Journal articles on the topic 'Hippocampus (brain)'
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1
Ismael, Saifudeen, Golnoush Mirzahosseini, Heba A. Ahmed, Arum Yoo, Modar Kassan, Kafait U. Malik, and Tauheed Ishrat. "Renin-Angiotensin System Alterations in the Human Alzheimer’s Disease Brain." Journal of Alzheimer's Disease 84, no. 4 (December 7, 2021): 1473–84. http://dx.doi.org/10.3233/jad-215051.
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Background: Understanding Alzheimer’s disease (AD) in terms of its various pathophysiological pathways is essential to unravel the complex nature of the disease process and identify potential therapeutic targets. The renin-angiotensin system (RAS) has been implicated in several brain diseases, including traumatic brain injury, ischemic stroke, and AD. Objective: This study was designed to evaluate the protein expression levels of RAS components in postmortem cortical and hippocampal brain samples obtained from AD versus non-AD individuals. Methods: We analyzed RAS components in the cortex and hippocampus of postmortem human brain samples by western blotting and immunohistochemical techniques in comparison with age-matched non-demented controls. Results: The expression of AT1R increased in the hippocampus, whereas AT2R expression remained almost unchanged in the cortical and hippocampal regions of AD compared to non-AD brains. The Mas receptor was downregulated in the hippocampus. We also detected slight reductions in ACE-1 protein levels in both the cortex and hippocampus of AD brains, with minor elevations in ACE-2 in the cortex. We did not find remarkable differences in the protein levels of angiotensinogen and Ang II in either the cortex or hippocampus of AD brains, whereas we observed a considerable increase in the expression of brain-derived neurotrophic factor in the hippocampus. Conclusion: The current findings support the significant contribution of RAS components in AD pathogenesis, further suggesting that strategies focusing on the AT1R and AT2R pathways may lead to novel therapies for the management of AD.
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Leskinen, Sandra, Harshal Shah, Morana Vojnic, Beril Yaffe, Shonna Schneider, Randy D'Amico, and A. Gabriella Wernicke. "RADT-03. A CASE OF PARTIAL HIPPOCAMPAL-AVOIDANCE WHOLE BRAIN RADIOTHERAPY IN A PATIENT WITH METASTATIC INFILTRATION OF THE LEFT HIPPOCAMPUS." Neuro-Oncology 25, Supplement_5 (November 1, 2023): v48. http://dx.doi.org/10.1093/neuonc/noad179.0192.
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Abstract In addition to surgical resection and systemic therapy, whole brain radiotherapy (WBRT) is a crucial modality in the treatment of cancers that have metastasized to the brain. It has been shown to improve intracranial disease control and overall survival. However, WBRT also increases the risk of radiation-associated damage to sensitive structures like the hippocampus, often resulting in neurocognitive dysfunction and decline. Hippocampal avoidance WBRT (HAWBRT) has been shown to reduce neurocognitive sequalae without worsening survival outcomes or increasing the risk of metastasis to the spared region compared to conventional WBRT. In cases where both hippocampi cannot be completely spared, the effectiveness of partial hippocampal avoidance on neurocognitive function and tumor control have been poorly described. We present the case of a patient diagnosed with triple negative invasive ductal carcinoma of the breast and disease metastatic to the brain, lung, bones, adrenal glands, and liver. Brain imaging revealed multiple brain metastases, two of which were noted near the left hippocampus. The patient underwent partial HAWBRT with complete avoidance of the right hippocampus and partial avoidance of the left. At 1-year follow-up, there was no evidence of metastasis in or near the partially spared left hippocampus. The patient’s neurocognitive functional status remained consistent with the findings of prospective randomized trials in which total bilateral hippocampal sparing was performed. To our knowledge, no such case has been presented in the literature. Further studies assessing the role of partial hippocampal avoidance in WBRT are needed.
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Spivak, Yulia S., Anna A. Karan, Yulia V. Dobryakova, Tatiana M. Medvedeva, Vladimir A. Markevich, and Alexey P. Bolshakov. "Deep Brain Stimulation of the Medial Septal Area Can Modulate Gene Expression in the Hippocampus of Rats under Urethane Anesthesia." International Journal of Molecular Sciences 23, no. 11 (May 27, 2022): 6034. http://dx.doi.org/10.3390/ijms23116034.
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We studied the effects of stimulation of the medial septal area on the gene expression in the dorsal and ventral hippocampus. Rats under urethane anesthesia were implanted with a recording electrode in the right hippocampus and stimulating electrode in the dorsal medial septum (dMS) or medial septal nucleus (MSN). After one-hour-long deep brain stimulation, we collected ipsi- and contralateral dorsal and ventral hippocampi. Quantitative PCR showed that deep brain stimulation did not cause any changes in the intact contralateral dorsal and ventral hippocampi. A comparison of ipsi- and contralateral hippocampi in the control unstimulated animals showed that electrode implantation in the ipsilateral dorsal hippocampus led to a dramatic increase in the expression of immediate early genes (c-fos, arc, egr1, npas4), neurotrophins (ngf, bdnf) and inflammatory cytokines (il1b and tnf, but not il6) not only in the area close to implantation site but also in the ventral hippocampus. Moreover, the stimulation of MSN but not dMS further increased the expression of c-fos, egr1, npas4, bdnf, and tnf in the ipsilateral ventral but not dorsal hippocampus. Our data suggest that the activation of medial septal nucleus can change the gene expression in ventral hippocampal cells after their priming by other stimuli.
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Goda, Jayant S., Debnarayan Dutta, Uday Krishna, Savita Goswami, Vikas Kothavade, Sadhna Kannan, Madan Maitre, Nazia Bano, Tejpal Gupta, and Rakesh Jalali. "Hippocampal radiotherapy dose constraints for predicting long-term neurocognitive outcomes: mature data from a prospective trial in young patients with brain tumors." Neuro-Oncology 22, no. 11 (March 30, 2020): 1677–85. http://dx.doi.org/10.1093/neuonc/noaa076.
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Abstract Background Hippocampus is considered to be the seat for neurocognitive functions. Avoidance of hippocampus during radiotherapy to brain may serve to preserve various domains of neurocognition. We aimed to derive radiotherapy dose constraints to hippocampi for preserving neurocognition in young patients with brain tumors by measuring various neurocognitive parameters. Methods Forty-eight patients with residual/progressive benign or low-grade brain tumors treated with stereotactic conformal radiotherapy (SCRT) to a dose of 54 Gy in 30 fractions underwent prospective neuropsychological assessments at baseline before SCRT and at 6 months and 2, 3, 4, and 5 years. Hippocampi were drawn as per the Radiation Therapy Oncology Group atlas. Longitudinal change in intelligence quotient scores was correlated with hippocampal doses. Results Mean volume of bilateral hippocampi was 4.35 cc (range: 2.12–8.41 cc). Craniopharyngioma was the commonest histologic subtype. A drop of >10% in mean full-scale intelligence quotient (FSIQ) scores at 3 and 5 years post SCRT was observed in patients in whom left hippocampus received a mean dose of 30.7 Gy (P = 0.04) and 31 Gy (P = 0.04), respectively. Mean performance quotient (PQ) scores dropped > 10% at 5 years when the left hippocampus received a dose of > 32 Gy (P = 0.03). There was no significant correlation of radiotherapy doses with verbal quotient, or with doses received by the right hippocampus. Multivariate analysis revealed young age (<13 y) and left hippocampus dose predicted for clinically relevant decline in certain neurocognitive domains. Conclusions A mean dose of ≤30 Gy to the left hippocampus as a dose constraint for preserving intelligence quotient is suggested. Key Points 1. Children and young adults with benign and low-grade gliomas survive long after therapy. 2. Higher dose to the hippocampi may result in long-term neurocognitive impairment. 3. Mean dose of <30 Gy to left hippocampus could be used as a pragmatic dose constraint to prevent long-term neurocognitive decline.
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Kazda, Tomas, Adela Misove, Petr Burkon, Petr Pospisil, Ludmila Hynkova, Iveta Selingerova, Adam Dziacky, et al. "Incidence of Hippocampal Metastases: Laterality and Implications for Unilateral Hippocampal Avoiding Whole Brain Radiotherapy." BioMed Research International 2018 (December 13, 2018): 1–7. http://dx.doi.org/10.1155/2018/2459608.
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Introduction. Hippocampi sparing whole brain radiotherapy (WBRT) is an evolving approach in the treatment of patients with multiple brain metastases, pursuing mitigation of verbal memory decline as a consequence of hippocampal radiation injury. Accumulating data are showing different postradiotherapy changes in the left and right hippocampus with a theoretical proposal of only unilateral (dominant, left) hippocampal sparing during WBRT. Method. The aim of this retrospective study is to describe spatial distribution of brain metastases on MRI in a cohort of 260 patients (2595 metastases) and to evaluate distribution separately in the left and right hippocampus and in respective hippocampal avoiding zones (HAZ, region with subtherapeutic radiation dose), including evaluation of location of metastatic mass centre. Results. The median number of brain metastases was three, with lung cancer being the most common type of primary tumour; 36% had single metastasis. Almost 8% of patients had metastasis within hippocampus (1.1% of all metastases) and 18.1% of patients within HAZ (3.3% of all metastases). No statistically significant difference was observed in the laterality of hippocampal involvement, also when the location of centre of metastases was analyzed. There were more patients presenting the centre of metastasis within left (15) versus right (6) HAZ approaching the borderline of statistical significance. Conclusion. No significant difference in the laterality of BM seeding within hippocampal structures was observed. The hypothesized unilateral sparing WBRT would have theoretical advantage in about 50% reduction in the risk of subsequent recurrence within spared regions.
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Henin, Simon, Anita Shankar, Helen Borges, Adeen Flinker, Werner Doyle, Daniel Friedman, Orrin Devinsky, György Buzsáki, and Anli Liu. "Spatiotemporal dynamics between interictal epileptiform discharges and ripples during associative memory processing." Brain 144, no. 5 (April 23, 2021): 1590–602. http://dx.doi.org/10.1093/brain/awab044.
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Abstract We describe the spatiotemporal course of cortical high-gamma activity, hippocampal ripple activity and interictal epileptiform discharges during an associative memory task in 15 epilepsy patients undergoing invasive EEG. Successful encoding trials manifested significantly greater high-gamma activity in hippocampus and frontal regions. Successful cued recall trials manifested sustained high-gamma activity in hippocampus compared to failed responses. Hippocampal ripple rates were greater during successful encoding and retrieval trials. Interictal epileptiform discharges during encoding were associated with 15% decreased odds of remembering in hippocampus (95% confidence interval 6–23%). Hippocampal interictal epileptiform discharges during retrieval predicted 25% decreased odds of remembering (15–33%). Odds of remembering were reduced by 25–52% if interictal epileptiform discharges occurred during the 500–2000 ms window of encoding or by 41% during retrieval. During encoding and retrieval, hippocampal interictal epileptiform discharges were followed by a transient decrease in ripple rate. We hypothesize that interictal epileptiform discharges impair associative memory in a regionally and temporally specific manner by decreasing physiological hippocampal ripples necessary for effective encoding and recall. Because dynamic memory impairment arises from pathological interictal epileptiform discharge events competing with physiological ripples, interictal epileptiform discharges represent a promising therapeutic target for memory remediation in patients with epilepsy.
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Davidson, Terry L., and Richard J. Stevenson. "Vulnerability of the Hippocampus to Insults: Links to Blood–Brain Barrier Dysfunction." International Journal of Molecular Sciences 25, no. 4 (February 6, 2024): 1991. http://dx.doi.org/10.3390/ijms25041991.
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The hippocampus is a critical brain substrate for learning and memory; events that harm the hippocampus can seriously impair mental and behavioral functioning. Hippocampal pathophysiologies have been identified as potential causes and effects of a remarkably diverse array of medical diseases, psychological disorders, and environmental sources of damage. It may be that the hippocampus is more vulnerable than other brain areas to insults that are related to these conditions. One purpose of this review is to assess the vulnerability of the hippocampus to the most prevalent types of insults in multiple biomedical domains (i.e., neuroactive pathogens, neurotoxins, neurological conditions, trauma, aging, neurodegenerative disease, acquired brain injury, mental health conditions, endocrine disorders, developmental disabilities, nutrition) and to evaluate whether these insults affect the hippocampus first and more prominently compared to other brain loci. A second purpose is to consider the role of hippocampal blood–brain barrier (BBB) breakdown in either causing or worsening the harmful effects of each insult. Recent research suggests that the hippocampal BBB is more fragile compared to other brain areas and may also be more prone to the disruption of the transport mechanisms that act to maintain the internal milieu. Moreover, a compromised BBB could be a factor that is common to many different types of insults. Our analysis indicates that the hippocampus is more vulnerable to insults compared to other parts of the brain, and that developing interventions that protect the hippocampal BBB may help to prevent or ameliorate the harmful effects of many insults on memory and cognition.
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Zhang, Jia-He, Takashi Tasaki, Manabu Tsukamoto, Ke-Yong Wang, Kin-ya Kubo, and Kagaku Azuma. "Deletion of Wnt10a Is Implicated in Hippocampal Neurodegeneration in Mice." Biomedicines 10, no. 7 (June 25, 2022): 1500. http://dx.doi.org/10.3390/biomedicines10071500.
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The hippocampus plays an important role in maintaining normal cognitive function and is closely associated with the neuropathogenesis of dementia. Wnt signaling is relevant to neuronal development and maturation, synaptic formation, and plasticity. The role of Wnt10a in hippocampus-associated cognition, however, is largely unclear. Here, we examined the morphological and functional alterations in the hippocampus of Wnt10a-knockout (Wnt10a-/-) mice. Neurobehavioral tests revealed that Wnt10a-/- mice exhibited spatial memory impairment and anxiety-like behavior. Immunostaining and Western blot findings showed that the protein expressions of β-catenin, brain-derived neurotrophic factor, and doublecortin were significantly decreased and that the number of activated microglia increased, accompanied by amyloid-β accumulation, synaptic dysfunction, and microglia-associated neuroinflammation in the hippocampi of Wnt10a-/- mice. Our findings revealed that the deletion of Wnt10a decreased neurogenesis, impaired synaptic function, and induced hippocampal neuroinflammation, eventually leading to hippocampal neurodegeneration and memory deficit, possibly through the β-catenin signaling pathway, providing a novel insight into preventive approaches for hippocampus-dependent cognitive impairment.
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Zhang, X.-D., L.-R. Zhao, J.-M. Zhou, Y.-Y. Su, J. Ke, Y. Cheng, J.-L. Li, and W. Shen. "Altered hippocampal functional connectivity in primary Sjögren syndrome: a resting-state fMRI study." Lupus 29, no. 5 (February 19, 2020): 446–54. http://dx.doi.org/10.1177/0961203320908936.
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Structural and metabolic abnormalities in the hippocampus have been associated with the pathophysiological mechanism of central nervous system involvement in primary Sjögren syndrome (pSS). Nevertheless, how hippocampal function is altered in pSS remains unknown. The purpose of our study is to investigate the alterations in hippocampal functional connectivity (FC) in pSS by using resting-state functional magnetic resonance imaging (rs-fMRI). Thirty-eight patients with pSS and 38 age- and education level-matched healthy controls (HCs) underwent magnetic resonance imaging examination. Prior to each MRI examination, neuropsychological tests were performed. Left and right hippocampal FCs were analyzed by using seed-based whole-brain correlation and compared between pSS and HCs. Spearman correlation analysis was performed between the z-value of hippocampal FC in brain regions with significant difference between the two groups and neuropsychological tests/clinical data in pSS. Compared with the controls, the patients with pSS showed decreased hippocampal FC between the left hippocampus and the right inferior occipital gray (IOG)/inferior temporal gray (ITG), as well as between the right hippocampus and right IOG/middle occipital gray (MOG), left MOG, and left middle temporal gray. In addition, increased hippocampal FCs were detected between the left hippocampus and left putamen, as well as between the right hippocampus and right cerebellum posterior lobe. Moreover, the visual reproduction score positively correlated with the FC between right hippocampus and right IOG/MOG. The white matter hyperintensity score negatively correlated with the FC between left hippocampus and right IOG/ITG. In conclusion, patients with pSS suffered decreased hippocampal FC mainly sited in the occipital and temporal cortex with right hippocampal laterality. Altered hippocampal FC might be a potential biomarker in detecting brain function changes and guiding neuroprotection in pSS.
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Perosa, Valentina, Anastasia Priester, Gabriel Ziegler, Arturo Cardenas-Blanco, Laura Dobisch, Marco Spallazzi, Anne Assmann, et al. "Hippocampal vascular reserve associated with cognitive performance and hippocampal volume." Brain 143, no. 2 (January 29, 2020): 622–34. http://dx.doi.org/10.1093/brain/awz383.
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Abstract Medial temporal lobe dependent cognitive functions are highly vulnerable to hypoxia in the hippocampal region, yet little is known about the relationship between the richness of hippocampal vascular supply and cognition. Hippocampal vascularization patterns have been categorized into a mixed supply from both the posterior cerebral artery and the anterior choroidal artery or a single supply by the posterior cerebral artery only. Hippocampal arteries are small and affected by pathological changes when cerebral small vessel disease is present. We hypothesized, that hippocampal vascularization patterns may be important trait markers for vascular reserve and modulate (i) cognitive performance; (ii) structural hippocampal integrity; and (iii) the effect of cerebral small vessel disease on cognition. Using high-resolution 7 T time-of-flight angiography we manually classified hippocampal vascularization patterns in older adults with and without cerebral small vessel disease in vivo. The presence of a mixed supplied hippocampus was an advantage in several cognitive domains, including verbal list learning and global cognition. A mixed supplied hippocampus also was an advantage for verbal memory performance in cerebral small vessel disease. Voxel-based morphometry showed higher anterior hippocampal grey matter volume in mixed, compared to single supply. We discuss that a mixed hippocampal supply, as opposed to a single one, may increase the reliability of hippocampal blood supply and thereby provide a hippocampal vascular reserve that protects against cognitive impairment.
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Romagnoli, Martina, Elisa Porcellini, Ilaria Carbone, Robert Veerhuis, and Federico Licastro. "Impaired Innate Immunity Mechanisms in the Brain of Alzheimer’s Disease." International Journal of Molecular Sciences 21, no. 3 (February 8, 2020): 1126. http://dx.doi.org/10.3390/ijms21031126.
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Among environmental factors likely associated with Alzheimer’s disease (AD), persistent virus infections, and age-related progressive decline of immune competence might play a pivotal role. However, AD antimicrobial brain immune responses are poorly investigated. The present study focused on genes involved in antimicrobial defenses, especially against virus infections, in the AD brain. In particular, mRNA levels of IRF7, MED23, IL28B, and IFN-α genes were analyzed in hippocampus and temporal cortex brain samples from AD and non-demented controls. All subjects were also genotyped for APOE ε, IRF7, MED23, and IL28B gene polymorphisms. Most AD patients showed decreased mRNA levels of all investigated genes in the hippocampus and temporal cortex. However, a small group of AD patients showed increased hippocampal mRNA expression of MED23, IL28B, and IFN-α. mRNA levels of MED23, IL28B, IFN-α from the hippocampus and those of MED23 from the temporal cortex were further decreased in APOE ε4 allele AD carriers. Moreover, rs6598008 polymorphism of IRF7 was significantly associated with decreased hippocampal expression of IRF7, MED23, IL28B, and IFN-α. These findings suggest that AD brains show impaired innate antimicrobial gene expression profiles, and individual genetic makeup, such as positivity for the APOE ε4 and IRF7 A alleles, might affect brain immune efficiency.
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Green, C. R., L. T. Watts, S. M. Kobus, G. I. Henderson, J. N. Reynolds, and J. F. Brien. "Effects of chronic prenatal ethanol exposure on mitochondrial glutathione and 8-iso-prostaglandin F2α concentrations in the hippocampus of the perinatal guinea pig." Reproduction, Fertility and Development 18, no. 5 (2006): 517. http://dx.doi.org/10.1071/rd05128.
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It is hypothesised that oxidative stress is a key mechanism of ethanol neurobehavioural teratogenicity, resulting in altered endogenous antioxidant status and increased membrane lipid peroxidation in the hippocampus of chronic prenatal ethanol exposure (CPEE) offspring. To test this hypothesis, timed pregnant guinea-pigs (term, approximately gestational day (GD) 68) received chronic daily oral administration of (i) 4 g ethanol kg–1 maternal bodyweight, (ii) isocaloric sucrose with pair feeding, or (iii) water. At GD 65 (term fetus) and postnatal day (PD) 0 (neonate), individual offspring were killed, the brain was excised and the hippocampi were dissected. Glutathione (GSH) concentration was measured in the cytosolic and mitochondrial fractions of hippocampal homogenate. The occurrence of lipid peroxidation was determined by measuring the concentration of 8-iso-prostaglandin F2α (8-iso-PGF2α). There was CPEE-induced decreased brain weight and hippocampal weight at GD 65 and PD 0, decreased mitochondrial GSH concentration in the hippocampus at PD 0, with no change in mitochondrial GSH concentration at GD 65 or cytosolic GSH concentration at GD 65 or PD 0, and no change in mitochondrial or whole-homogenate 8-iso-PGF2α concentration in the hippocampus at GD 65 or PD 0. The data demonstrate that CPEE produces selective mitochondrial dysfunction in the hippocampus of the neonatal guinea-pig, involving GSH depletion.
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Stojanovic, Tamara, David Velarde Gamez, Gabor Jorrid Schuld, Daniel Bormann, Maureen Cabatic, Pavel Uhrin, Gert Lubec, and Francisco J. Monje. "Age-Dependent and Pathway-Specific Bimodal Action of Nicotine on Synaptic Plasticity in the Hippocampus of Mice Lacking the miR-132/212 Genes." Cells 11, no. 2 (January 13, 2022): 261. http://dx.doi.org/10.3390/cells11020261.
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Nicotine addiction develops predominantly during human adolescence through smoking. Self-administration experiments in rodents verify this biological preponderance to adolescence, suggesting evolutionary-conserved and age-defined mechanisms which influence the susceptibility to nicotine addiction. The hippocampus, a brain region linked to drug-related memory storage, undergoes major morpho-functional restructuring during adolescence and is strongly affected by nicotine stimulation. However, the signaling mechanisms shaping the effects of nicotine in young vs. adult brains remain unclear. MicroRNAs (miRNAs) emerged recently as modulators of brain neuroplasticity, learning and memory, and addiction. Nevertheless, the age-dependent interplay between miRNAs regulation and hippocampal nicotinergic signaling remains poorly explored. We here combined biophysical and pharmacological methods to examine the impact of miRNA-132/212 gene-deletion (miRNA-132/212−/−) and nicotine stimulation on synaptic functions in adolescent and mature adult mice at two hippocampal synaptic circuits: the medial perforant pathway (MPP) to dentate yrus (DG) synapses (MPP-DG) and CA3 Schaffer collaterals to CA1 synapses (CA3–CA1). Basal synaptic transmission and short-term (paired-pulse-induced) synaptic plasticity was unaltered in adolescent and adult miRNA-132/212−/− mice hippocampi, compared with wild-type controls. However, nicotine stimulation promoted CA3–CA1 synaptic potentiation in mature adult (not adolescent) wild-type and suppressed MPP-DG synaptic potentiation in miRNA-132/212−/− mice. Altered levels of CREB, Phospho-CREB, and acetylcholinesterase (AChE) expression were further detected in adult miRNA-132/212−/− mice hippocampi. These observations propose miRNAs as age-sensitive bimodal regulators of hippocampal nicotinergic signaling and, given the relevance of the hippocampus for drug-related memory storage, encourage further research on the influence of miRNAs 132 and 212 in nicotine addiction in the young and the adult brain.
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Komoltsev, Ilia G., and Natalia V. Gulyaeva. "Brain Trauma, Glucocorticoids and Neuroinflammation: Dangerous Liaisons for the Hippocampus." Biomedicines 10, no. 5 (May 15, 2022): 1139. http://dx.doi.org/10.3390/biomedicines10051139.
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Glucocorticoid-dependent mechanisms of inflammation-mediated distant hippocampal damage are discussed with a focus on the consequences of traumatic brain injury. The effects of glucocorticoids on specific neuronal populations in the hippocampus depend on their concentration, duration of exposure and cell type. Previous stress and elevated level of glucocorticoids prior to pro-inflammatory impact, as well as long-term though moderate elevation of glucocorticoids, may inflate pro-inflammatory effects. Glucocorticoid-mediated long-lasting neuronal circuit changes in the hippocampus after brain trauma are involved in late post-traumatic pathology development, such as epilepsy, depression and cognitive impairment. Complex and diverse actions of the hypothalamic–pituitary–adrenal axis on neuroinflammation may be essential for late post-traumatic pathology. These mechanisms are applicable to remote hippocampal damage occurring after other types of focal brain damage (stroke, epilepsy) or central nervous system diseases without obvious focal injury. Thus, the liaisons of excessive glucocorticoids/dysfunctional hypothalamic–pituitary–adrenal axis with neuroinflammation, dangerous to the hippocampus, may be crucial to distant hippocampal damage in many brain diseases. Taking into account that the hippocampus controls both the cognitive functions and the emotional state, further research on potential links between glucocorticoid signaling and inflammatory processes in the brain and respective mechanisms is vital.
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Sudarman, A. Gunawan Santoso, Fatimah, Rasyid, and Leny Latifah. "Volumetric Hippocampal Magnetic Resonance Imaging and Electroenchepalogram OF Epilepsy." International Journal of Advanced Technology and Social Sciences 2, no. 2 (February 29, 2024): 255–70. http://dx.doi.org/10.59890/ijatss.v2i2.1433.
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Hippocampal volumetry is a method of measuring the volume or size of hippocampal structures in the brain, can be used as a diagnostic aid and monitoring of disease progression conditions or neurological disorders as well as response to treatment. Analyze volumetric measurement of Hippocampus MRI examination Brain 3D T2 FSE with EEG study results in cases of Epilepsy. Patient data was obtained through MRI examination of Brain 3D T2 FSE to measure volumetric hippocampus. These volumetric results are compared with EEG interpretation in cases of epilepsy. Statistical analysis was performed to identify the correlation between volumetric changes in the hippocampus and EEG results. There was no difference in the volume of the left hippocampus smaller than the right based on MRI measurements of Brain 3D T2 FSE in cases of epilepsy. Most (77.27%) shrank right and left. Left lobe temporal brain wave images in all epilepsy patients with irregular ups and downs show abnormalities based on EEG measurements. Brain wave images of the right temporal lobe in epilepsy patients are all normal. Volumetric imaging for epileptic patients cannot establish the diagnosis of epilepsy, because it cannot show an sensibility between the left and right hemisper images
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Konopka-Filippow, Monika, Ewa Sierko, Dominika Hempel, Rafał Maksim, Natalia Samołyk-Kogaczewska, Tomasz Filipowski, Ewa Rożkowska, et al. "The Learning Curve and Inter-Observer Variability in Contouring the Hippocampus under the Hippocampal Sparing Guidelines of Radiation Therapy Oncology Group 0933." Current Oncology 29, no. 4 (April 8, 2022): 2564–74. http://dx.doi.org/10.3390/curroncol29040210.
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Hippocampal-sparing brain radiotherapy (HS-BRT) in cancer patients results in preservation of neurocognitive function after brain RT which can contribute to patients’ quality of life (QoL). The crucial element in HS-BRT treatment planning is appropriate contouring of the hippocampus. Ten doctors delineated the left and right hippocampus (LH and RH, respectively) on 10 patients’ virtual axial images of brain CT fused with T1-enhanced MRI (1 mm) according to the RTOG 0933 atlas recommendations. Variations in the spatial localization of the structure were described in three directions: right–left (X), cranio-caudal (Y), and forward–backward (Z). Discrepancies concerned three-dimensional localization, shape, volume and size of the hippocampus. The largest differences were observed in the first three delineated cases which were characterized by larger hippocampal volumes than the remaining seven cases. The volumes of LH of more than half of hippocampus contours were marginally bigger than those of RH. Most differences in delineation of the hippocampus were observed in the area of the posterior horn of the lateral ventricle. Conversely, a large number of hippocampal contours overlapped near the brainstem and the anterior horn of the lateral ventricle. The most problematic area of hippocampal contouring is the posterior horn of the lateral ventricle. Training in the manual contouring of the hippocampus during HS-BRT treatment planning under the supervision of experienced radiation oncologists is necessary to achieve optimal outcomes. This would result in superior outcomes of HS-BRT treatment and improvement in QoL of patients compared to without HS-BRT procedure. Correct delineation of the hippocampus is problematic. This study demonstrates difficulties in HS-BRT treatment planning and highlights critical points during hippocampus delineation.
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Cardilini, Adam P. A., Sarah Micallef, Valerie R. Bishop, Craig D. H. Sherman, Simone L. Meddle, and Katherine L. Buchanan. "Environmental Influences on Neuromorphology in the Non-Native Starling Sturnus vulgaris." Brain, Behavior and Evolution 92, no. 1-2 (2018): 63–70. http://dx.doi.org/10.1159/000491672.
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Cognitive traits are predicted to be under intense selection in animals moving into new environments and may determine the success, or otherwise, of dispersal and invasions. In particular, spatial information related to resource distribution is an important determinant of neural development. Spatial information is predicted to vary for invasive species encountering novel environments. However, few studies have tested how cognition or neural development varies intraspecifically within an invasive species. In Australia, the non-native common starling Sturnus vulgaris inhabits a range of habitats that vary in seasonal resource availability and distribution. We aimed to identify variations in the brain mass and hippocampus volume of starlings in Australia related to environmental variation across two substantially different habitat types. Specifically, we predicted variation in brain mass and hippocampal volume in relation to environmental conditions, latitude, and climatic variables. To test this, brain mass and volumes of the hippocampus and two control brain regions (telencephalon and tractus septomesencephalicus) were quantified from starling brains gathered from across the species’ range in south eastern Australia. When comparing across an environmental gradient, there was a significant interaction between sex and environment for overall brain mass, with greater sexual dimorphism in brain mass in inland populations compared to those at the coast. There was no significant difference in hippocampal volume in relation to environmental measures (hippocampus volume, n = 17) for either sex. While these data provide no evidence for intraspecific environmental drivers for changes in hippocampus volume in European starlings in Australia, they do suggest that environmental factors contribute to sex differences in brain mass. This study identifies associations between the brain volume of a non-native species and the environment; further work in this area is required to elucidate the mechanisms driving this relationship.
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Miura, Kosei, Hiromasa Kurosaki, Nobuko Utsumi, and Hideyuki Sakurai. "Use of a Head-Tilting Baseplate During Tomotherapy to Shorten the Irradiation Time and Protect the Hippocampus and Lens in Hippocampal Sparing-Whole Brain Radiotherapy." Technology in Cancer Research & Treatment 20 (January 1, 2021): 153303382098682. http://dx.doi.org/10.1177/1533033820986824.
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Purpose: The aim of this study is to comparatively examine the possibility of reducing the exposure dose to organs at risk, such as the hippocampus and lens, and improving the dose distribution of the planned target volume with and without the use of a head-tilting base plate in hippocampal-sparing whole-brain radiotherapy using tomotherapy. Methods: Five paired images of planned head computed tomography without and with tilt were analyzed. The hippocampus and planning target volume were contoured according to the RTOG 0933 contouring atlas protocol. The hippocampal zone to be avoided was delineated using a 5-mm margin. The prescribed radiation dose was 30 Gy in 10 fractions. The absorbed dose to planning target volume dose, absorbed dose to the organ at risk, and irradiation time were evaluated. The paired t-test was used to analyze the differences between hippocampal-sparing whole-brain radiotherapy with head tilts and without head tilts. Results: Hippocampal-sparing whole-brain radiotherapy with tilt was not superior in planning target volume doses using the homogeneity index than that without tilt; however, it showed better values, and for Dmean and D2%, the values were closer to 30 Gy. Regarding the hippocampus, dose reduction with tilt was significantly greater at Dmax, Dmean, and Dmin, whereas regarding the lens, it was significantly greater at Dmax and Dmin. The irradiation time was also predominantly shorter. Conclusion: In our study, a tilted hippocampal-sparing whole-brain radiotherapy reduced the irradiation time by >10%. Therefore, our study indicated that hippocampal-sparing whole-brain radiotherapy with tomotherapy should be performed with a tilt. The head-tilting technique might be useful during hippocampal-sparing whole-brain radiotherapy. This method could decrease the radiation exposure time, while sparing healthy organs, including the hippocampus and lens.
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Kouhnavardi, Shima, Maureen Cabatic, M. Carmen Mañas-Padilla, Marife-Astrid Malabanan, Tarik Smani, Ana Cicvaric, Edison Alejandro Muñoz Aranzalez, et al. "miRNA-132/212 Deficiency Disrupts Selective Corticosterone Modulation of Dorsal vs. Ventral Hippocampal Metaplasticity." International Journal of Molecular Sciences 24, no. 11 (May 31, 2023): 9565. http://dx.doi.org/10.3390/ijms24119565.
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Cortisol is a potent human steroid hormone that plays key roles in the central nervous system, influencing processes such as brain neuronal synaptic plasticity and regulating the expression of emotional and behavioral responses. The relevance of cortisol stands out in the disease, as its dysregulation is associated with debilitating conditions such as Alzheimer’s Disease, chronic stress, anxiety and depression. Among other brain regions, cortisol importantly influences the function of the hippocampus, a structure central for memory and emotional information processing. The mechanisms fine-tuning the different synaptic responses of the hippocampus to steroid hormone signaling remain, however, poorly understood. Using ex vivo electrophysiology and wild type (WT) and miR-132/miR-212 microRNAs knockout (miRNA-132/212−/−) mice, we examined the effects of corticosterone (the rodent’s equivalent to cortisol in humans) on the synaptic properties of the dorsal and ventral hippocampus. In WT mice, corticosterone predominantly inhibited metaplasticity in the dorsal WT hippocampi, whereas it significantly dysregulated both synaptic transmission and metaplasticity at dorsal and ventral regions of miR–132/212−/− hippocampi. Western blotting further revealed significantly augmented levels of endogenous CREB and a significant CREB reduction in response to corticosterone only in miR–132/212−/− hippocampi. Sirt1 levels were also endogenously enhanced in the miR–132/212−/− hippocampi but unaltered by corticosterone, whereas the levels of phospo-MSK1 were only reduced by corticosterone in WT, not in miR–132/212−/− hippocampi. In behavioral studies using the elevated plus maze, miRNA-132/212−/− mice further showed reduced anxiety-like behavior. These observations propose miRNA-132/212 as potential region-selective regulators of the effects of steroid hormones on hippocampal functions, thus likely fine-tuning hippocampus-dependent memory and emotional processing.
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Dexte, Micki. "Brain Atrophy Rates in Normal Aging and Alzheimer Disease." Neuroscience and Neurological Surgery 1, no. 1 (February 27, 2017): 01–02. http://dx.doi.org/10.31579/2578-8868/009.
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The objectives of this study were to (1) compare atrophy rates associated with normal aging and Alzheimer disease (AD) using the semi-automated Boundary Shift Integral (BSI) method and manual tracing of the entorhinal cortex (ERC) and hippocampus and (2) calculate power of BSI vs. ERC and hippocampal volume changes for clinical trials in AD. We quantified whole brain and ventricular BSI atrophy rates and ERC and hippocampal atrophy rates from longitudinal MRI data in 20 AD patients and 22 age-matched healthy controls.
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Dexte, Micki. "Brain Atrophy Rates in Normal Aging and Alzheimer Disease." Neuroscience and Neurological Surgery 1, no. 1 (February 27, 2017): 01–02. http://dx.doi.org/10.31579/2578-8868/009.
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The objectives of this study were to (1) compare atrophy rates associated with normal aging and Alzheimer disease (AD) using the semi-automated Boundary Shift Integral (BSI) method and manual tracing of the entorhinal cortex (ERC) and hippocampus and (2) calculate power of BSI vs. ERC and hippocampal volume changes for clinical trials in AD. We quantified whole brain and ventricular BSI atrophy rates and ERC and hippocampal atrophy rates from longitudinal MRI data in 20 AD patients and 22 age-matched healthy controls.
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Crum, W. R., F. Danckaers, T. Huysmans, M. C. Cotel, S. Natesan, M. M. Modo, J. Sijbers, S. C. R. Williams, S. Kapur, and A. C. Vernon. "Chronic exposure to haloperidol and olanzapine leads to common and divergent shape changes in the rat hippocampus in the absence of grey-matter volume loss." Psychological Medicine 46, no. 15 (August 12, 2016): 3081–93. http://dx.doi.org/10.1017/s0033291716001768.
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BackgroundOne of the most consistently reported brain abnormalities in schizophrenia (SCZ) is decreased volume and shape deformation of the hippocampus. However, the potential contribution of chronic antipsychotic medication exposure to these phenomena remains unclear.MethodWe examined the effect of chronic exposure (8 weeks) to clinically relevant doses of either haloperidol (HAL) or olanzapine (OLZ) on adult rat hippocampal volume and shape using ex vivo structural MRI with the brain retained inside the cranium to prevent distortions due to dissection, followed by tensor-based morphometry (TBM) and elastic surface-based shape deformation analysis. The volume of the hippocampus was also measured post-mortem from brain tissue sections in each group.ResultsChronic exposure to either HAL or OLZ had no effect on the volume of the hippocampus, even at exploratory thresholds, which was confirmed post-mortem. In contrast, shape deformation analysis revealed that chronic HAL and OLZ exposure lead to both common and divergent shape deformations (q = 0.05, FDR-corrected) in the rat hippocampus. In particular, in the dorsal hippocampus, HAL exposure led to inward shape deformation, whereas OLZ exposure led to outward shape deformation. Interestingly, outward shape deformations that were common to both drugs occurred in the ventral hippocampus. These effects remained significant after controlling for hippocampal volume suggesting true shape changes.ConclusionsChronic exposure to either HAL or OLZ leads to both common and divergent effects on rat hippocampal shape in the absence of volume change. The implications of these findings for the clinic are discussed.
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Chandra, Sawarya. "Hippocampus Prosthesis for Memory Impairment." International Journal for Research in Applied Science and Engineering Technology 11, no. 7 (July 31, 2023): 526–34. http://dx.doi.org/10.22214/ijraset.2023.54431.
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Abstract: Hippocampus is the area of the brain that is vital for functions as learning, memory and mood setting. It also reacts to injury or neurodegeneration with robust plasticity. Damage to the hippocampus leads to loss of ability to convert short-term memory to new long-term memories. This can happen due to epilepsy, stroke, dimentia or head injuries. Hippocampal injuries typically lead to cognitive dysfunction, depression, and/or epilepsy. Neural stem cell grafting early after injury has promise for preventing neurological deficits. It modulates aberrant hippocampal post-injury plasticity.and adds new inhibitory GABA-ergic interneurons into the hippocampus. Hippocampal memory prosthesis is a Brain Machine Interface (BMI) device developed for restoring or enhancing memory functions. The objective is to restore the long-term memory function in a stimulus-specific manner by using a multi-input, multi-output (MIMO) nonlinear dynamical model which might serve as a boon for patients suffering from Alzheimer’s disease.
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Hristova, Katerina, Cristina Martinez-Gonzalez, Thomas C. Watson, Neela K. Codadu, Kevan Hashemi, Peter C. Kind, Matthew F. Nolan, and Alfredo Gonzalez-Sulser. "Medial septal GABAergic neurons reduce seizure duration upon optogenetic closed-loop stimulation." Brain 144, no. 5 (March 26, 2021): 1576–89. http://dx.doi.org/10.1093/brain/awab042.
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Abstract Seizures can emerge from multiple or large foci in temporal lobe epilepsy, complicating focally targeted strategies such as surgical resection or the modulation of the activity of specific hippocampal neuronal populations through genetic or optogenetic techniques. Here, we evaluate a strategy in which optogenetic activation of medial septal GABAergic neurons, which provide extensive projections throughout the hippocampus, is used to control seizures. We utilized the chronic intrahippocampal kainate mouse model of temporal lobe epilepsy, which results in spontaneous seizures and as is often the case in human patients, presents with hippocampal sclerosis. Medial septal GABAergic neuron populations were immunohistochemically labelled and were not reduced in epileptic conditions. Genetic labelling with mRuby of medial septal GABAergic neuron synaptic puncta and imaging across the rostral to caudal extent of the hippocampus, also indicated an unchanged number of putative synapses in epilepsy. Furthermore, optogenetic stimulation of medial septal GABAergic neurons consistently modulated oscillations across multiple hippocampal locations in control and epileptic conditions. Finally, wireless optogenetic stimulation of medial septal GABAergic neurons, upon electrographic detection of spontaneous hippocampal seizures, resulted in reduced seizure durations. We propose medial septal GABAergic neurons as a novel target for optogenetic control of seizures in temporal lobe epilepsy.
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Chan, Russell W., Alex T. L. Leong, Leon C. Ho, Patrick P. Gao, Eddie C. Wong, Celia M. Dong, Xunda Wang, et al. "Low-frequency hippocampal–cortical activity drives brain-wide resting-state functional MRI connectivity." Proceedings of the National Academy of Sciences 114, no. 33 (July 31, 2017): E6972—E6981. http://dx.doi.org/10.1073/pnas.1703309114.
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The hippocampus, including the dorsal dentate gyrus (dDG), and cortex engage in bidirectional communication. We propose that low-frequency activity in hippocampal–cortical pathways contributes to brain-wide resting-state connectivity to integrate sensory information. Using optogenetic stimulation and brain-wide fMRI and resting-state fMRI (rsfMRI), we determined the large-scale effects of spatiotemporal-specific downstream propagation of hippocampal activity. Low-frequency (1 Hz), but not high-frequency (40 Hz), stimulation of dDG excitatory neurons evoked robust cortical and subcortical brain-wide fMRI responses. More importantly, it enhanced interhemispheric rsfMRI connectivity in various cortices and hippocampus. Subsequent local field potential recordings revealed an increase in slow oscillations in dorsal hippocampus and visual cortex, interhemispheric visual cortical connectivity, and hippocampal–cortical connectivity. Meanwhile, pharmacological inactivation of dDG neurons decreased interhemispheric rsfMRI connectivity. Functionally, visually evoked fMRI responses in visual regions also increased during and after low-frequency dDG stimulation. Together, our results indicate that low-frequency activity robustly propagates in the dorsal hippocampal–cortical pathway, drives interhemispheric cortical rsfMRI connectivity, and mediates visual processing.
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Velakoulis, Dennis, Stephen J. Wood, Patrick D. McGorry, and Christos Pantelis. "Evidence for Progression of Brain Structural Abnormalities in Schizophrenia: Beyond the Neurodevelopmental Model." Australian & New Zealand Journal of Psychiatry 34, no. 1_suppl (February 2000): A113—A126. http://dx.doi.org/10.1177/000486740003401s17.
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Objective Clinical, neuroimaging, neuropathological and neuropsychological evidence suggests that, in schizophrenia, there is structural and functional disturbance of the hippocampus. The purpose of this paper is to present published findings concerning the nature, timing and course of these putative disturbances of hippocampal function and the pathophysiological mechanisms involved, and to explore whether schizophrenia is a disorder of neurodevelopment, neurodegeneration or a combination of both processes. Method The available cross-sectional and longitudinal evidence for hippocampal involvement in schizophrenia is reviewed and a model of hippocampal involvement in this disorder, which derives from our own cross-sectional and longitudinal hippocampal imaging data, is described. Results We propose a three-hit model in which an early neurodevelopmental lesion renders the hippocampus vulnerable to further insult later in life during the transition phase to active illness. The available evidence suggests that the left hippocampus is particularly vulnerable during these early stages, while further insult involving the hippocampus bilaterally occurs in those who develop a chronic form of the illness. Conclusions Intervention strategies should target the most vulnerable stages of the illness, in particular the transition phase to psychosis, when novel treatments may prevent the illness or ameliorate its effects.
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Kaverina, Mariya, Arina Kuleva, and Olga Krotkova. "The Role of the Hippocampus in Detecting the Novelty of Impressions: A Literature Review." Russian Journal of Cognitive Science 9, no. 1-2 (June 30, 2022): 27–43. http://dx.doi.org/10.47010/22.1-2.2.
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The article presents a review of modern studies of the hippocampus’s functions in the implementation of cognitive phenomena, a review which covers a wide range of experimental areas, including high-precision brain morphometry, functional neuroimaging, electroencephalography, deep navigational electrode implantation, and dosed radiation effects on the brain. Literary sources demonstrate the involvement of the hippocampus in almost all spheres and aspects of human mental activity, from memory to eye movements, from circadian rhythms to spatial navigation. The literature review allows us to generalize the results of many works and to speak about the basic characteristic of the hippocampus’s functional activity in information processing: that the hippocampus is a comparator which continuously marks impressions of the current experience according to the degree of novelty. The authors see such a functional analysis as much more productive than attempts to correspond brain structures with mental processes (perception, memory, attention) and, accordingly, than the customary discussion in the scientific literature of the hippocampus functioning mainly as a brain substrate of memory
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Shen, Renrui. "How Fructose Affects the Hippocampus." Journal of Clinical Medicine Research 3, no. 3 (September 24, 2022): 98. http://dx.doi.org/10.32629/jcmr.v3i3.951.
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This review explores the effects of fructose on the hippocampus: hippocampal function and structure, hippocampal neurogenesis, and hippocampal cognitive function. First, this result confirms that excess fructose intake affects the microstructure of pathways connecting the hippocampus to other brain areas. Fructose has the potential to affect neurogenesis in the hippocampus, and a diet high in fructose can impair learning and memory, leading to cognitive impairment. However, further research is needed to apply animal experiments to humans in the future. The literature review focused on the effects of fructose, but a balanced intake of other nutrients also needed to be considered.
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Hall, Matthew, Yazmin Odia, Toba Niazi, Reshma Naidoo, Golnar Alamdari, Rupesh Kotecha, Martin Tom, et al. "RADT-35. CHANGE IN HIPPOCAMPAL VOLUME AS A FUNCTION OF RADIATION DOSE: RESULTS FROM A PROSPECTIVE TRIAL WITH STANDARDIZED IMAGING AND MORPHOMETRIC EVALUATION." Neuro-Oncology 23, Supplement_6 (November 2, 2021): vi48. http://dx.doi.org/10.1093/neuonc/noab196.192.
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Abstract PURPOSE/OBJECTIVES MRIs in pediatric and adult brain tumor patients (Age< 35) were prospectively collected at baseline and during follow-up to measure volumetric changes in multiple brain substructures with neurocognitive, laboratory, and quality-of-life assessments. In this planned interim analysis, we model early outcomes for change in hippocampal volume at 6 months following radiotherapy. MATERIALS AND METHODS As of 5/15/2021, 50 patients enrolled on this prospective study and 41 completed 6-month post-treatment assessments after fractionated intensity-modulated proton therapy. Left and right hippocampus volumes were independently measured on T1 sagittal precontrast MRI at baseline and 6-months after radiotherapy using both automated software and physician-delineated contours. The relationship between mean hippocampus dose and change in volume was assessed by Pearson’s correlation coefficient. A linear mixed-effects model was applied to evaluate other predictors associated with change in hippocampal volume, assuming random effects of subjects. RESULTS Mean hippocampus dose was strongly correlated with change in hippocampal volume at 6 months following radiotherapy (r=−0.727, 95% CI [-0.820,-0.596], p< 0.001). Changes in hippocampal volumes over time were similar between software and physician contours. Hippocampal volume was significantly reduced for mean doses ≥10 Gy (mean Δ -10.8% ± 5.5%, p< 0.001), while no significant volume change was observed with mean doses < 10 Gy (mean Δ +0.7% ± 3.9%). In the mixed-effects model, only mean hippocampus dose was significantly associated with hippocampal volume change (p< 0.001). The final model predicted a -3.4% change in hippocampal volume for every 10 Gy increase in mean dose. CONCLUSIONS Change in hippocampal volume was correlated with hippocampus mean dose at 6 months following radiotherapy. Future analyses will assess volume change in the hippocampus and other brain substructures over time as a function of radiation dose and correlate with measured neurocognitive and other effects.
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He, Bing Song, Xue Ping Zhang, and Yong Gang Shi. "Hippocampus Segmentation Techniques: A Survey." Advanced Materials Research 760-762 (September 2013): 2086–90. http://dx.doi.org/10.4028/www.scientific.net/amr.760-762.2086.
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Since the volume of hippocampal formation has been found to be an early biomarker for MCI and Alzheimer's disease, hippocampus segmentation plays a significant role in clinical diagnosis. Because hippocampus in MR images presents features of low contrast, low signal-to-noise ratio and discontinuous boundaries, accurate segmentation still remains a challenging task. We presented a survey of the methods used to segment the hippocampal formation in MR images of human brain and concluded with a discussion on the trend of the future research in hippocampus segmentation.
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Ang, Mary Jasmin, Sueun Lee, Mai Wada, Poornima D. E. Weerasinghe-Mudiyanselage, Sung-Ho Kim, Taekyun Shin, Tae-Il Jeon, Seung-Soon Im, and Changjong Moon. "SREBP-1c Deficiency Affects Hippocampal Micromorphometry and Hippocampus-Dependent Memory Ability in Mice." International Journal of Molecular Sciences 22, no. 11 (June 5, 2021): 6103. http://dx.doi.org/10.3390/ijms22116103.
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Changes in structural and functional neuroplasticity have been implicated in various neurological disorders. Sterol regulatory element-binding protein (SREBP)-1c is a critical regulatory molecule of lipid homeostasis in the brain. Recently, our findings have shown the potential involvement of SREBP-1c deficiency in the alteration of novel modulatory molecules in the hippocampus and occurrence of schizophrenia-like behaviors in mice. However, the possible underlying mechanisms, related to neuronal plasticity in the hippocampus, are yet to be elucidated. In this study, we investigated the hippocampus-dependent memory function and neuronal architecture of hippocampal neurons in SREBP-1c knockout (KO) mice. During the passive avoidance test, SREBP-1c KO mice showed memory impairment. Based on Golgi staining, the dendritic complexity, length, and branch points were significantly decreased in the apical cornu ammonis (CA) 1, CA3, and dentate gyrus (DG) subregions of the hippocampi of SREBP-1c KO mice, compared with those of wild-type (WT) mice. Additionally, significant decreases in the dendritic diameters were detected in the CA3 and DG subregions, and spine density was also significantly decreased in the apical CA3 subregion of the hippocampi of KO mice, compared with that of WT mice. Alterations in the proportions of stubby and thin-shaped dendritic spines were observed in the apical subcompartments of CA1 and CA3 in the hippocampi of KO mice. Furthermore, the corresponding differential decreases in the levels of SREBP-1 expression in the hippocampal subregions (particularly, a significant decrease in the level in the CA3) were detected by immunofluorescence. This study suggests that the contributions of SREBP-1c to the structural plasticity of the mouse hippocampus may have underlain the behavioral alterations. These findings offer insights into the critical role of SREBP-1c in hippocampal functioning in mice.
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Pereira, D., M. Freschi, R. Frittoli, A. C. Londe, T. Amaral, S. Dertkigil, A. P. Del Rio, F. Cendes, L. Rittner, and S. Appenzeller. "AB0457 HIPPOCAMPAL SUBFIELDS VOLUMES REDUCTION IN PATIENTS WITH SYSTEMIC SCLEROSIS: A LONGITUDINAL MAGNETIC RESONANCE IMAGING (MRI) VOLUMETRIC STUDY." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 1255.2–1256. http://dx.doi.org/10.1136/annrheumdis-2021-eular.3815.
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Background:Systemic sclerosis (SSc) is a multisystem disease characterized by functional and structural abnormalities of small blood vessels, fibrosis of the skin and internal organs. In addition, volume reduction and shape abnormality of the hippocampus have been demonstrated in rheumatic and neurodegenerative diseases. However, the neuroanatomy of the hippocampus is complex and is not a uniform structure, consisting of subfields with distinct morphology: cornu ammonis (CA) subfields CA1–4, dentate gyrus (DG), fimbria, and adjacent subiculum and presubiculum [1].Objectives:To investigate the hippocampal subfields volumes reduction in SSc patients using MRI.Methods:In this study we included 37 SSc patients (33 women, mean age of 53.46, SD ± 12.29; range 30 - 78) and 37 healthy controls (HC) (31 women, mean age of 48.41, SD±12.20; range 29 - 80). Cognitive evaluation was performed using the Montreal Cognitive Assessment (MoCA), mood disorders were determined through Beck’s Depression (BDI) and Beck’s Anxiety Inventories (BAI). SSc patients were further assessed for clinical and laboratory SSc manifestations, disease activity (Valentini Activity Index), severity activity (Medsger Severity Index). MRI protocol consisted of: Sagittal T1-weighted images performed with a Philips 3.0T MRI scanner. MRI brain structure volumetric was done through volBrain [2]. After 48 months MRI acquisition were repeated in 26 SSc patients and 12 healthy volunteers. Statistics was performed according nature of the variable.Results:We observed a significant reduction in hippocampal subfields volumes in SSc patients when compared to controls: Total hippocampi (SSc: mean volume = 4.78 cm3; SD = 0.38; HC: mean volume = 5.01 cm3; SD = 0.38; p = 0.033). Reduction in volume of the total hippocampi was associated with Raynaud’s phenomenon (p = 0.006). A longitudinal study showed a reduction in volume of the hippocampus subfields volumes when compared to patient’s baseline: Total hippocampi (mean initial volume = 4.78 cm3; mean follow-up volume = 4.50 cm3, p = 0.027); Total CA1 (mean initial volume = 1.59 cm3; mean follow-up volume = 1.58 cm3, p < 0.0001); Reduction in volume of the total hippocampi was associated with presence of current use of prednisone (p = 0.008). Reduction in left CA1 left associated with current use of prednisone (p = 0.014). Reduction in total subiculum was associated with presence of calcinosis (p = 0.023). No significant changes were observed in hippocampal subfields volumes in controls over the follow-up period.Conclusion:This study provides evidence of hippocampus subfields volumes reductions in SSc patients when compared to controls and was associated with Raynaud’s phenomenon, current use of losartan and correlated with BAI scores. Also, a longitudinal study showed a reduction in volume of the hippocampus subfields volumes when compared to patient’s baseline associated with calcinosis and current use of prednisone.References:[1]Eichenbaum, Howard. “A cortical–hippocampal system for declarative memory.” Nature Reviews Neuroscience 1.1 (2000): 41-50.[2]Manjon JV, Coupe P (2016) volBrain: an online MRI brain volumetry system. Front Neuroinform 10:30.Disclosure of Interests:None declared.
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Vikner, Tomas, Anders Eklund, Nina Karalija, Jan Malm, Katrine Riklund, Ulman Lindenberger, Lars Bäckman, Lars Nyberg, and Anders Wåhlin. "Cerebral arterial pulsatility is linked to hippocampal microvascular function and episodic memory in healthy older adults." Journal of Cerebral Blood Flow & Metabolism 41, no. 7 (January 14, 2021): 1778–90. http://dx.doi.org/10.1177/0271678x20980652.
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Microvascular damage in the hippocampus is emerging as a central cause of cognitive decline and dementia in aging. This could be a consequence of age-related decreases in vascular elasticity, exposing hippocampal capillaries to excessive cardiac-related pulsatile flow that disrupts the blood-brain barrier and the neurovascular unit. Previous studies have found altered intracranial hemodynamics in cognitive impairment and dementia, as well as negative associations between pulsatility and hippocampal volume. However, evidence linking features of the cerebral arterial flow waveform to hippocampal function is lacking. We used a high-resolution 4D flow MRI approach to estimate global representations of the time-resolved flow waveform in distal cortical arteries and in proximal arteries feeding the brain in healthy older adults. Waveform-based clustering revealed a group of individuals featuring steep systolic onset and high amplitude that had poorer hippocampus-sensitive episodic memory (p = 0.003), lower whole-brain perfusion (p = 0.001), and weaker microvascular low-frequency oscillations in the hippocampus (p = 0.035) and parahippocampal gyrus (p = 0.005), potentially indicating compromised neurovascular unit integrity. Our findings suggest that aberrant hemodynamic forces contribute to cerebral microvascular and hippocampal dysfunction in aging.
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Zhang, Yi, Chengxuan Qiu, Olof Lindberg, Lena Bronge, Peter Aspelin, Lars Bäckman, Laura Fratiglioni, and Lars-Olof Wahlund. "Acceleration of hippocampal atrophy in a non-demented elderly population: the SNAC-K study." International Psychogeriatrics 22, no. 1 (December 4, 2009): 14–25. http://dx.doi.org/10.1017/s1041610209991396.
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ABSTRACTBackground:Brain atrophy in Alzheimer's disease (AD) includes not only AD-specific brain atrophy but also the atrophy induced by normal aging. Atrophy of the hippocampus has been one diagnostic marker of AD, but it was also found to emerge in healthy adults, along with increasing age. It was reported that the important age when age-related shrinkage of the hippocampus starts was around the mid-40s. The aim is to study the aging atrophy speed and acceleration of brain atrophy in a cross-sectional database, to identify the age at which acceleration of hippocampal atrophy starts in non-demented elderly persons.Methods:544 subjects (aged 60–97 years; 318 female and 226 male) were recruited into the MRI study by using a subsample of an epidemiological sample of 3363 healthy non-demented elderly people (over 60 years of age). Hippocampus and ventricle sizes were measured.Results:The normalized volumes (by intracranial volume, ICV) of the hippocampus in males were smaller than those in females. The right hippocampus was larger than the left. The expansion of the lateral ventricles (2.80% per year in males, 2.95% in females) and third ventricle (1.58% and 2.28%, respectively) was more marked than the hippocampal shrinkage (0.68% and 0.79%, respectively). The suggested age at which acceleration of hippocampal atrophy starts is 72 years.Conclusions:Males present smaller hippocampus volumes (normalized by ICV) than females; however, females are more vulnerable to hippocampal atrophy in a non-demented elderly population. An acceleration of hippocampal atrophy may emerge and start around 72 years of age in a non-demented elderly population.
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King, R., D. Jecmen, A. Alkozei, A. C. Raikes, M. A. Grandner, and W. D. Killgore. "0082 Hippocampal Gray Matter Volume in Healthy Adult Population is Associated with Habitual Sleep Duration." Sleep 43, Supplement_1 (April 2020): A33—A34. http://dx.doi.org/10.1093/sleep/zsaa056.080.
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Abstract Introduction The hippocampus is well known for its role in sleep and memory consolidation in adolescents, and has been shown to demonstrate neural plasticity and neuronal regeneration. However, the relationship between sleep and hippocampal gray matter volume in healthy adults remains to be fully characterized. We hypothesized that total sleep time (TST), as measured by actigraphy, would correlate positively with gray matter volume (GMV) in the hippocampus, a key memory region of the brain. Methods Forty-five healthy normal sleeping adults between 20–45 years of age wore an actigraph for seven days to quantify habitual sleep duration and underwent magnetic resonance imaging during the actigraphy period. Voxel based morphometry in SPM12 was used to estimate GMV at the whole brain level. A region-of-interest mask was used to constrain data analysis to the left and right hippocampi. Results Habitual sleep duration per night correlated positively with gray matter volume within part of the left hippocampus (x=-36,y=-20,z=-18; k=32, pFWE-corr=0.093), controlling for age, sex, total intracranial volume, intelligence scores and mood. No correlation was found between TST and hippocampal GMV in the right hippocampus. Conclusion Longer sleep time was associated with greater gray matter volume in the left hippocampus. This finding is consistent with what has been observed in healthy children and extend these findings to healthy normal sleeping adults. While TST and GMV are correlated, the causal association cannot be established here. Further research may explore the effects of sleep extension on GMV and how these volume differences associate with various aspects of cognition, particularly memory. It should be noted that this study only included healthy adults with sleep durations between 6–9 hours per night. Future studies would benefit from including adults with a greater variance in their sleep patterns to better understand the relationship between sleep and hippocampal volume, and its potential effects on memory performance. Support Defense Advanced Research Projects Agency Young Faculty Award: DARPA-12-12-11-YFA11-FP-029
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Bellani, Marcella, Monica Baiano, and Paolo Brambilla. "Brain anatomy of major depression I. Focus on hippocampus." Epidemiology and Psychiatric Sciences 19, no. 4 (December 2010): 298–301. http://dx.doi.org/10.1017/s1121189x00000634.
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Pignataro, Giuseppe, Samaneh Maysami, Francesca E. Studer, Andrew Wilz, Roger P. Simon, and Detlev Boison. "Downregulation of Hippocampal Adenosine Kinase after Focal Ischemia as Potential Endogenous Neuroprotective Mechanism." Journal of Cerebral Blood Flow & Metabolism 28, no. 1 (April 25, 2007): 17–23. http://dx.doi.org/10.1038/sj.jcbfm.9600499.
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The rate of ischemic brain injury varies with the brain region, requiring only hours in striatum but days in hippocampus. Such maturation implies the existence of endogenous neuroprotective mechanisms. Adenosine is an endogenous neuroprotectant regulated by adenosine kinase (ADK). To investigate, whether adenosine might play a role in protecting the hippocampus after focal ischemia, we subjected transgenic mice, which overexpress ADK in hippocampal neurons (Adk-tg mice) to transient middle cerebral artery occlusion (MCAO). Although the hippocampus of wild-type (wt) mice was consistently spared from injury after 60 mins of MCAO, hippocampal injury became evident in Adk-tg mice after only 15 mins of MCAO. To determine, whether downregulation of hippocampal ADK might qualify as candidate mechanism mediating endogenous neuroprotection, we evaluated ADK expression in wt mice after several periods of reperfusion after 15 or 60 mins of MCAO. After 60 mins of MCAO, hippocampal ADK was significantly reduced in both hemispheres after 1, 3, and 24 h of reperfusion. Reduction of ADK-immunoreactivity corresponded to a 2.2-fold increase in hippocampal adenosine at 3 h of reperfusion. Remarkably, a significant reduction of ADK immunoreactivity was also found in the ipsilateral (stroked) hippocampus after 15 mins of MCAO and 3 h of reperfusion. Thus, transient downregulation of hippocampal ADK after stroke might be a protective mechanism during maturation hippocampal cell loss.
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Zach, P., A. Bartoš, A. Lagutina, Z. Wurst, P. Gallina, T. Rai, K. Kieslich, et al. "Easy Identification of Optimal Coronal Slice on Brain Magnetic Resonance Imaging to Measure Hippocampal Area in Alzheimer’s Disease Patients." BioMed Research International 2020 (September 24, 2020): 1–6. http://dx.doi.org/10.1155/2020/5894021.
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Introduction. Measurement of an- hippocampal area or volume is useful in clinical practice as a supportive aid for diagnosis of Alzheimer’s disease. Since it is time-consuming and not simple, it is not being used very often. We present a simplified protocol for hippocampal atrophy evaluation based on a single optimal slice in Alzheimer’s disease. Methods. We defined a single optimal slice for hippocampal measurement on brain magnetic resonance imaging (MRI) at the plane where the amygdala disappears and only the hippocampus is present. We compared an absolute area and volume of the hippocampus on this optimal slice between 40 patients with Alzheimer disease and 40 age-, education- and gender-mateched elderly controls. Furthermore, we compared these results with those relative to the size of the brain or the skull: the area of the optimal slice normalized to the area of the brain at anterior commissure and the volume of the hippocampus normalized to the total intracranial volume. Results. Hippocampal areas on the single optimal slice and hippocampal volumes on the left and right in the control group were significantly higher than those in the AD group. Normalized hippocampal areas and volumes on the left and right in the control group were significantly higher compared to the AD group. Absolute hippocampal areas and volumes did not significantly differ from corresponding normalized hippocampal areas as well as normalized hippocampal volumes using comparisons of areas under the receiver operating characteristic curves. Conclusion. The hippocampal area on the well-defined optimal slice of brain MRI can reliably substitute a complicated measurement of the hippocampal volume. Surprisingly, brain or skull normalization of these variables does not add any incremental differentiation between Alzheimer disease patients and controls or give better results.
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Fajnerová, Iveta, David Greguš, Jaroslav Hlinka, Tereza Nekovářová, Antonín Škoch, Tomáš Zítka, Jan Romportl, Eva Žáčková, and Jiří Horáček. "Could Prolonged Usage of GPS Navigation Implemented in Augmented Reality Smart Glasses Affect Hippocampal Functional Connectivity?" BioMed Research International 2018 (June 13, 2018): 1–10. http://dx.doi.org/10.1155/2018/2716134.
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Background. Augmented reality (AR) glasses with GPS navigation represent the rapidly evolving technology which spares (and externalizes) navigational capacities. Regarding the expected everyday usage of this device, its impact on neuroplastic brain changes and navigation abilities should be evaluated. Aims. This study aimed to assess possible changes in functional connectivity (FC) of hippocampus and other brain regions involved in spatial navigation. Methods. Thirty-three healthy participants completed two resting state functional magnetic resonance imaging (rsfMRI) measurements at the baseline and after 3 months. For this period, the experimental group (n = 17) has had used AR device (Vuzix M100) with incorporated GPS guidance system during navigation in real world. Participants from the control group (n = 16) have not used any GPS device while navigating during walking. The rsfMRI FC of right and left hippocampi was analyzed using a seed-driven approach. Virtual city task was used to test navigational abilities both before and after the usage of AR device. Results. We identified strong functional coupling of right and left hippocampi at the baseline (p < 0.05, FDR corrected). Mild changes in bilateral hippocampal FC (p < 0.05, FDR uncorrected) were observed in both assessed groups mainly between the bilateral hippocampi and between each hippocampus and temporal regions and cerebellum. However, the experimental group showed FC decrease after three months of using GPS navigation implemented in AR glasses in contrast to FC increase in the control group without such intervention. Importantly, no effect of intervention on navigational abilities was observed. Discussion. Our observation supports the assumption that externalization of spatial navigation to technological device (GPS in AR glasses) can decrease the functional coupling between hippocampus and associated brain regions. Considering some limitations of the present study, further studies should elucidate the mechanism of the observed changes and their impact on cognitive abilities.
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Falkai, P. "Clinical and neurobiological effects of aerobic endurance training in multi-episode schizophrenia patients." European Psychiatry 33, S1 (March 2016): S41. http://dx.doi.org/10.1016/j.eurpsy.2016.01.890.
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Schizophrenia is a severe brain disorder characterised by positive, negative, affective and cognitive symptoms and can be viewed as a disorder of impaired neural plasticity. Aerobic exercise has a profound impact on the plasticity of the brain of both rodents and humans such as inducing the proliferation and differentiation of neural progenitor cells of the hippocampus in mice and rats. Aerobic exercise enhances LTP and leads to a better performance in hippocampus related memory tasks, eventually by increasing metabolic and synaptic plasticity related proteins in the hippocampus. In healthy humans, regular aerobic exercise increases hippocampal volume and seems to diminish processes of ageing like brain atrophy and cognitive decline.Disclosure of interestThe author has not supplied his declaration of competing interest.
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Sartim, Ariandra G., Amanda J. Sales, Francisco S. Guimarães, and Sâmia RL Joca. "Hippocampal mammalian target of rapamycin is implicated in stress-coping behavior induced by cannabidiol in the forced swim test." Journal of Psychopharmacology 32, no. 8 (July 3, 2018): 922–31. http://dx.doi.org/10.1177/0269881118784877.
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Background: Cannabidiol is a non-psychotomimetic compound with antidepressant-like effects. However, the mechanisms and brain regions involved in cannabidiol effects are not yet completely understood. Brain-derived neurotrophic factor/tropomyosin-receptor kinase B/mammalian target of rapamycin (BDNF-TrkB-mTOR) signaling, especially in limbic structures, seems to play a central role in mediating the effects of antidepressant drugs. Aim: Since it is not yet known if BDNF-TrkB-mTOR signaling in the hippocampus is critical to the antidepressant-like effects of cannabidiol, we investigated the effects produced by cannabidiol (10/30/60 nmol/0.2 µL) micro-injection into the hippocampus of mice submitted to the forced swim test and to the open field test. Methods: Independent groups received intra-hippocampal injections of rapamycin (mTOR inhibitor, 0.2 nmol/0.2 µL) or K252 (Trk antagonist, 0.01 nmol/0.2 µL), before the systemic (10 mg/kg) or hippocampal (10 nmol/0.2µL) injection of cannabidiol, and were submitted to the same tests. BDNF levels were analyzed in the hippocampus of animals treated with cannabidiol (10 mg/kg). Results: Systemic cannabidiol administration induced antidepressant-like effects and increased BDNF levels in the dorsal hippocampus. Rapamycin, but not K252a, injection into the dorsal hippocampus prevented the antidepressant-like effect induced by systemic cannabidiol treatment (10 mg/kg). Differently, hippocampal administration of cannabidiol (10 nmol/0.2 µL) reduced immobility time, an effect that was blocked by both rapamycin and K252a local microinjection. Conclusion: Altogether, our data suggest that the hippocampal BDNF-TrkB-mTOR pathway is vital for cannabidiol-induced antidepressant-like effect when the drug is locally administered. However, other brain regions may also be involved in cannabidiol-induced antidepressant effect upon systemic administration.
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Toh, You Sheng, and Carol Anne Hargreaves. "Analysis of 2D and 3D Convolution Models for Volumetric Segmentation of the Human Hippocampus." Big Data and Cognitive Computing 7, no. 2 (April 23, 2023): 82. http://dx.doi.org/10.3390/bdcc7020082.
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Extensive medical research has revealed evidence of a strong association between hippocampus atrophy and age-related diseases such as Alzheimer’s disease (AD). Therefore; segmentation of the hippocampus is an important task that can help clinicians and researchers in diagnosing cognitive impairment and uncovering the mechanisms behind hippocampal changes and diseases of the brain. The main aim of this paper was to provide a fair comparison of 2D and 3D convolution-based architectures for the specific task of hippocampus segmentation from brain MRI volumes to determine whether 3D convolution models truly perform better in hippocampus segmentation and also to assess any additional costs in terms of time and computational resources. Our optimized model, which used 50 epochs and a mini-batch size of 2, achieved the best validation loss and Dice Similarity Score (DSC) of 0.0129 and 0.8541, respectively, across all experiment runs. Based on the model comparisons, we concluded that 2D convolution models can surpass their 3D counterparts in terms of both hippocampus segmentation performance and training efficiency. Our automatic hippocampus segmentation demonstrated potential savings of thousands of clinician person-hours spent on manually analyzing and segmenting brain MRI scans
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Hall, Matthew, Yazmin Odia, Katherine Von Werne, Toba Niazi, Ossama Maher, Ziad Khatib, Alexander Mohler, et al. "RONC-13. Change in hippocampus volume as a function of radiation dose: Results from a prospective trial with standardized imaging and morphometric evaluation." Neuro-Oncology 24, Supplement_1 (June 1, 2022): i179. http://dx.doi.org/10.1093/neuonc/noac079.667.
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Abstract PURPOSE/OBJECTIVES: MRIs were prospectively collected at baseline and during follow-up in pediatric and young adult brain tumor patients (Age<35) to measure volumetric changes in multiple brain substructures with neurocognitive, laboratory, and quality-of-life assessments. In this planned interim analysis, we model early outcomes for change in hippocampal volume at 6 and 12 months following radiotherapy. MATERIALS/METHODS: As of 2/6/2021, 60 patients enrolled on this prospective study and 41 completed 6 and 12-month post-treatment assessments after fractionated intensity-modulated proton therapy. Left and right hippocampus volumes were independently measured on T1 sagittal precontrast MRI at baseline, 6-months, and 12-months after radiotherapy using automated software and physician-delineated contours. The relationship between mean hippocampus dose and change in volume was assessed by Pearson’s correlation coefficient. A linear mixed-effects model was applied to evaluate other predictors associated with change in hippocampal volume, assuming random effects of subjects. RESULTS: Mean hippocampus dose was strongly correlated with change in hippocampal volume at 12 months following radiotherapy (r=−0.707, 95% CI [-0.805,-0.572], p<0.001). Changes in hippocampal volumes over time were similar between software and physician contours. In the mixed-effects model, only mean hippocampus dose was significantly associated with hippocampal volume change (p<0.001) at both 6 and 12 months. The final model predicted changes in hippocampal volume of -3.6% and -10.1% for every 10 Gy increase in mean dose at 6 and 12 months, respectively. Hippocampal volume was significantly reduced for mean doses >5 Gy (meanΔ -38.1%±20.3%, p<0.001), while no significant volume change was observed with mean doses ≤5 Gy (meanΔ -1.7%±5.0%). CONCLUSIONS: Change in hippocampal volume was correlated with hippocampus mean dose at 6 and 12 months following radiotherapy. Future analyses will assess volumetric changes in additional brain substructures as a function of radiation dose and correlate with measured neurocognitive and quality-of-life effects.
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Nam, Sung, Misun Seo, Jin-Seok Seo, Hyewhon Rhim, Sang-Soep Nahm, Ik-Hyun Cho, Byung-Joon Chang, Hyeon-Joong Kim, Sun-Hye Choi, and Seung-Yeol Nah. "Ascorbic Acid Mitigates D-galactose-Induced Brain Aging by Increasing Hippocampal Neurogenesis and Improving Memory Function." Nutrients 11, no. 1 (January 15, 2019): 176. http://dx.doi.org/10.3390/nu11010176.
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Ascorbic acid is essential for normal brain development and homeostasis. However, the effect of ascorbic acid on adult brain aging has not been determined. Long-term treatment with high levels of D-galactose (D-gal) induces brain aging by accumulated oxidative stress. In the present study, mice were subcutaneously administered with D-gal (150 mg/kg/day) for 10 weeks; from the seventh week, ascorbic acid (150 mg/kg/day) was orally co-administered for four weeks. Although D-gal administration alone reduced hippocampal neurogenesis and cognitive functions, co-treatment of ascorbic acid with D-gal effectively prevented D-gal-induced reduced hippocampal neurogenesis through improved cellular proliferation, neuronal differentiation, and neuronal maturation. Long-term D-gal treatment also reduced expression levels of synaptic plasticity-related markers, i.e., synaptophysin and phosphorylated Ca2+/calmodulin-dependent protein kinase II, while ascorbic acid prevented the reduction in the hippocampus. Furthermore, ascorbic acid ameliorated D-gal-induced downregulation of superoxide dismutase 1 and 2, sirtuin1, caveolin-1, and brain-derived neurotrophic factor and upregulation of interleukin 1 beta and tumor necrosis factor alpha in the hippocampus. Ascorbic acid-mediated hippocampal restoration from D-gal-induced impairment was associated with an enhanced hippocampus-dependent memory function. Therefore, ascorbic acid ameliorates D-gal-induced impairments through anti-oxidative and anti-inflammatory effects, and it could be an effective dietary supplement against adult brain aging.
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Pooja, Kumari, Sushma Tomar, Archana Rani, Manoj Kumar, and Sanjula Singh. "Volumetric study of Hippocampus by magnetic resonance imaging." Journal of Anatomical Sciences 29, no. 1 (June 1, 2021): 01–06. http://dx.doi.org/10.46351/jas.v29i1pp01-06.
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Introduction: Hippocampus is one of the major components of the brain, lies on ventral aspect of brain in temporal lobe of each cerebral hemisphere. It plays an important role in memory and therefore volumetric evaluation was done to establish normal values. The aim was to do a gender-wise comparison of right and left hippocampus volume in the age group of 21-40 years. Materials and methods: Magnetic resonance imaging was done in 50 patients (20 females and 30 males) of age 21-40 years with complaint of epilepsy or headache. Magnetic resonance imaging was done in 50 patients (20 females and 30 males) of age 21-40 years with complaint of epilepsy or headache. Results: Average of total volume of right side of hippocampus was 6.75 cm3 and of left side 6.21 cm3. In females, average volume of right hippocampus was 6.57 cm3 and left side 5.94 cm3. In males, average volume of right hippocampus was 6.88 cm3 while that of left was 6.37 cm3. Total average volume in females was 6.26 cm3 and in males was 6.62 cm3. Conclusions: The total volume of right hippocampus was more than that of left side. The total average hippocampal volume of males was more than of females. Keywords: Hippocampus, Volume, Brain, Magnetic resonance imaging
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Kurth, Florian, and Eileen Luders. "Hippocampal Asymmetry Increases with Age." Anatomia 2, no. 4 (October 16, 2023): 328–35. http://dx.doi.org/10.3390/anatomia2040029.
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It is unclear whether differences between the two brain hemispheres become larger or smaller with increasing age. Given that the hippocampus is particularly susceptible to age-related changes, here, we set out to investigate the correlation between chronological age and hippocampal asymmetry, both for the hippocampal complex as a whole and in cytoarchitectonically defined subregions (cornu ammonis 1, 2, 3, dentate gyrus, subiculum, and entorhinal cortex). We analyzed T1-weighted data of the brain from a sample of 725 healthy individuals (406 women/319 men) spanning a wide age range (36–100 years) from The Lifespan Human Connectome Project in Aging. Correlations between the absolute asymmetry index and chronological age were positive for all six subregions and also for the hippocampal complex as a whole, albeit effects the effects were not significant for the dentate gyrus. This suggests that, overall, hippocampal asymmetry increases with increasing age (i.e., the left and right hippocampi become more different over time). Given that the subregions of the hippocampal complex serve different brain functions, follow-up research is needed to explore the functional implications within the framework of brain aging. In addition, longitudinal studies will be necessary to confirm the observed cross-sectional effects.
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Heller-Wight, Abi, Connor Phipps, Jennifer Sexton, Meghan Ramirez, and David E. Warren. "Hippocampal Resting State Functional Connectivity Associated with Physical Activity in Periadolescent Children." Brain Sciences 13, no. 11 (November 7, 2023): 1558. http://dx.doi.org/10.3390/brainsci13111558.
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Periadolescence is a neurodevelopmental period characterized by structural and functional brain changes that are associated with cognitive maturation. The development of the functional connectivity of the hippocampus contributes to cognitive maturation, especially memory processes. Notably, hippocampal development is influenced by lifestyle factors, including physical activity. Physical activity has been associated with individual variability in hippocampal functional connectivity. However, this relationship has not been characterized in a developmental cohort. In this study, we aimed to fill this gap by investigating the relationship between physical activity and the functional connectivity of the hippocampus in a cohort of periadolescents aged 8–13 years (N = 117). The participants completed a physical activity questionnaire, reporting the number of days per week they performed 60 min of physical activity; then, they completed a resting-state functional MRI scan. We observed that greater physical activity was significantly associated with differences in hippocampal functional connectivity in frontal and temporal regions. Greater physical activity was associated with decreased connectivity between the hippocampus and the right superior frontal gyrus and increased connectivity between the hippocampus and the left superior temporal sulcus. Capturing changes in hippocampal functional connectivity during key developmental periods may elucidate how lifestyle factors including physical activity influence brain network connectivity trajectories, cognitive development, and future disease risk.
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Raja, Deepika, Sneha Ravichandran, Baskaran Chandrasekaran, Rajagopal Kadavigere, M. G. Ramesh Babu, Meshari Almeshari, Amjad R. Alyahyawi, Yasser Alzamil, Ahmad Abanomy, and Suresh Sukumar. "Association between Physical Activity Levels and Brain Volumes in Adults Visiting Radio-Imaging Center of Tertiary Care Hospital." International Journal of Environmental Research and Public Health 19, no. 24 (December 19, 2022): 17079. http://dx.doi.org/10.3390/ijerph192417079.
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Background and aim: There is evidence to support the favorable impact of physical activity (PA) on brain volume. However, the empirical evidence exploring the relationship between physical and sedentary behavior remains mixed. We aimed to explore the relationship between PA and sedentary behavior and brain volume. Methods: The study sample (n = 150, mean age = 39.7 years) included patients interviewed with the International Physical Activity Questionnaire (IPAQ) who underwent an MRI brain scan. From the images obtained, we measured total intracranial, gray matter, and white matter volume along with the hippocampus, amygdala, parahippocampal gyrus, and posterior cingulate cortex (PCC). Multivariable linear regression analysis was done. Results and discussion: Left hippocampus and overall PA were positively and significantly associated (β = 0.71, p = 0.021) whereas time spent on vigorous physical activity showed a negative association (β = −0.328, p = 0.049) with left hippocampal volume. Conclusion: We found a positive association between total PA and the left hippocampus, whereas vigorous PA showed a negative association with the left hippocampus.
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Castro, Carla Cristina Miranda, Sayonara Pereira Silva, Lívia Nascimento Rabelo, José Pablo Gonçalves Queiroz, Laura Damasceno Campos, Larissa Camila Silva, and Felipe Porto Fiuza. "Age, Education Years, and Biochemical Factors Are Associated with Selective Neuronal Changes in the Elderly Hippocampus." Cells 11, no. 24 (December 13, 2022): 4033. http://dx.doi.org/10.3390/cells11244033.
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Brain aging involves regional alterations of specific cellular subpopulations in the human hippocampus: a network hub for memory consolidation. The present study investigates whether age, sex, education years, and the concentration of neuropathological and inflammatory proteins influence neuronal-type marker expression in the elderly hippocampus. We analyzed the digital images (1 µm/pixel) of postmortem hippocampal sections from 19 non-demented individuals (from 78 to 99 years). This material was obtained from the “Aging Dementia and TBI Study” open database. Brain samples were processed through in situ hybridization (ISH) for the immunodetection of VGLUT1 (glutamatergic transporter) and GAT1 (GABAergic transporter) and mRNAs and Luminex protein quantifications. After image acquisition, we delineated the dentate gyrus, CA 3/2, and CA1 hippocampal subdivisions. Then, we estimated the area fraction in which the ISH markers were expressed. Increased VGLUT1 was observed in multiple hippocampal subfields at late ages. This glutamatergic marker is positively correlated with beta-amyloid and tau proteins and negatively correlated with interleukin-7 levels. Additionally, education years are positively correlated with GAT1 in the hippocampus of elderly women. This GABAergic marker expression is associated with interferon-gamma and brain-derived neurotrophic factor levels. These associations can help to explain how hippocampal sub-regions and neurotransmitter systems undergo distinct physiological changes during normal aging.
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Haggerty, Daniel C., and Daoyun Ji. "Initiation of sleep-dependent cortical-hippocampal correlations at wakefulness-sleep transition." Journal of Neurophysiology 112, no. 7 (October 1, 2014): 1763–74. http://dx.doi.org/10.1152/jn.00783.2013.
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Sleep is involved in memory consolidation. Current theories propose that sleep-dependent memory consolidation requires active communication between the hippocampus and neocortex. Indeed, it is known that neuronal activities in the hippocampus and various neocortical areas are correlated during slow-wave sleep. However, transitioning from wakefulness to slow-wave sleep is a gradual process. How the hippocampal-cortical correlation is established during the wakefulness-sleep transition is unknown. By examining local field potentials and multiunit activities in the rat hippocampus and visual cortex, we show that the wakefulness-sleep transition is characterized by sharp-wave ripple events in the hippocampus and high-voltage spike-wave events in the cortex, both of which are accompanied by highly synchronized multiunit activities in the corresponding area. Hippocampal ripple events occur earlier than the cortical high-voltage spike-wave events, and hippocampal ripple incidence is attenuated by the onset of cortical high-voltage spike waves. This attenuation leads to a temporary weak correlation in the hippocampal-cortical multiunit activities, which eventually evolves to a strong correlation as the brain enters slow-wave sleep. The results suggest that the hippocampal-cortical correlation is established through a concerted, two-step state change that first synchronizes the neuronal firing within each brain area and then couples the synchronized activities between the two regions.