Journal articles: 'Neurogenesis'

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Morgun, A. V., E. D. Osipova, E. B. Boytsova, A. N. Shuvaev, Yu K. Komleva, L. V. Trufanova, E. F. Vais, and A. B. Salmina. "Astroglia-mediated regulation of cell development in the model of neurogenic niche in vitro treated with Aβ1-42." Biomeditsinskaya Khimiya 65, no. 5 (2019): 366–73. http://dx.doi.org/10.18097/pbmc20196505366.

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Neurogenesis is a complex process which governs embryonic brain development and is importants for brain plasticity throughout the whole life. Postnatal neurogenesis occurs in neurogenic niches that regulate the processes of proliferation and differentiation of stem and progenitor cells under the action of stimuli that trigger the mechanisms of neuroplasticity. Cells of glial and endothelial origin are the key regulators of neurogenesis. It is known that physiological neurogeneses is crucial for memory formation, whereas reparative neurogenesis provides partial repair of altered brain structure and compensation of neurological deficits caused by brain injury. Dysregulation of neurogenesis is a characteristics of various neurodevelopmental and neurodegenerative diseases, particularly, Alzheimer's disease which is very important medical and social problem. In the in vitro model of the neurogenic niche using hippocampal neurospheres as a source of stem/progenitor cells and astrocytes, we studied effects of astrocyte activation on the expression of markers of different stages of cell proliferation and differentiation. We found that aberrant mechanisms of development of stem and progenitor cells, caused by the beta-amyloid (Aβ1-42), can be partially restored by targeted activation of GFAP-expressing cells in the neurogenic niche.

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Kowalczyk, Anna, Robert K. Filipkowski, Marcin Rylski, Grzegorz M. Wilczynski, Filip A. Konopacki, Jacek Jaworski, Maria A. Ciemerych, Piotr Sicinski, and Leszek Kaczmarek. "The critical role of cyclin D2 in adult neurogenesis." Journal of Cell Biology 167, no. 2 (October 25, 2004): 209–13. http://dx.doi.org/10.1083/jcb.200404181.

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Adult neurogenesis (i.e., proliferation and differentiation of neuronal precursors in the adult brain) is responsible for adding new neurons in the dentate gyrus of the hippocampus and in the olfactory bulb. We describe herein that adult mice mutated in the cell cycle regulatory gene Ccnd2, encoding cyclin D2, lack newly born neurons in both of these brain structures. In contrast, genetic ablation of cyclin D1 does not affect adult neurogenesis. Furthermore, we show that cyclin D2 is the only D-type cyclin (out of D1, D2, and D3) expressed in dividing cells derived from neuronal precursors present in the adult hippocampus. In contrast, all three cyclin D mRNAs are present in the cultures derived from 5-day-old hippocampi, when developmental neurogenesis in the dentate gyrus takes place. Thus, our results reveal the existence of molecular mechanisms discriminating adult versus developmental neurogeneses.

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Talan, Jamie. "Neurogenesis." Neurology Today 18, no. 7 (April 2018): 62–66. http://dx.doi.org/10.1097/01.nt.0000532356.12905.0c.

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Valeri, Andrea, and Emanuela Mazzon. "Cannabinoids and Neurogenesis: The Promised Solution for Neurodegeneration?" Molecules 26, no. 20 (October 19, 2021): 6313. http://dx.doi.org/10.3390/molecules26206313.

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The concept of neurons as irreplaceable cells does not hold true today. Experiments and evidence of neurogenesis, also, in the adult brain give hope that some compounds or drugs can enhance this process, helping to reverse the outcomes of diseases or traumas that once were thought to be everlasting. Cannabinoids, both from natural and artificial origins, already proved to have several beneficial effects (e.g., anti-inflammatory, anti-oxidants and analgesic action), but also capacity to increase neuronal population, by replacing the cells that were lost and/or regenerate a damaged nerve cell. Neurogenesis is a process which is not highly represented in literature as neuroprotection, though it is as important as prevention of nervous system damage, because it can represent a possible solution when neuronal death is already present, such as in neurodegenerative diseases. The aim of this review is to resume the experimental evidence of phyto- and synthetic cannabinoids effects on neurogenesis, both in vitro and in vivo, in order to elucidate if they possess also neurogenetic and neurorepairing properties.

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Wang, Ning, Yang Lu, Kui Wang, Wei-song Li, Pan Lu, Shan Lei, Rong Li, et al. "Simvastatin Attenuates Neurogenetic Damage and Improves Neurocongnitive Deficits Induced by Isoflurane in Neonatal Rats." Cellular Physiology and Biochemistry 46, no. 2 (2018): 618–32. http://dx.doi.org/10.1159/000488630.

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Background/Aims: Isoflurane inhibited neurogenesis and induced subsequent neurocognitive deficits in developing brain. Simvastatin exerts neuroprotection in a wide range of brain injury models. In the present study, we investigated whether simvastatin could attenuate neurogenetic inhibition and cognitive deficits induced by isoflurane exposure in neonatal rats. Methods: Sprague-Dawley rats at postnatal day (PND) 7 and neural stem cells (NSCs) were treated with either gas mixture, isoflurane, or simvastatin 60 min prior to isoflurane exposure, respectively. The rats were decapitated at PND 8 and PND 10 for detection of neurogenesis in the subventricular zone (SVZ) and subgranular zone (SGZ) of the hippocampus by immunostaining. NSC proliferation, viability and apoptosis were assessed by immunohistochemistry, CCK-8 and TUNEL, respectively. The protein expressions of caspase-3, p-Akt and p-GSK-3β both in vivo and vitro were assessed by western blotting. Cognitive functions were assessed by Morris Water Maze test and context fear conditioning test at the adult. Results: Isoflurane exposure inhibited neurogenesis in the SVZ and SGZ, decreased NSC proliferation and viability, promoted NSC apoptosis and led to late cognitive deficits. Furthermore, isoflurane increased caspase-3 expression and decreased protein expressions of p-Akt and p-GSK-3β both in vivo and in vitro. Pretreatment with simvastatin attenuated isoflurane-elicited changes in NSCs and cognitive function. Co-treatment with LY294002 reversed the effect of simvastatin on NSCs in vitro. Conclusion: We for the first time showed that simvastatin, by upregulating Akt/GSK-3β signaling pathway, alleviated isoflurane-induced neurogenetic damage and neurocognitive deficits in developing rat brain.

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Walton, R. M. "Postnatal Neurogenesis." Veterinary Pathology 49, no. 1 (August 8, 2011): 155–65. http://dx.doi.org/10.1177/0300985811414035.

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Crusio, Wim E. "Adult Neurogenesis." Genes, Brain and Behavior 7, no. 7 (October 2008): 831–32. http://dx.doi.org/10.1111/j.1601-183x.2008.00424_6.x.

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Farley, Suzanne. "Exciting neurogenesis." Nature Reviews Neuroscience 5, no. 7 (July 2004): 514. http://dx.doi.org/10.1038/nrn1446.

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Whalley, Katherine. "Upsetting neurogenesis." Nature Reviews Neuroscience 9, no. 4 (April 2008): 250–51. http://dx.doi.org/10.1038/nrn2358.

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de Souza, Natalie. "Predicting neurogenesis." Nature Methods 8, no. 8 (July 28, 2011): 616–17. http://dx.doi.org/10.1038/nmeth0811-616a.

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Zheng, Jie, Ming Yi, and You Wan. "Hippocampal neurogenesis." PAIN 157, no. 2 (February 2016): 506–7. http://dx.doi.org/10.1097/j.pain.0000000000000418.

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Barnea, Anat. "Wild Neurogenesis." Brain, Behavior and Evolution 75, no. 2 (2010): 86–87. http://dx.doi.org/10.1159/000306483.

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Stuart, Duncan K., Steven A. Torrence, and Margaret I. Law. "Leech neurogenesis." Developmental Biology 136, no. 1 (November 1989): 17–39. http://dx.doi.org/10.1016/0012-1606(89)90128-0.

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Torrence, Steven A., Margaret I. Law, and Duncan K. Stuart. "Leech neurogenesis." Developmental Biology 136, no. 1 (November 1989): 40–60. http://dx.doi.org/10.1016/0012-1606(89)90129-2.

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Aimone, James, Sebastian Jessberger, and Fred Gage. "Adult neurogenesis." Scholarpedia 2, no. 2 (2007): 2100. http://dx.doi.org/10.4249/scholarpedia.2100.

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Centanin, L., and J. Wittbrodt. "Retinal neurogenesis." Development 141, no. 2 (December 31, 2013): 241–44. http://dx.doi.org/10.1242/dev.083642.

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Martino, Gianvito, Erica Butti, and Marco Bacigaluppi. "Neurogenesis or non-neurogenesis: that is the question." Journal of Clinical Investigation 124, no. 3 (February 24, 2014): 970–73. http://dx.doi.org/10.1172/jci74419.

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Kim, Il Bin, and Seon-Cheol Park. "Neural Circuitry–Neurogenesis Coupling Model of Depression." International Journal of Molecular Sciences 22, no. 5 (February 28, 2021): 2468. http://dx.doi.org/10.3390/ijms22052468.

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Depression is characterized by the disruption of both neural circuitry and neurogenesis. Defects in hippocampal activity and volume, indicative of reduced neurogenesis, are associated with depression-related behaviors in both humans and animals. Neurogenesis in adulthood is considered an activity-dependent process; therefore, hippocampal neurogenesis defects in depression can be a result of defective neural circuitry activity. However, the mechanistic understanding of how defective neural circuitry can induce neurogenesis defects in depression remains unclear. This review highlights the current findings supporting the neural circuitry-regulated neurogenesis, especially focusing on hippocampal neurogenesis regulated by the entorhinal cortex, with regard to memory, pattern separation, and mood. Taken together, these findings may pave the way for future progress in neural circuitry–neurogenesis coupling studies of depression.

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Kim, Il Bin, and Seon-Cheol Park. "The Entorhinal Cortex and Adult Neurogenesis in Major Depression." International Journal of Molecular Sciences 22, no. 21 (October 29, 2021): 11725. http://dx.doi.org/10.3390/ijms222111725.

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Depression is characterized by impairments in adult neurogenesis. Reduced hippocampal function, which is suggestive of neurogenesis impairments, is associated with depression-related phenotypes. As adult neurogenesis operates in an activity-dependent manner, disruption of hippocampal neurogenesis in depression may be a consequence of neural circuitry impairments. In particular, the entorhinal cortex is known to have a regulatory effect on the neural circuitry related to hippocampal function and adult neurogenesis. However, a comprehensive understanding of how disruption of the neural circuitry can lead to neurogenesis impairments in depression remains unclear with respect to the regulatory role of the entorhinal cortex. This review highlights recent findings suggesting neural circuitry-regulated neurogenesis, with a focus on the potential role of the entorhinal cortex in hippocampal neurogenesis in depression-related cognitive and emotional phenotypes. Taken together, these findings may provide a better understanding of the entorhinal cortex-regulated hippocampal neurogenesis model of depression.

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Lazic, Stanley E. "Using causal models to distinguish between neurogenesis-dependent and -independent effects on behaviour." Journal of The Royal Society Interface 9, no. 70 (September 28, 2011): 907–17. http://dx.doi.org/10.1098/rsif.2011.0510.

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There has been a substantial amount of research on the relationship between hippocampal neurogenesis and behaviour over the past 15 years, but the causal role that new neurons have on cognitive and affective behavioural tasks is still far from clear. This is partly due to the difficulty of manipulating levels of neurogenesis without inducing off-target effects, which might also influence behaviour. In addition, the analytical methods typically used do not directly test whether neurogenesis mediates the effect of an intervention on behaviour. Previous studies may have incorrectly attributed changes in behavioural performance to neurogenesis because the role of known (or unknown) neurogenesis-independent mechanisms was not formally taken into consideration during the analysis. Causal models can tease apart complex causal relationships and were used to demonstrate that the effect of exercise on pattern separation is via neurogenesis-independent mechanisms. Many studies in the neurogenesis literature would benefit from the use of statistical methods that can separate neurogenesis-dependent from neurogenesis-independent effects on behaviour.

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Coplan, Jeremy D., Shariful Syed, Tarique D. Perera, Sasha L. Fulton, Mary Ann Banerji, Andrew J. Dwork, and John G. Kral. "Glucagon-Like Peptide-1 as Predictor of Body Mass Index and Dentate Gyrus Neurogenesis: Neuroplasticity and the Metabolic Milieu." Neural Plasticity 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/917981.

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Glucagon-like peptide-1 (GLP-1) regulates carbohydrate metabolism and promotes neurogenesis. We reported an inverse correlation between adult body mass and neurogenesis in nonhuman primates. Here we examine relationships between physiological levels of the neurotrophic incretin, plasma GLP-1 (pGLP-1), and body mass index (BMI) in adolescence to adult neurogenesis and associations with a diabesity diathesis and infant stress. Morphometry, fasting pGLP-1, insulin resistance, and lipid profiles were measured in early adolescence in 10 stressed and 4 unstressed male bonnet macaques. As adults, dentate gyrus neurogenesis was assessed by doublecortin staining. High pGLP-1, low body weight, and low central adiposity, yet peripheral insulin resistance and high plasma lipids, during adolescence were associated with relatively high adult neurogenesis rates. High pGLP-1 also predicted low body weight with, paradoxically, insulin resistance and high plasma lipids. No rearing effects for neurogenesis rates were observed. We replicated an inverse relationship between BMI and neurogenesis. Adolescent pGLP-1 directly predicted adult neurogenesis. Two divergent processes relevant to human diabesity emerge—high BMI, low pGLP-1, and low neurogenesis and low BMI, high pGLP-1, high neurogenesis, insulin resistance, and lipid elevations. Diabesity markers putatively reflect high nutrient levels necessary for neurogenesis at the expense of peripheral tissues.

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Boonstra, R., L. Galea, S. Matthews, and J. M. Wojtowicz. "Adult neurogenesis in natural populations." Canadian Journal of Physiology and Pharmacology 79, no. 4 (April 1, 2001): 297–302. http://dx.doi.org/10.1139/y00-135.

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The dogma that the adult brain produces no new neurons has been overturned, but the critics are still asking, so what? Is adult neurogenesis a biologically relevant phenomenon, or is it perhaps harmful because it disrupts the existing neuronal circuitry? Considering that the phenomenon is evolutionarily conserved in all mammalian species examined to date and that its relevance has been well documented in non-mammalian species, it seems self-evident that neurogenesis in adult mammals must have a role. In birds, it has been established that neurogenesis varies dramatically with seasonal changes in song production. In chickadees, the learning behaviour related to finding stored food is also correlated with seasonal adult neurogenesis. Such studies are still nonexistent in mammals, but the related evidence suggests that neurogenesis does vary seasonally in hamsters and shows sexual differences in meadow voles. To promote studies on natural populations asking fundamental questions of the purpose and function of neurogenesis, we organized a Workshop on "Hippocampal Neurogenesis in Natural Populations" in Toronto in May 2000. The Workshop highlighted recent discoveries in neurogenesis from the lab, and focused on its functional consequences. The consensus at the Workshop was that demonstration of a role for neurogenesis in natural behaviours will ultimately be essential if we are to understand the purpose and function of neurogenesis in humans.Key words: neurogenesis, hippocampus, dentate gyrus, learning, memory, wild population.

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Leung, Joseph Wai-Hin, Kwok-Kuen Cheung, Shirley Pui-Ching Ngai, Hector Wing-Hong Tsang, and Benson Wui-Man Lau. "Protective Effects of Melatonin on Neurogenesis Impairment in Neurological Disorders and Its Relevant Molecular Mechanisms." International Journal of Molecular Sciences 21, no. 16 (August 6, 2020): 5645. http://dx.doi.org/10.3390/ijms21165645.

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Neurogenesis is the process by which functional new neurons are generated from the neural stem cells (NSCs) or neural progenitor cells (NPCs). Increasing lines of evidence show that neurogenesis impairment is involved in different neurological illnesses, including mood disorders, neurogenerative diseases, and central nervous system (CNS) injuries. Since reversing neurogenesis impairment was found to improve neurological outcomes in the pathological conditions, it is speculated that modulating neurogenesis is a potential therapeutic strategy for neurological diseases. Among different modulators of neurogenesis, melatonin is a particularly interesting one. In traditional understanding, melatonin controls the circadian rhythm and sleep–wake cycle, although it is not directly involved in the proliferation and survival of neurons. In the last decade, it was reported that melatonin plays an important role in the regulation of neurogenesis, and thus it may be a potential treatment for neurogenesis-related disorders. The present review aims to summarize and discuss the recent findings regarding the protective effects of melatonin on the neurogenesis impairment in different neurological conditions. We also address the molecular mechanisms involved in the actions of melatonin in neurogenesis modulation.

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Bond, Allison M., Daniel A. Berg, Stephanie Lee, Alan S. Garcia-Epelboim, Vijay S. Adusumilli, Guo-li Ming, and Hongjun Song. "Differential Timing and Coordination of Neurogenesis and Astrogenesis in Developing Mouse Hippocampal Subregions." Brain Sciences 10, no. 12 (November 26, 2020): 909. http://dx.doi.org/10.3390/brainsci10120909.

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Neocortical development has been extensively studied and therefore is the basis of our understanding of mammalian brain development. One fundamental principle of neocortical development is that neurogenesis and gliogenesis are temporally segregated processes. However, it is unclear how neurogenesis and gliogenesis are coordinated in non-neocortical regions of the cerebral cortex, such as the hippocampus, also known as the archicortex. Here, we show that the timing of neurogenesis and astrogenesis in the Cornu Ammonis (CA) 1 and CA3 regions of mouse hippocampus mirrors that of the neocortex; neurogenesis occurs embryonically, followed by astrogenesis during early postnatal development. In contrast, we find that neurogenesis in the dentate gyrus begins embryonically but is a protracted process which peaks neonatally and continues at low levels postnatally. As a result, astrogenesis, which occurs during early postnatal development, overlaps with the process of neurogenesis in the dentate gyrus. During all stages, neurogenesis overwhelms astrogenesis in the dentate gyrus. In addition, we find that the timing of peak astrogenesis varies by hippocampal subregion. Together, our results show differential timing and coordination of neurogenesis and astrogenesis in developing mouse hippocampal subregions and suggest that neurogenesis and gliogenesis occur simultaneously during dentate gyrus development, challenging the conventional principle that neurogenesis and gliogenesis are temporally separated processes.

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Sun, Yunjuan, Kunlin Jin, Jocelyn T. Childs, Lin Xie, Xiao Ou Mao, and David A. Greenberg. "Neuronal Nitric Oxide Synthase and Ischemia-Induced Neurogenesis." Journal of Cerebral Blood Flow & Metabolism 25, no. 4 (February 2, 2005): 485–92. http://dx.doi.org/10.1038/sj.jcbfm.9600049.

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Nitric oxide (NO) influences infarct size after focal cerebral ischemia and also regulates neurogenesis in the adult brain. These observations suggest that therapeutic approaches to stroke that target NO signaling may provide neuroprotection and also enhance brain repair through cell replacement. However, ischemic injury and neurogenesis are both affected differently depending on which isoform of NO synthase is the source of NO. In addition, ischemia itself stimulates neurogenesis, and ischemia-induced neurogenesis may be regulated differently than neurogenesis in nonischemic brain. To determine how neuronal NO synthase affects ischemia-induced neurogenesis, transient focal cerebral ischemia was produced in wild-type mice and in knockout mice lacking neuronal NO synthase, and BrdU incorporation and doublecortin immunoreactivity were measured in the principal neuroproliferative regions of the adult brain. Knockout of neuronal NO synthase reduced infarct size and increased both basal and ischemia-induced neurogenesis, suggesting that NO from this source is an inhibitory regulator of neurogenesis in the ischemic brain. 7-Nitroindazole, an NO synthase inhibitor that preferentially affects the neuronal isoform, also increased neurogenesis in rats when administered by the intracerebroventricular route. Selective inhibition of neuronal NO synthase may have the potential to both reduce infarct size and enhance neurogenesis in stroke.

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Zhang, Rui Lan, and Michael Chopp. "Neurogenesis in Stroke Treatment." European Neurological Review 6, no. 4 (2011): 246. http://dx.doi.org/10.17925/enr.2011.06.04.246.

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Findings of stroke-induced neurogenesis in the adult brain have raised hopes that amplification of endogenous neurogenesis contributes to improvement of neurological outcomes. This article briefly reviews stroke-induced neurogenesis and emerging potential therapies aimed at amplification of endogenous neurogenesis during stroke recovery.

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Asl, Sara Solimani, Cyrus Jalili, Tayebeh Artimani, Mahdi Ramezani, and Fatemeh Mirzaei. "Inflammasome can Affect Adult Neurogenesis: A Review Article." Open Neurology Journal 15, no. 1 (July 7, 2021): 25–30. http://dx.doi.org/10.2174/1874205x02115010025.

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Adult neurogenesis is the process of producing new neurons in the adult brain and is limited to two major areas: the hippocampal dentate gyrus and the Subventricular Zone (SVZ). Adult neurogenesis is affected by some physiological, pharmacological, and pathological factors. The inflammasome is a major signalling platform that regulates caspase-1 and induces proinflammatory cytokines production such as interleukin-1β (IL1-β) and IL-18. Inflammasomes may be stimulated through multiple signals, and some of these signaling factors can affect neurogenesis. In the current review, “adult neurogenesis and inflammasome” were searched in PubMed, Scopus, and Google Scholar. Reviewing various research works showed correlations between inflammasome and neurogenesis by different intermediate factors, such as interferons (IFN), interleukins (IL), α-synuclein, microRNAs, and natural compounds. Concerning the significant role of neurogenesis in the health of the nervous system and memory, understanding factors inducing neurogenesis is crucial for identifying new therapeutic aims. Hence in this review, we will discuss the different mechanisms by which inflammasome influences adult neurogenesis.

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Jiranugrom, Piyanart, Ik Dong Yoo, Min Woo Park, Ji Hwan Ryu, Jong-Seok Moon, and Sun Shin Yi. "NOX4 Deficiency Exacerbates the Impairment of Cystatin C-Dependent Hippocampal Neurogenesis by a Chronic High Fat Diet." Genes 11, no. 5 (May 19, 2020): 567. http://dx.doi.org/10.3390/genes11050567.

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Hippocampal neurogenesis is linked with a cognitive process under a normal physiological condition including learning, memory, pattern separation, and cognitive flexibility. Hippocampal neurogenesis is altered by multiple factors such as the systemic metabolic changes. NADPH oxidase 4 (NOX4) has been implicated in the regulation of brain function. While the role of NOX4 plays in the brain, the mechanism by which NOX4 regulates hippocampal neurogenesis under metabolic stress is unclear. In this case, we show that NOX4 deficiency exacerbates the impairment of hippocampal neurogenesis by inhibiting neuronal maturation by a chronic high fat diet (HFD). NOX4 deficiency resulted in less hippocampal neurogenesis by decreasing doublecortin (DCX)-positive neuroblasts, a neuronal differentiation marker, and their branched-dendrites. Notably, NOX4 deficiency exacerbates the impairment of hippocampal neurogenesis by chronic HFD. Moreover, NOX4 deficiency had a significant reduction of Cystatin C levels, which is critical for hippocampal neurogenesis, under chronic HFD as well as normal chow (NC) diet. Furthermore, the reduction of Cystatin C levels was correlated with the impairment of hippocampal neurogenesis in NOX4 deficient and wild-type (WT) mice under chronic HFD. Our results suggest that NOX4 regulates the impairment of Cystatin C-dependent hippocampal neurogenesis under chronic HFD.

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Shou, J., R. C. Murray, P. C. Rim, and A. L. Calof. "Opposing effects of bone morphogenetic proteins on neuron production and survival in the olfactory receptor neuron lineage." Development 127, no. 24 (December 15, 2000): 5403–13. http://dx.doi.org/10.1242/dev.127.24.5403.

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In olfactory epithelium (OE) cultures, bone morphogenetic proteins (BMPs) can strongly inhibit neurogenesis. Here we provide evidence that BMPs also promote, and indeed are required, for OE neurogenesis. Addition of the BMP antagonist noggin inhibited neurogenesis in OE-stromal cell co-cultures. Bmp2, Bmp4 and Bmp7 were expressed by OE stroma, and low concentrations of BMP4 (below the threshold for inhibition of neurogenesis) stimulated neurogenesis; BMP7 did not exhibit a stimulatory effect at any concentration tested. Stromal cell conditioned medium also stimulated neurogenesis; part of this effect was due to the presence within it of a noggin-binding factor or factors. Studies of the pro-neurogenic effect of BMP4 indicated that it did not increase progenitor cell proliferation, but rather promoted survival of newly generated olfactory receptor neurons. These findings indicate that BMPs exert both positive and negative effects on neurogenesis, depending on ligand identity, ligand concentration and the particular cell in the lineage that is responding. In addition, they reveal the presence of a factor or factors, produced by OE stroma, that can synergize with BMP4 to stimulate OE neurogenesis.

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LaDage, Lara D., Timothy C. Roth, Rebecca A. Fox, and Vladimir V. Pravosudov. "Ecologically relevant spatial memory use modulates hippocampal neurogenesis." Proceedings of the Royal Society B: Biological Sciences 277, no. 1684 (November 25, 2009): 1071–79. http://dx.doi.org/10.1098/rspb.2009.1769.

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The adult hippocampus in birds and mammals undergoes neurogenesis and the resulting new neurons appear to integrate structurally and functionally into the existing neural architecture. However, the factors underlying the regulation of new neuron production is still under scrutiny. In recent years, the concept that spatial memory affects adult hippocampal neurogenesis has gained acceptance, although results attempting to causally link memory use to neurogenesis remain inconclusive, possibly owing to confounds of motor activity, task difficulty or training for the task. Here, we show that ecologically relevant, spatial memory-based experiences of food caching and retrieving directly affect hippocampal neurogenesis in mountain chickadees ( Poecile gambeli ). We found that restricting memory experiences in captivity caused significantly lower rates of neurogenesis, as determined by doublecortin expression, compared with captive individuals provided with such experiences. However, neurogenesis rates in both groups of captive birds were still greatly lower than those in free-ranging conspecifics. These findings show that ecologically relevant spatial memory experiences can directly modulate neurogenesis, separate from other confounds that may also independently affect neurogenesis.

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Mattova, Simona, Patrik Simko, Nicol Urbanska, and Terezia Kiskova. "Bioactive Compounds and Their Influence on Postnatal Neurogenesis." International Journal of Molecular Sciences 24, no. 23 (November 22, 2023): 16614. http://dx.doi.org/10.3390/ijms242316614.

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Since postnatal neurogenesis was revealed to have significant implications for cognition and neurological health, researchers have been increasingly exploring the impact of natural compounds on this process, aiming to uncover strategies for enhancing brain plasticity. This review provides an overview of postnatal neurogenesis, neurogenic zones, and disorders characterized by suppressed neurogenesis and neurogenesis-stimulating bioactive compounds. Examining recent studies, this review underscores the multifaceted effects of natural compounds on postnatal neurogenesis. In essence, understanding the interplay between postnatal neurogenesis and natural compounds could bring novel insights into brain health interventions. Exploiting the therapeutic abilities of these compounds may unlock innovative approaches to enhance cognitive function, mitigate neurodegenerative diseases, and promote overall brain well-being.

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Jiang, Mei, Se Eun Jang, and Li Zeng. "The Effects of Extrinsic and Intrinsic Factors on Neurogenesis." Cells 12, no. 9 (April 29, 2023): 1285. http://dx.doi.org/10.3390/cells12091285.

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In the mammalian brain, neurogenesis is maintained throughout adulthood primarily in two typical niches, the subgranular zone (SGZ) of the dentate gyrus and the subventricular zone (SVZ) of the lateral ventricles and in other nonclassic neurogenic areas (e.g., the amygdala and striatum). During prenatal and early postnatal development, neural stem cells (NSCs) differentiate into neurons and migrate to appropriate areas such as the olfactory bulb where they integrate into existing neural networks; these phenomena constitute the multistep process of neurogenesis. Alterations in any of these processes impair neurogenesis and may even lead to brain dysfunction, including cognitive impairment and neurodegeneration. Here, we first summarize the main properties of mammalian neurogenic niches to describe the cellular and molecular mechanisms of neurogenesis. Accumulating evidence indicates that neurogenesis plays an integral role in neuronal plasticity in the brain and cognition in the postnatal period. Given that neurogenesis can be highly modulated by a number of extrinsic and intrinsic factors, we discuss the impact of extrinsic (e.g., alcohol) and intrinsic (e.g., hormones) modulators on neurogenesis. Additionally, we provide an overview of the contribution of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection to persistent neurological sequelae such as neurodegeneration, neurogenic defects and accelerated neuronal cell death. Together, our review provides a link between extrinsic/intrinsic factors and neurogenesis and explains the possible mechanisms of abnormal neurogenesis underlying neurological disorders.

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Bortolasci, Chiara C., Briana Spolding, Srisaiyini Kidnapillai, Timothy Connor, Trang T. T. Truong, Zoe S. J. Liu, Bruna Panizzutti, et al. "Transcriptional Effects of Psychoactive Drugs on Genes Involved in Neurogenesis." International Journal of Molecular Sciences 21, no. 21 (November 6, 2020): 8333. http://dx.doi.org/10.3390/ijms21218333.

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Although neurogenesis is affected in several psychiatric diseases, the effects and mechanisms of action of psychoactive drugs on neurogenesis remain unknown and/or controversial. This study aims to evaluate the effects of psychoactive drugs on the expression of genes involved in neurogenesis. Neuronal-like cells (NT2-N) were treated with amisulpride (10 µM), aripiprazole (0.1 µM), clozapine (10 µM), lamotrigine (50 µM), lithium (2.5 mM), quetiapine (50 µM), risperidone (0.1 µM), or valproate (0.5 mM) for 24 h. Genome wide mRNA expression was quantified and analysed using gene set enrichment analysis, with the neurogenesis gene set retrieved from the Gene Ontology database and the Mammalian Adult Neurogenesis Gene Ontology (MANGO) database. Transcription factors that are more likely to regulate these genes were investigated to better understand the biological processes driving neurogenesis. Targeted metabolomics were performed using gas chromatography-mass spectrometry. Six of the eight drugs decreased the expression of genes involved in neurogenesis in both databases. This suggests that acute treatment with these psychoactive drugs negatively regulates the expression of genes involved in neurogenesis in vitro. SOX2 and three of its target genes (CCND1, BMP4, and DKK1) were also decreased after treatment with quetiapine. This can, at least in part, explain the mechanisms by which these drugs decrease neurogenesis at a transcriptional level in vitro. These results were supported by the finding of increased metabolite markers of mature neurons following treatment with most of the drugs tested, suggesting increased proportions of mature relative to immature neurons consistent with reduced neurogenesis.

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Kaslin, Jan, Julia Ganz, and Michael Brand. "Proliferation, neurogenesis and regeneration in the non-mammalian vertebrate brain." Philosophical Transactions of the Royal Society B: Biological Sciences 363, no. 1489 (February 5, 2007): 101–22. http://dx.doi.org/10.1098/rstb.2006.2015.

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Post-embryonic neurogenesis is a fundamental feature of the vertebrate brain. However, the level of adult neurogenesis decreases significantly with phylogeny. In the first part of this review, a comparative analysis of adult neurogenesis and its putative roles in vertebrates are discussed. Adult neurogenesis in mammals is restricted to two telencephalic constitutively active zones. On the contrary, non-mammalian vertebrates display a considerable amount of adult neurogenesis in many brain regions. The phylogenetic differences in adult neurogenesis are poorly understood. However, a common feature of vertebrates (fish, amphibians and reptiles) that display a widespread adult neurogenesis is the substantial post-embryonic brain growth in contrast to birds and mammals. It is probable that the adult neurogenesis in fish, frogs and reptiles is related to the coordinated growth of sensory systems and corresponding sensory brain regions. Likewise, neurons are substantially added to the olfactory bulb in smell-oriented mammals in contrast to more visually oriented primates and songbirds, where much fewer neurons are added to the olfactory bulb. The second part of this review focuses on the differences in brain plasticity and regeneration in vertebrates. Interestingly, several recent studies show that neurogenesis is suppressed in the adult mammalian brain. In mammals, neurogenesis can be induced in the constitutively neurogenic brain regions as well as ectopically in response to injury, disease or experimental manipulations. Furthermore, multipotent progenitor cells can be isolated and differentiated in vitro from several otherwise silent regions of the mammalian brain. This indicates that the potential to recruit or generate neurons in non-neurogenic brain areas is not completely lost in mammals. The level of adult neurogenesis in vertebrates correlates with the capacity to regenerate injury, for example fish and amphibians exhibit the most widespread adult neurogenesis and also the greatest capacity to regenerate central nervous system injuries. Studying these phenomena in non-mammalian vertebrates may greatly increase our understanding of the mechanisms underlying regeneration and adult neurogenesis. Understanding mechanisms that regulate endogenous proliferation and neurogenic permissiveness in the adult brain is of great significance in therapeutical approaches for brain injury and disease.

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Paizanis, Eleni, Michel Hamon, and Laurence Lanfumey. "Hippocampal Neurogenesis, Depressive Disorders, and Antidepressant Therapy." Neural Plasticity 2007 (2007): 1–7. http://dx.doi.org/10.1155/2007/73754.

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There is a growing body of evidence that neural stem cells reside in the adult central nervous system where neurogenesis occurs throughout lifespan. Neurogenesis concerns mainly two areas in the brain: the subgranular zone of the dentate gyrus in the hippocampus and the subventricular zone, where it is controlled by several trophic factors and neuroactive molecules. Neurogenesis is involved in processes such as learning and memory and accumulating evidence implicates hippocampal neurogenesis in the physiopathology of depression. We herein review experimental and clinical data demonstrating that stress and antidepressant treatments affect neurogenesis in opposite direction in rodents. In particular, the stimulation of hippocampal neurogenesis by all types of antidepressant drugs supports the view that neuroplastic phenomena are involved in the physiopathology of depression and underlie—at least partly—antidepressant therapy.

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LaDage, Lara D. "Factors That Modulate Neurogenesis: A Top-Down Approach." Brain, Behavior and Evolution 87, no. 3 (2016): 184–90. http://dx.doi.org/10.1159/000446906.

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Although hippocampal neurogenesis in the adult brain has been conserved across the vertebrate lineage, laboratory studies have primarily examined this phenomenon in rodent models. This approach has been successful in elucidating important factors and mechanisms that can modulate rates of hippocampal neurogenesis, including hormones, environmental complexity, learning and memory, motor stimulation, and stress. However, recent studies have found that neurobiological research on neurogenesis in rodents may not easily translate to, or explain, neurogenesis patterns in nonrodent systems, particularly in species examined in the field. This review examines some of the evolutionary and ecological variables that may also modulate neurogenesis patterns. This ‘top-down' and more naturalistic approach, which incorporates ecology and natural history, particularly of nonmodel species, may allow for a more comprehensive understanding of the functional significance of neurogenesis.

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Liu, He, and Ni Song. "Molecular Mechanism of Adult Neurogenesis and its Association with Human Brain Diseases." Journal of Central Nervous System Disease 8 (January 2016): JCNSD.S32204. http://dx.doi.org/10.4137/jcnsd.s32204.

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Recent advances in neuroscience challenge the old dogma that neurogenesis occurs only during embryonic development. Mounting evidence suggests that functional neurogenesis occurs throughout adulthood. This review article discusses molecular factors that affect adult neurogenesis, including morphogens, growth factors, neurotransmitters, transcription factors, and epigenetic factors. Furthermore, we summarize and compare current evidence of associations between adult neurogenesis and human brain diseases such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and brain tumors.

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Spritzer, Mark D., and Ethan A. Roy. "Testosterone and Adult Neurogenesis." Biomolecules 10, no. 2 (February 3, 2020): 225. http://dx.doi.org/10.3390/biom10020225.

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It is now well established that neurogenesis occurs throughout adulthood in select brain regions, but the functional significance of adult neurogenesis remains unclear. There is considerable evidence that steroid hormones modulate various stages of adult neurogenesis, and this review provides a focused summary of the effects of testosterone on adult neurogenesis. Initial evidence came from field studies with birds and wild rodent populations. Subsequent experiments with laboratory rodents have tested the effects of testosterone and its steroid metabolites upon adult neurogenesis, as well as the functional consequences of induced changes in neurogenesis. These experiments have provided clear evidence that testosterone increases adult neurogenesis within the dentate gyrus region of the hippocampus through an androgen-dependent pathway. Most evidence indicates that androgens selectively enhance the survival of newly generated neurons, while having little effect on cell proliferation. Whether this is a result of androgens acting directly on receptors of new neurons remains unclear, and indirect routes involving brain-derived neurotrophic factor (BDNF) and glucocorticoids may be involved. In vitro experiments suggest that testosterone has broad-ranging neuroprotective effects, which will be briefly reviewed. A better understanding of the effects of testosterone upon adult neurogenesis could shed light on neurological diseases that show sex differences.

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Zoungrana, Linda Ines, Meredith Krause-Hauch, Hao Wang, Mohammad Kasim Fatmi, Lauryn Bates, Zehui Li, Parth Kulkarni, Di Ren, and Ji Li. "The Interaction of mTOR and Nrf2 in Neurogenesis and Its Implication in Neurodegenerative Diseases." Cells 11, no. 13 (June 28, 2022): 2048. http://dx.doi.org/10.3390/cells11132048.

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Neurogenesis occurs in the brain during embryonic development and throughout adulthood. Neurogenesis occurs in the hippocampus and under normal conditions and persists in two regions of the brain—the subgranular zone (SGZ) in the dentate gyrus of the hippocampus and the subventricular zone (SVZ) of the lateral ventricles. As the critical role in neurogenesis, the neural stem cells have the capacity to differentiate into various cells and to self-renew. This process is controlled through different methods. The mammalian target of rapamycin (mTOR) controls cellular growth, cell proliferation, apoptosis, and autophagy. The transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2) is a major regulator of metabolism, protein quality control, and antioxidative defense, and is linked to neurogenesis. However, dysregulation in neurogenesis, mTOR, and Nrf2 activity have all been associated with neurodegenerative diseases such as Alzheimer’s, Huntington’s, and Parkinson’s. Understanding the role of these complexes in both neurogenesis and neurodegenerative disease could be necessary to develop future therapies. Here, we review both mTOR and Nrf2 complexes, their crosstalk and role in neurogenesis, and their implication in neurodegenerative diseases.

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Niklison-Chirou, Maria Victoria, Massimiliano Agostini, Ivano Amelio, and Gerry Melino. "Regulation of Adult Neurogenesis in Mammalian Brain." International Journal of Molecular Sciences 21, no. 14 (July 9, 2020): 4869. http://dx.doi.org/10.3390/ijms21144869.

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Adult neurogenesis is a multistage process by which neurons are generated and integrated into existing neuronal circuits. In the adult brain, neurogenesis is mainly localized in two specialized niches, the subgranular zone (SGZ) of the dentate gyrus and the subventricular zone (SVZ) adjacent to the lateral ventricles. Neurogenesis plays a fundamental role in postnatal brain, where it is required for neuronal plasticity. Moreover, perturbation of adult neurogenesis contributes to several human diseases, including cognitive impairment and neurodegenerative diseases. The interplay between extrinsic and intrinsic factors is fundamental in regulating neurogenesis. Over the past decades, several studies on intrinsic pathways, including transcription factors, have highlighted their fundamental role in regulating every stage of neurogenesis. However, it is likely that transcriptional regulation is part of a more sophisticated regulatory network, which includes epigenetic modifications, non-coding RNAs and metabolic pathways. Here, we review recent findings that advance our knowledge in epigenetic, transcriptional and metabolic regulation of adult neurogenesis in the SGZ of the hippocampus, with a special attention to the p53-family of transcription factors.

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LU, BAI, and JAY H. CHANG. "Regulation of neurogenesis by neurotrophins: implications in hippocampus-dependent memory." Neuron Glia Biology 1, no. 4 (November 2004): 377–84. http://dx.doi.org/10.1017/s1740925x05000232.

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Neurogenesis, the generation of new neurons from neural precursor cells (NPCs), is a multi-step process that includes the proliferation of NPCs, fate determination, migration, and neuronal maturation. Neurogenesis is regulated by several extrinsic factors, such as enriched environment, physical exercise, hormones and stress, many of which also induce the expression of neurotrophins. In this review, we summarize studies on the role of neurotrophins in neurogenesis during development and in adults. We discuss the functional significance of neurogenesis in learning and memory, and how neurotrophins regulate this process. In this context, we describe recent experiments linking adult neurogenesis to long-term synaptic plasticity in the hippocampal dentate gyrus. Further study of the relationship between neurotrophins, adult neurogenesis and dentate synaptic plasticity might provide new insights into the mechanisms by which gene–environment interactions control cognition and brain plasticity.

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Inta, agos, and Peter Gass. "Is Forebrain Neurogenesis a Potential Repair Mechanism after Stroke?" Journal of Cerebral Blood Flow & Metabolism 35, no. 7 (May 13, 2015): 1220–21. http://dx.doi.org/10.1038/jcbfm.2015.95.

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The use of adult subventricular zone (SVZ) neurogenesis as brain repair strategy after stroke represents a hot topic in neurologic research. Recent radiocarbon-14 dating has revealed a lack of poststroke neurogenesis in the adult human neocortex; however, adult neurogenesis has been shown to occur, even under physiologic conditions, in the human striatum. Here, these results are contrasted with experimental poststroke neurogenesis in the murine brain. Both in humans and in rodents, the SVZ generates predominantly calretinin (CR)-expressing GABAergic interneurons, which cannot replace the broad spectrum of neuronal subtypes damaged by stroke. Therefore, SVZ neurogenesis may represent a repair mechanism only after genetic manipulation redirecting its differentiation.

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Rastoldo, Guillaume, and Brahim Tighilet. "The Vestibular Nuclei: A Cerebral Reservoir of Stem Cells Involved in Balance Function in Normal and Pathological Conditions." International Journal of Molecular Sciences 25, no. 3 (January 24, 2024): 1422. http://dx.doi.org/10.3390/ijms25031422.

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In this review, we explore the intriguing realm of neurogenesis in the vestibular nuclei—a critical brainstem region governing balance and spatial orientation. We retrace almost 20 years of research into vestibular neurogenesis, from its discovery in the feline model in 2007 to the recent discovery of a vestibular neural stem cell niche. We explore the reasons why neurogenesis is important in the vestibular nuclei and the triggers for activating the vestibular neurogenic niche. We develop the symbiotic relationship between neurogenesis and gliogenesis to promote vestibular compensation. Finally, we examine the potential impact of reactive neurogenesis on vestibular compensation, highlighting its role in restoring balance through various mechanisms.

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Greenberg, David. "Neurogenesis and Stroke." CNS & Neurological Disorders - Drug Targets 6, no. 5 (October 1, 2007): 321–25. http://dx.doi.org/10.2174/187152707783220901.

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DEMPSEY, ROBERT J. "Neurogenesis in Adults." Neurosurgery 64, no. 4 (April 1, 2009): N12. http://dx.doi.org/10.1227/01.neu.0000349644.11011.00.

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Hastings, Nicholas B., and Elizabeth Gould. "Neurons inhibit neurogenesis." Nature Medicine 9, no. 3 (March 2003): 264–66. http://dx.doi.org/10.1038/nm0303-264.

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Lee, Jacqueline E. "NeuroD and Neurogenesis." Developmental Neuroscience 19, no. 1 (1997): 27–32. http://dx.doi.org/10.1159/000111182.

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SONI, DEEPA, and ROBERT M. FRIEDLANDER. "Pregnancy Stimulated Neurogenesis." Neurosurgery 52, no. 6 (June 2003): NA. http://dx.doi.org/10.1227/01.neu.0000309185.19353.9a.

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KOMOTAR, RICARDO J., MICHAEL SUGHRUE, and E. SANDER CONNOLLY. "Inflammation and Neurogenesis." Neurosurgery 54, no. 3 (March 2004): NA. http://dx.doi.org/10.1227/01.neu.0000309605.99960.26.

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Snyder, Jason S. "Questioning human neurogenesis." Nature 555, no. 7696 (March 2018): 315–16. http://dx.doi.org/10.1038/d41586-018-02629-3.

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Journal articles on the topic 'Neurogenesis'

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