Relevant bibliographies by topics / Neuropathology

Academic literature on the topic 'Neuropathology'

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Published: 4 June 2021
Last updated: 27 July 2024

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Journal articles on the topic "Neuropathology"

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Mattsson-Carlgren, Niklas, Lea T. Grinberg, Adam Boxer, Rik Ossenkoppele, Magnus Jonsson, William Seeley, Alexander Ehrenberg, et al. "Cerebrospinal Fluid Biomarkers in Autopsy-Confirmed Alzheimer Disease and Frontotemporal Lobar Degeneration." Neurology 98, no. 11 (February 16, 2022): e1137-e1150. http://dx.doi.org/10.1212/wnl.0000000000200040.

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Background and ObjectivesTo determine how fully automated Elecsys CSF immunoassays for β-amyloid (Aβ) and tau biomarkers and an ultrasensitive Simoa assay for neurofilament light chain (NFL) correlate with neuropathologic changes of Alzheimer disease (AD) and frontotemporal lobar degeneration (FTLD).MethodsWe studied 101 patients with antemortem CSF and neuropathology data. CSF samples were collected a mean of 2.9 years before death (range 0.2–7.5 years). CSF was analyzed for Aβ40, Aβ42, total tau (T-tau), tau phosphorylated at amino acid residue 181 (P-tau), P-tau/Aβ42 and Aβ42/Aβ40 ratios, and NFL. Neuropathology measures included Thal phases, Braak stages, Consortium to Establish a Registry for Alzheimer's Disease (CERAD) scores, AD neuropathologic change (ADNC), and primary and contributory pathologic diagnoses. Associations between CSF biomarkers and neuropathologic features were tested in regression models adjusted for age, sex, and time from sampling to death.ResultsCSF biomarkers were associated with neuropathologic measures of Aβ (Thal, CERAD score), tau (Braak stage), and overall ADNC. The CSF P-tau/Aβ42 and Aβ42/Aβ40 ratios had high sensitivity, specificity, and overall diagnostic performance for intermediate-high ADNC (area under the curve range 0.95–0.96). Distinct biomarker patterns were seen in different FTLD subtypes, with increased NFL and reduced P-tau/T-tau in FTLD–TAR DNA-binding protein 43 and reduced T-tau in progressive supranuclear palsy compared to other FTLD variants.DiscussionCSF biomarkers, including P-tau, T-tau, Aβ42, Aβ40, and NFL, support in vivo identification of AD neuropathology and correlate with FTLD neuropathology.Classification of EvidenceThis study provides Class II evidence that distinct CSF biomarker patterns, including for P-tau, T-tau, Aβ42, Aβ40, and NFL, are associated with AD and FTLD neuropathology.
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Wallace, Lindsay M. K., Olga Theou, Sultan Darvesh, David A. Bennett, Aron S. Buchman, Melissa K. Andrew, Susan A. Kirkland, John D. Fisk, and Kenneth Rockwood. "Neuropathologic burden and the degree of frailty in relation to global cognition and dementia." Neurology 95, no. 24 (September 28, 2020): e3269-e3279. http://dx.doi.org/10.1212/wnl.0000000000010944.

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ObjectiveTo test the hypothesis that degree of frailty and neuropathologic burden independently contribute to global cognition and odds of dementia.MethodsThis was a secondary analysis of a prospective cohort study of older adults living in Illinois. Participants underwent an annual neuropsychological and clinical evaluation. We included 625 participants (mean age 89.7 ± 6.1 years; 67.5% female) who died and underwent autopsy. We quantified neuropathology using an index measure of 10 neuropathologic features: β-amyloid deposition, hippocampal sclerosis, Lewy bodies, tangle density, TDP-43, cerebral amyloid angiopathy, arteriolosclerosis, atherosclerosis, and gross and chronic cerebral infarcts. Clinical consensus determined dementia status, which we coded as no cognitive impairment, mild cognitive impairment, or dementia. A battery of 19 tests spanning multiple domains quantified global cognition. We operationalized frailty using a 41-item frailty index. We employed regression analyses to model relationships between neuropathology, frailty, and dementia.ResultsBoth frailty and a neuropathology index were independently associated with global cognition and dementia status. These results held after controlling for traditional pathologic measures in a sample of participants with Alzheimer clinical syndrome. Frailty improved the fit of the model for dementia status (χ2[2] 72.64; p < 0.0001) and explained an additional 11%–12% of the variance in the outcomes.ConclusionDementia is a multiply determined condition, to which both general health, as captured by frailty, and neuropathology significantly contribute. This integrative view of dementia and health has implications for prevention and therapy; specifically, future research should evaluate frailty as a means of dementia risk reduction.
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Blackburn, Jessica, Diana L. Thomas, Anna Hughes, and Christopher R. Pierson. "Neuropathology of Septo-optic Dysplasia: A Report of 4 Autopsy Cases." Journal of Child Neurology 36, no. 2 (September 14, 2020): 105–15. http://dx.doi.org/10.1177/0883073820954071.

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Septo-optic dysplasia (SOD) is defined by the presence of 2 or more features in a diagnostic triad: (1) optic nerve hypoplasia, (2) pituitary dysfunction, and (3) midline forebrain anomalies. SOD arises due to diverse pathogenetic mechanisms including acquired and genetic factors, and it shows considerable clinical and phenotypic variability. Our knowledge of SOD is incomplete in part because of a paucity of published neuropathology data, so we reviewed the autopsy neuropathology of 4 SOD patients. All patients met SOD criteria according to the triad. Additional neuropathologic findings included malformations involving non-forebrain structures and possible secondary phenomena. Autopsies demonstrate that SOD patients often have additional neuropathologic findings beyond the triad and we feel that use of the term SOD-complex appropriately underscores this diversity and its likely clinical impact. This study suggests that autopsies enhance our understanding of SOD and may be an asset in performing needed clinical and phenotypic correlation studies.
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Saito, Yuko, and Shigeo Murayama. "Neuropathology." Rinsho Shinkeigaku 51, no. 11 (2011): 1168–71. http://dx.doi.org/10.5692/clinicalneurol.51.1168.

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Squier, M. V. "Neuropathology." AVMA Medical & Legal Journal 2, no. 2 (March 1996): 37–42. http://dx.doi.org/10.1177/135626229600200202.

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Hart, Michael N. "Neuropathology." Journal of Neuropathology and Experimental Neurology 64, no. 10 (October 2005): 923. http://dx.doi.org/10.1097/01.jnen.0000182984.87106.1f.

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Tremblay, G. F. "Neuropathology." Neurology 39, no. 2 (February 1, 1989): 313. http://dx.doi.org/10.1212/wnl.39.2.313.

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Almira-Suarez, Maria Isabel, and Maria Beatriz Lopes. "Neuropathology." American Journal of Surgical Pathology 37, no. 11 (November 2013): 1768. http://dx.doi.org/10.1097/pas.0000000000000084.

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Pinckard, J. Keith. "Neuropathology." Academic Forensic Pathology 2, no. 1 (March 2012): vi—vii. http://dx.doi.org/10.1177/192536211200200101.

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Renshaw, Andrew. "Neuropathology." Advances in Anatomic Pathology 13, no. 1 (January 2006): 62. http://dx.doi.org/10.1097/01.pap.0000201830.69849.b9.

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Dissertations / Theses on the topic "Neuropathology"

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Spillantini, Maria Grazia. "Molecular neuropathology of Alzheimer's disease." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.282037.

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Huseby, Carol. "Molecular Neuropathology in Alzheimer's Disease." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1543314678552794.

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Betts, Joanne. "The molecular neuropathology of mitochondrial disease." Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.421187.

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Tofaris, George Kynacov. "Molecular neuropathology of Lewy body disorders." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619824.

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Davis, Brittany. "Modelling the neuropathology of Ehmt1 haploinsufficiency." Thesis, Cardiff University, 2014. http://orca.cf.ac.uk/73068/.

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EHMT1 is a gene that encodes an epigenetic regulator important for normal brain development. Disruption in EHMT1 is associated with a number of neurodevelopment and psychiatric conditions, like schizophrenia, Autism Spectrum Disorders, developmental delays and intellectual disabilities. In order to help elucidate the role of Ehmt1 in cortical development two models are examined: the differentiation of mouse pyramidal neurons lacking one copy of the gene and a forebrain-specific Ehmt1-haploinsufficient mouse model. Ehmt1+/- cells demonstrated changes in cell cycle, with significant differences in proliferation rates at embryonic stem cell and neural progenitor stages. Ehmt1+/- cells demonstrated significantly different transcriptional profiles in early and late stages of progenitor development, which suggested these cells, underwent precocious differentiation. In addition, the dysregulation of mRNA expression in a number of the Nrsf/Rest repressor complex members and Rest target genes was found; and Ehmt1+/- cells did not survive as post-mitotic neurons. The forebrain-specific Ehmt1-haploinsufficient mouse model, Ehmt1D6Cre/+, importantly showed normal Mendelian birth ratios, survival, motor coordination and function and no gross morphological changes in brain structure. However, these mice demonstrated differences in activity levels and anxiety-related measurements; deficits in sensorimotor gating and object recognition; and significant differences in a number of electrophysiological measurements, including abnormal event-related neural responses in the cortex and high frequency oscillatory patterns. Taken together, these data suggest that Ehmt1 expression is important for normal pyramidal development and Ehmt1 haploinsufficiency throughout development manifests cortical dysfunction, which leads to marked behavioural and electrophysiological abnormalities.
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Tabata, Rena Christina. "Neuropathology induced by sterol glucosides in mice." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/24178.

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Sterol glucosides are a family of compounds characterized by a carbohydrate unit bound to a tetracyclic carbon chain. They are found in high concentrations in cycad seeds which have been linked to the etiology of amyotrophic lateral scierosis-parkinsonism dementia complex (ALS-PDC). The neurotoxicities of the three main cycad sterol glucosides, campesterol β-D-glucoside, stigmasterol β-Dglucoside (SG), and β-sitosterol β-D-glucoside (BSSG) have been demonstrated previously in vitro. In the present study, we demonstrate that SC and BSSG exert neurotoxic effects in vivo. An outbred strain of mice was fed BSSG or SG (1000 μg daily) for a period of 15 wk and sacrificed immediately after or at 17 wk later. A battery of behavioural tests, including rotarod, wirehang, modified leg extension reflex test, treadmill, and open field were used to monitor behavioural disturbances. An array of histological measures was also conducted to assess the cellular impact of BSSG and SG. Behavioural test performance scores revealed that BSSG and SG impaired spinal reflexes and decreased overall movement. In addition to this, SC was found to impair motor coordination and strength. Also, ventral plane videography of performance on a treadmill and open field tests indicated that SG-exposed animals were more anxious and tended to drag and shuffle their limbs during forward movement. The cellular impact of dietary BSSG and SG exposures were also different. Animals exposed to each of the sterol glucosides showed an upregulation of activating transcription factor-3 and an increase in the incidence of phosphorylation of junser⁷³ in response to stress. However, BSSG-exposure induced neurodegeneration that primarily targeted large motor neurons whereas SC impacted a more diverse motor neuron population, including large and small motor neurons. Exposure to each of the sterol glucoside caused intense proliferation of astrocytes and microglia as well as a depletion of dopamine levels in the substantia nigra and striatum. Lastly, SG-exposure induced the pathological aggregation of either tau or transactivating DNA binding protein-43 in some animals. The insights gained from this study will be useful for elucidating the pathogenesis of ALS-PDC and related disorders.
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Nagy, Zsuzsanna. "Aspects of the neuropathology of Alzheimer's disease." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240537.

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Bleshoy, Hans. "Neuropathology and sensitivity in the keratoconic cornea." Thesis, City University London, 1990. http://openaccess.city.ac.uk/7670/.

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Corneal touch threshold (CTT) was investigated by aesthesiometry in patients with keratoconusq with and without contact lens wear. Using a matching control group it was established that CTT was significantly higher for the central corneal position in keratoconus. No difference inCTT was found in four peripheral corneal positions in keratoconic and normal corneas. Central CTT correlated inversely with central corneal curvature and central corneal thickness. Central corneal curvature was the most significant single factor to correlate with central CTT and indicates that CTT increases (sensitivity reduces) as the cornea steepens. Corneal surface irregularityq as measured by mire image distortion, correlated positively with central CTT as did corneal scarring. Central CTT did not show a relationship with duration of the disease nor the visibility of the corneal nerve fibres. Lid margin touch thresholds (LTT) were investigated for the central position on the lower and upper eyelid margins. No statistical differences were found between keratoconic and normal eyes nor between upper and lower eyelid margins. The magnitude of LTT was in the order of that established for the peripheral corneal CTT. Innervation of the human corneal stroma and epithelium was investigated by light and electron microscopy in the central and mid-peripheral positions. All nerve bundles were located in the anterior two thirds of the. corneas. In keratoconic corneas mid-peripheral stromal nerve bundles were disorganised and irregular taking up the shape of the adjacent collagen lamellae. Nerve bundles had a regular oval appearance in the control corneas. In both groups Schwann cell cytoplasm was sparse and of varying degree of electron density; axon varicosities were not uncommon and axon content with respect to organelles were similar. The axon density showed large variation in keratoconic: specimens and averaged more than threefold that of control specimens for stromal and epithelial nerves. The control corneas showed a greater proportion of large diameter stromal axons than in keratoconic corneas. This result was reversed for epithelial axons. The results are discussed with respect to the disease process and influence on tactile sensitivity.
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Pitts, Georgia Eloise Rollo. "Neuropathology and cognitive dysfunction after early hypoglycaemia." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/10025822/.

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Hypoglycaemia is the most common metabolic problem in neonatal medicine, occurring during the first days of life and usually resolving within the same time frame. However, some neonates and infants experience severe and recurrent episodes of hypoglycaemia, the most common aetiologies being congenital hyperinsulinism (CHI) and ketotic hypoglycaemia (KH). Children with CHI are at risk of lasting brain injury, while children with KH are considered to be protected from adverse sequelae owing to the presence of ketone bodies during hypoglycaemia. This thesis investigated the neuropsychological and neuroimaging profiles of these two patient groups in neurologically normal school-aged children. Thirty-one patients with CHI and twenty-one patients with KH participated in the study alongside a cohort of healthy controls. A comprehensive battery of neuropsychological tests revealed specific impairments in attention and motor skills in both patient groups, with additional impairments observed in children with CHI. Automated and manual measurements of subcortical volumes, as well as whole brain analyses (voxel based morphometry and tract based spatial statistics) were conducted. Compared to controls, patients with CHI have reduced volume of subcortical structures, as well as extensive white matter volume loss (accompanied by decreased intracranial volume) and reduced white matter integrity across the entire brain. Patients with KH did not significantly differ from controls on any brain measures, but the only significant difference between patient groups was in thalamic and intracranial volumes. Integrity of subcortical structures and white matter was found to be predictive of scores in memory, motor skills and attention. This study is the first to show the extent of brain abnormality as a result of CHI in neurologically normal children. Furthermore, the finding that both patient groups share a similar cognitive profile refutes the notion that children with KH are protected from adverse sequelae. The implications of these findings are discussed.
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Henkes, Greta. "Neuropathologie primärer und sekundärer Mitochondriopathien im Rahmen entzündlicher Muskelerkrankungen." Doctoral thesis, Universitätsbibliothek Leipzig, 2011. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-71313.

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Idiopathische Myositiden stellen die größte Gruppe der erworbenen Myopathien im Erwachsenenalter dar. Die Pathogenese dieser Erkrankungen ist sehr heterogen und nicht in allen Einzelheiten geklärt. Das Auftreten von mitochondrialen Veränderungen und mtDNADeletionen in idiopathischen Myositiden und deren pathophysiologische Bedeutung ist in der Literatur ein kontrovers diskutiertes Thema. Nach der Präsentation des bekannten Wissens über diese Erkrankungen wird in vorliegender Arbeit dieses Thema anhand lichtmikroskopischer Methoden unter Anwendung histologischer Spezialmethoden an Muskelbiopsien von 98 Patienten untersucht. Ziel der Arbeit ist es, mit verschiedenen histologischen Färbemethoden Hinweise für Mitochondrien-Alterationen und feinstrukturelle Charakteristika von primären Mitochondrialen Myopathien in idiopathischen Myositiden zu detektieren. Ein besonderer Schwerpunkt liegt auf der Anwendung einer neuen immunhistochemischen Methode unter Anwendung eines monoklonalen antimitochondrialen Antikörpers. Es wird der Fall eines Mädchens mit muskeldystrophischer Symptomatik dargestellt, dessen Muskelbiopsie im Alter von 7 Jahren die myohistologische Diagnose einer juvenilen Dermatomyositis und Hinweise auf eine mitochondriale Dysfunktion ergab. Die Ergebnisse der immunhistochemischen Methode korrelieren gut mit anderen bekannten mitochondrialen Färbungen, sind sensitiver und stellen möglicherweise eine gute Ergänzung zu den bekannten mitochondrialen Markern und Färbungen dar. Die beobachteten mitochondrialen Dysfunktionen sprechen für die gestörte Mitochondrienfunktion und eine früh im Krankheitsverlauf, am ehesten sekundäre, Beteiligung der Mitochondrien im Krankheitsprozess dieser primär nicht mitochondrialen Erkrankungen
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Books on the topic "Neuropathology"

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Berry, Colin L., ed. Neuropathology. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-71353-8.

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Love, Seth, ed. Neuropathology. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-59554-7.

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A, Cancilla Pasquale, Vogel F. Stephen 1919-, Kaufman Nathan 1915-, United States and Canadian Academy of Pathology. Meeting, and Long Course on the Nervous System (1989 : San Francisco, Calif.), eds. Neuropathology. Baltimore: Williams & Wilkins, 1990.

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Hume, Adams J., and Berry Colin Leonard 1937-, eds. Neuropathology. Berlin: Springer-Verlag, 1988.

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Hilton, David A., and Aditya G. Shivane. Neuropathology Simplified. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-66830-3.

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Garcia, Julio H., Julio Escalona-Zapata, Uriel Sandbank, and Jorge Cervós-Navarro, eds. Diagnostic Neuropathology. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-662-06585-3.

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Friede, Reinhard L. Developmental Neuropathology. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73697-1.

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Hilton, David A., and Aditya G. Shivane. Neuropathology Simplified. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14605-8.

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Adle-Biassette, Homa, Brian N. Harding, and Jeffrey Golden, eds. Developmental Neuropathology. Oxford, UK: John Wiley & Sons, Ltd, 2018. http://dx.doi.org/10.1002/9781119013112.

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Garcia, Julio H., Julio Escalona-Zapata, and Uriel Sandbank, eds. Diagnostic Neuropathology. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-662-11468-1.

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Book chapters on the topic "Neuropathology"

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Perry, Arie, and Bernd W. Scheithauer. "Neuropathology." In Essentials of Anatomic Pathology, 359–422. Totowa, NJ: Humana Press, 2006. http://dx.doi.org/10.1007/978-1-60327-173-8_8.

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Graham, D. I. "Neuropathology." In Spinal Cord Disease, 61–96. London: Springer London, 1997. http://dx.doi.org/10.1007/978-1-4471-0911-2_7.

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Graham, D. I. "Neuropathology." In Clinical Medicine and the Nervous System, 41–78. London: Springer London, 1992. http://dx.doi.org/10.1007/978-1-4471-3353-7_6.

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Martin, Sarah E., Arie Perry, and Eyas M. Hattab. "Neuropathology." In Essentials of Anatomic Pathology, 667–749. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-23380-2_14.

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Shaw, Cheng-Mei, and Ellsworth C. Alvord. "Neuropathology." In Neurosurgery, 39–68. London: Springer London, 2005. http://dx.doi.org/10.1007/1-84628-051-6_3.

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Graham, D. I. "Neuropathology." In Spinal Cord Disease, 61–96. London: Springer London, 1997. http://dx.doi.org/10.1007/978-1-4471-0569-5_7.

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Cairns, N. J. "Neuropathology." In The Molecular Biology of Down Syndrome, 61–74. Vienna: Springer Vienna, 1999. http://dx.doi.org/10.1007/978-3-7091-6380-1_4.

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Hattab, Eyas M., Matthew C. Hagen, Bernd W. Scheithauer, and Arie Perry. "Neuropathology." In Essentials of Anatomic Pathology, 601–80. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6043-6_14.

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Anagnostou, Evdokia, Deepali Mankad, Joshua Diehl, Catherine Lord, Sarah Butler, Andrea McDuffie, Lisa Shull, et al. "Neuropathology." In Encyclopedia of Autism Spectrum Disorders, 2018–23. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1698-3_682.

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Shaw, Cheng-Mei, and Ellsworth C. Alvord. "Neuropathology." In Tumor Neurosurgery, 39–68. London: Springer London, 2006. http://dx.doi.org/10.1007/978-1-84628-294-2_3.

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Conference papers on the topic "Neuropathology"

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Hassan, M. S., P. J. Bentley, and M. Galloway. "Support Vector Machines for Computer Assisted Diagnostic Neuropathology." In Proceedings. 19th IEEE International Symposium on Computer-Based Medical Systems. IEEE, 2006. http://dx.doi.org/10.1109/cbms.2006.150.

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Hall, Nicole, Kariann Lamon, Nicholas Whitton, and Kevin Murnane. "Dopamine Dysregulation and Beyond: Exploring Methamphetamine-Induced Neuropathology." In ASPET 2023 Annual Meeting Abstracts. American Society for Pharmacology and Experimental Therapeutics, 2023. http://dx.doi.org/10.1124/jpet.122.234370.

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Abas, Fazly S., Hamza N. Gokozan, Behiye Goksel, Jose J. Otero, and Metin N. Gurcan. "Intraoperative neuropathology of glioma recurrence: cell detection and classification." In SPIE Medical Imaging, edited by Metin N. Gurcan and Anant Madabhushi. SPIE, 2016. http://dx.doi.org/10.1117/12.2216448.

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Vandenberghe, Michel E., Yael Balbastre, Nicolas Souedet, Anne-Sophie Herard, Marc Dhenain, Frederique Frouin, and Thierry Delzescaux. "Robust supervised segmentation of neuropathology whole-slide microscopy images." In 2015 37th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2015. http://dx.doi.org/10.1109/embc.2015.7319234.

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Delĺera, E., J. Hultman, B. Kessler, K. Jäderlund, and K. Matiasek. "Neuropathology of painful episodic hypersensitivity in greyhound show dogs." In 67. Jahrestagung der Fachgruppe Pathologie der Deutschen Veterinärmedizinischen Gesellschaft. Georg Thieme Verlag KG, 2024. http://dx.doi.org/10.1055/s-0044-1787334.

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Kannan, Kasthuri S., Aristotelis Tsirigos, Jonathan Serrano, Lynn Ann Forrester, Arline Faustin, Cheddhi Thomas, David Capper, et al. "Abstract 11: Advancing methylation profiling in neuropathology: Diagnosis and clinical management." In Abstracts: AACR Precision Medicine Series: Integrating Clinical Genomics and Cancer Therapy; June 13-16, 2015; Salt Lake City, UT. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3265.pmsclingen15-11.

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Sarah, Wrigley, Cullinane Patrick, Jaunmuktane Zane, Revesz Tamas, Warner Tom, and De Pablo Fernandez Eduardo. "Natural history and neuropathology of patients presenting with pure autonomic failure." In Association of British Neurologists: Annual Meeting Abstracts 2023. BMJ Publishing Group Ltd, 2023. http://dx.doi.org/10.1136/jnnp-2023-abn.88.

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Auboyer, Laura, Amandine Virlogeux, Chiara Scaramuzzino, Sophie Lenoir, Rémi Carpentier, Morgane Louessard, Aurélie Genoux, et al. "I05 Increasing brain palmitoylation rescues behavior and neuropathology in huntington disease mice." In EHDN Abstracts 2021. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/jnnp-2021-ehdn.119.

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"BGRS/SB-2022 729 Modeling of neuropathology on zebrafish: traumatic brain injury." In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-420.

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Safransky, Michelle, Kaj Blennow, Henrik Zetterberg, Yorghos Tripodis, Brett Martin, Jason Weller, Breton Asken, et al. "Cerebrospinal Fluid Biomarkers for the Early Detection of Alzheimer’s Disease Neuropathology (S15.005)." In 2023 Annual Meeting Abstracts. Lippincott Williams & Wilkins, 2023. http://dx.doi.org/10.1212/wnl.0000000000203440.

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Reports on the topic "Neuropathology"

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Koob, George F., and Eric P. Zorrilla. Chronic Stress and Neuropathology: Neurochemical, Molecular, and Genetic Factors. Fort Belvoir, VA: Defense Technical Information Center, August 2005. http://dx.doi.org/10.21236/ada452205.

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Muggenburg, Bruce A., and Elizabeth Head. The Effects of Antioxidants and Experience on the Development of Age Dependent Cognitive Dysfunction and Neuropathology in Canines. Fort Belvoir, VA: Defense Technical Information Center, October 2002. http://dx.doi.org/10.21236/ada410295.

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Block, Michelle L. The Role of Protein Radicals in Chronic Neuroimmune Dysfunction and Neuropathology in Response to a Multiple-Hit Model of Gulf War Exposure. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613307.

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Elmann, Anat, Orly Lazarov, Joel Kashman, and Rivka Ofir. therapeutic potential of a desert plant and its active compounds for Alzheimer's Disease. United States Department of Agriculture, March 2015. http://dx.doi.org/10.32747/2015.7597913.bard.

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Abstract:
We chose to focus our investigations on the effect of the active forms, TTF and AcA, rather than the whole (crude) extract. 1. To establish cultivation program designed to develop lead cultivar/s (which will be selected from the different Af accessions) with the highest yield of the active compounds TTF and/or achillolide A (AcA). These cultivar/s will be the source for the purification of large amounts of the active compounds when needed in the future for functional foods/drug development. This task was completed. 2. To determine the effect of the Af extract, TTF and AcA on neuronal vulnerability to oxidative stress in cultured neurons expressing FAD-linked mutants.Compounds were tested in N2a neuroblastoma cell line. In addition, we have tested the effects of TTF and AcA on signaling events promoted by H₂O₂ in astrocytes and by β-amyloid in neuronal N2a cells. 3. To determine the effect of the Af extract, TTF and AcA on neuropathology (amyloidosis and tau phosphorylation) in cultured neurons expressing FAD-linked mutants. 4. To determine the effect of A¦ extract, AcA and TTF on FAD-linked neuropathology (amyloidosis, tau phosphorylation and inflammation) in transgenic mice. 5. To examine whether A¦ extract, TTF and AcA can reverse behavioral deficits in APPswe/PS1DE9 mice, and affect learning and memory and cognitive performance in these FAD-linked transgenic mice. Background to the topic.Neuroinflammation, oxidative stress, glutamate toxicity and amyloid beta (Ab) toxicity are involved in the pathogenesis of Alzheimer's diseases. We have previously purified from Achilleafragrantissimatwo active compounds: a protective flavonoid named 3,5,4’-trihydroxy-6,7,3’-trimethoxyflavone (TTF, Fl-72/2) and an anti-inflammatory sesquiterpenelactone named achillolide A (AcA). Major conclusions, solutions, achievements. In this study we could show that TTF and AcA protected cultured astrocytes from H₂O₂ –induced cell death via interference with cell signaling events. TTF inhibited SAPK/JNK, ERK1/2, MEK1 and CREBphosphorylation, while AcA inhibited only ERK1/2 and MEK1 phosphorylation. In addition to its protective activities, TTF had also anti-inflammatory activities, and inhibited the LPS-elicited secretion of the proinflammatorycytokinesInterleukin 6 (IL-6) and IL-1b from cultured microglial cells. Moreover, TTF and AcA protected neuronal cells from glutamate and Abcytotoxicity by reducing the glutamate and amyloid beta induced levels of intracellular reactive oxygen species (ROS) and via interference with cell signaling events induced by Ab. These compounds also reduced amyloid precursor protein net processing in vitro and in vivo in a mouse model for Alzheimer’s disease and improvedperformance in the novel object recognition learning and memory task. Conclusion: TTF and AcA are potential candidates to be developed as drugs or food additives to prevent, postpone or ameliorate Alzheimer’s disease. Implications, both scientific and agricultural.The synthesis ofAcA and TTF is very complicated. Thus, the plant itself will be the source for the isolation of these compounds or their precursors for synthesis. Therefore, Achilleafragrantissima could be developed into a new crop with industrial potential for the Arava-Negev area in Israel, and will generate more working places in this region.
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Kochanek, Patrick M. Emergency Interventions After Severe Traumatic Brain Injury in Rats: Effect on Neuropatholgy and Functional Outcome. Fort Belvoir, VA: Defense Technical Information Center, January 1999. http://dx.doi.org/10.21236/ada360938.

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