Có 20+ tài liệu thuộc chủ đề "cơ chế thần kinh"
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gene function and expression, 730 gene location and structure, 730 genetic variation, 730–731 inheritance and clinical features,. structure and mutations, 731 clinical diagnostic, 714 clinical manifestations, 713 cognitive ERP-S in, 259 delayed-response tests, 258 DJ1. gene function and expression, 726–727 gene location and structure, 726 genetic variation, 727. inheritance and clinical features, 726 structure and mutations, 728 etiology of, 248....
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This work may not be translated or copied in whole or in part without the written permission of the publisher (Springer Science+Business Media, LLC, 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. A major problem in doing chemistry on brain obtained at autopsy is the possibil- ity of artifacts...
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The Genetics of Alzheimer’s Disease and Parkinson’s Disease. Bak Faculty of Pharmaceutical Sciences, Department of Pharmacology and Pharmacotherapy, University of Copenhagen, DK-2100, Copenhagen, Denmark, [email protected]. Barker Department of Medicinal Chemistry and Molecular Pharmacology, Purdue University, West Lafayette, IN 47906, USA, [email protected]. Nike Beaubier Department of Pathology, Taub Center for the Study of. Alzheimer’s Disease and the Aging Brain, Columbia University...
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Science at that time was heavily a matter of classification, including classification of the new species of plants and animals being discovered in the Americas and other continents pre- viously unexplored by Europeans. Sydenham classified illnesses analogously to the way Linnaeus was classifying plants.. His model was what we now recog- nize to be malaria. This disease typically causes high...
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Mechanisms Versus Diagnoses 15 Navon R et al (1973) Am J Human Genet 25:287–292. O’Neill B et al (1978) Neurology Oonk JGW et al (1979) Neurology 29:380–384. Rapin I et al (1976) Arch Neurol Renshaw PF et al (1992) Ann Neurol Rosebush PI et al (1995) J Clin Psychiat 56:347–353. Molecular Mechanisms of Neuronal Death. Abstract Cellular homeostasis, maintenance of...
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In the second (caspase-8) part of the pathway, TRADD, which is bound to the TNF receptor, acts as a platform allowing the complex to interact with Fas- associated death domain (Yeh et al., 1998. Once FADD is bound to the complex, it recruits caspase-8 to form a cytoplasmic DISC protein com- plex that finally ends with the death of the...
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Because AD is the primary cause of dementia among the elderly population and ALS is the most common adult onset disorder of motor neurons, we take a global overview of the molecular mechanisms leading to neuronal cell death in both diseases.. Accompanying these features is a profound synaptic and neuronal loss in specific vulnerable brain regions including the hippocampus and...
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Consensus statement of the American Association for Geriatric Psychiatry, the Alzheimer’s Association, and the American Geriatrics Society. Takeuchi H, Kobayashi Y, Ishigaki S, Doyu M, Sobue G (2002) Mitochondrial localization of mutant superoxide dismutase 1 triggers caspase-dependent cell death in a cellular model of familial amyotrophic lateral sclerosis. Terry RD, Peck A, DeTeresa R, Schechter R, Horoupian DS (1981) Some...
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evident except in the model APP SL /PS-1 M146L mice developed by Blanchard et al.. (2003) where a loss (35%) of neurons in the pyramidal cell layer of the hippocampus was seen at 17 months of age (Schmitz et al., 2004). Recently, an intense sub- cortical monoaminergic neurodegeneration (50% neuronal loss) was observed in APP SWE /PS-1 dE9 (Liu et...
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or reduced in the brain of AD patients (Holmes et al., 2008). 3 Parkinson’s Disease (PD) 3.1 The Human Disease. Although PD can develop at any age, it begins most commonly in older adults, with a peak age at onset at around 60 years (von Campenhausen et al., 2005).. The likelihood of developing PD increases with age, with a lifetime...
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Ludolph et al., 1991). The susceptibility, nature (apoptotic or necrotic), and extent of the striatal damage depend upon the species, animal strain, age, dose administered, and administration schedule (acute versus chronic) (Alexi et al., 1998. Ouary et al., 2000. Striatal and nigral damage were also evident with significant neuronal loss and astroglial activation (Fernagut et al., 2004).. For instance, the...
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still essential elements in the laborious attempts to determine the etiology of a given disease, understand its progression, and the relationship between the observed clin- ical phenotypes and the histological features or hallmarks of the disease. Work on animal models of neurodegenerative disorders in the group of MJ and AG is financed by the Fondation de France, Institut pour la...
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Perez SE, Dar S, Ikonomovic MD, DeKosky ST, Mufson EJ (2007) Cholinergic forebrain degeneration in the APPswe/PS1DeltaE9 transgenic mouse. Periquet M, Fulga T, Myllykangas L, Schlossmacher MG, Feany MB (2007) Aggregated alpha- synuclein mediates dopaminergic neurotoxicity in vivo. Peters A, Rosene DL, Moss MB, Kemper TL, Abraham CR, Tigges J, Albert MS (1996) Neurobiological bases of age-related cognitive decline in...
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2.1 Thiamine Deficiency-Related Neurological Disorders. Beriberi (infantile and adult) and Wernicke’s encephalopathy (WE) are clinical manifestations attributed to thiamine deficiency. WE is a metabolic disease due to thiamine deficiency and is characterized by lesions in the thalamus, hypothalamus (including mammillary nuclei), and cerebellum (Victor et al., 1971. Similarly, a review of the literature describ- ing WE patients with HIV–AIDS revealed...
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Neurological symptoms are more obvious in rats with antimetabolite-induced niacin deficiencies than in the corn-fed dogs.. Dietary niacin deficiency reduces the levels of NAD and NADP coenzymes in the brain. A chronic toxic delirium may be the only clinical abnormal- ity, at least early in the course of the disorder. Administration of niacin is recommended in APE patients showing myoclonus...
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Cerebral edema results from the excess of fluid in the brain’s intra- and extracellular spaces. This chapter focuses on the major molecular mechanisms triggering brain edema, including alterations in ion chan- nels and transporters, matrix metalloproteinases, tight junction protein degradation, free radicals, and products of the arachidonic acid metabolism. We review present knowledge of the contribution to brain edema of...
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Zeynalov et al., 2008). Similarly, in a model of water intoxication, AQP4-null mice display a decreased brain water content and a significant improvement in survival (Manley et al., 2000. Zador et al., 2007).. However, in conditions in which vasogenic edema is significant, AQP4 deletion exacerbates brain edema (Zador et al., 2007). AQP4 function has been demonstrated to be of great...
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the COX-2 inhibitor nimesulide (Candelario-Jalil et al., 2007a). Inhibition of COX activity with indomethacin prevented BBB damage following intracerebral admin- istration of TNF-α in the rat. Indomethacin significantly reduced TNF-α-induced MMP-9 and MMP-3 expression and activity and attenuated free radical formation (Candelario-Jalil et al., 2007b).. The theories related to shifts in water that result in the imbalance associated with edema...
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Treatment with 1 g/day of methylprednisolone for 3–5 days reduces the inflammatory changes in the blood vessels during an acute exacerbation.. High-dose steroids reduce the MMP-9 in the brain as reflected in the CSF, preserving the integrity of the BBB (Rosenberg et al., 1996b).. Treatment of edema surrounding an intracerebral hemorrhage has recently been intensively studied because of the side-effect...
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Rosenberg GA, Dencoff JE, Correa N Jr., Reiners M, Ford CC (1996b) Effect of steroids on CSF matrix metalloproteinases in multiple sclerosis: relation to blood-brain barrier injury.. Rosenberg GA, Estrada EY, Dencoff JE (1998) Matrix metalloproteinases and TIMPs are associated with blood-brain barrier opening after reperfusion in rat brain. Rosenberg GA, Estrada E, Kyner WT (1990) Vasopressin-induced brain edema is...