Neurodegeneration最新文献

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Current Approaches to the Treatment of Alzheimer's Disease 目前治疗阿尔茨海默病的方法
Neurodegeneration Pub Date : 1996-12-01 DOI: 10.1006/neur.1996.0070
Gordon K. Wilcock
{"title":"Current Approaches to the Treatment of Alzheimer's Disease","authors":"Gordon K. Wilcock","doi":"10.1006/neur.1996.0070","DOIUrl":"10.1006/neur.1996.0070","url":null,"abstract":"<div><p>Alzheimer's disease is associated with multiple neurotransmitter deficits, most importantly in the cholinergic system. There are also other pathological processes. Strategies to combat these are discussed.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0070","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20066528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 78
Amyloid Precursor Protein mRNAs in Alzheimer's Disease 阿尔茨海默病中的淀粉样前体蛋白mrna
Neurodegeneration Pub Date : 1996-12-01 DOI: 10.1006/neur.1996.0055
Paul J. Harrison , Wendy H. Wighton-Benn , Josephine M. Heffernan , Maurice W. Sanders , R.Carl A. Pearson
{"title":"Amyloid Precursor Protein mRNAs in Alzheimer's Disease","authors":"Paul J. Harrison ,&nbsp;Wendy H. Wighton-Benn ,&nbsp;Josephine M. Heffernan ,&nbsp;Maurice W. Sanders ,&nbsp;R.Carl A. Pearson","doi":"10.1006/neur.1996.0055","DOIUrl":"10.1006/neur.1996.0055","url":null,"abstract":"<div><p>Hybridization studies of mRNA link genetic with neurochemical and neuropathological approaches to Alzheimer's disease (AD). Here we review the distribution and abundance of amyloid precursor protein mRNAs in normal and AD-afflicted brains. The expression of apolipoprotein E and presenilin mRNAs are also discussed.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0055","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20065847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 11
Structural Correlates of Cognition in Dementia: Quantification and Assessment of Synapse Change 认知在痴呆中的结构相关性:突触变化的量化和评估
Neurodegeneration Pub Date : 1996-12-01 DOI: 10.1006/neur.1996.0056
Steven T. DeKosky , Stephen W. Scheff , Scot D. Styren
{"title":"Structural Correlates of Cognition in Dementia: Quantification and Assessment of Synapse Change","authors":"Steven T. DeKosky ,&nbsp;Stephen W. Scheff ,&nbsp;Scot D. Styren","doi":"10.1006/neur.1996.0056","DOIUrl":"10.1006/neur.1996.0056","url":null,"abstract":"<div><p>Dementia results from a combination of structural and neurochemical pathologies. The most reliable index of cognition in both postmortem and biopsied AD brain is synapse loss.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0056","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20065848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 383
An Ultrastructural Study of the Ciliary Ganglia of the Cat and Monkey (Macaca fascicularis) Following Preganglionic Axotomy 猫猴(Macaca fascularis)睫状神经节前切开后睫状神经节超微结构研究
Neurodegeneration Pub Date : 1996-12-01 DOI: 10.1006/neur.1996.0049
Y.L. Zhang, C.K. Tan, W.C. Wong
{"title":"An Ultrastructural Study of the Ciliary Ganglia of the Cat and Monkey (Macaca fascicularis) Following Preganglionic Axotomy","authors":"Y.L. Zhang,&nbsp;C.K. Tan,&nbsp;W.C. Wong","doi":"10.1006/neur.1996.0049","DOIUrl":"10.1006/neur.1996.0049","url":null,"abstract":"<div><p>The present study describes ultrastructural changes in the ciliary ganglia of the cat and monkey following preganglionic axotomy. At 3, 5 and 7 days after operation, the nucleus of some neurons was irregular, with prominent indentations, and displaced to the periphery of the neuron. The surface of most neurons was irregular. Neurofilaments and glycogen-like granules were much increased in some neurons. At 21 and 28 days after operation, neurons again appeared normal. Dendritic profiles, packed with many mitochondria and glycogen-like granules, could often be observed from 3 days after operation. In longitudinal section such profiles represented expanded trunks of dendrites; dilated mitochondria and dense bodies were sometimes encountered within them. At later stages after operation, some of these profiles were synaptically contacted by, or closely associated with, axon terminals. In myelinated axons, mitochondria and glycogen-like granules were also increased in number and dilated profiles and dense bodies were found within the axoplasm. In unmyelinated axons, dilated profiles and myelin-like figures were present, as were vesiculo-tubular structures and dense bodies. Electron-dense and -lucent changes could both be observed in myelinated and unmyelinated axons. Almost all the axon terminals were affected 3 days after operation. Within such degenerating axon terminals, the synaptic vesicles had accumulated to form one or several clumps, sometimes the degenerating axon terminals had undergone filamentous hyperplasia. At 45 days after operation, hardly any axon terminals were encountered. Non-neuronal cells, including satellite cells, macrophages and Schwann cells, were actively involved in removing degenerating axons and other cell debris.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0049","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20065903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 4
Energy Metabolism, Oxidative Stress and Neuronal Degeneration in Alzheimer's Disease 阿尔茨海默病的能量代谢、氧化应激和神经元变性
Neurodegeneration Pub Date : 1996-12-01 DOI: 10.1006/neur.1996.0059
Neil R. Sims
{"title":"Energy Metabolism, Oxidative Stress and Neuronal Degeneration in Alzheimer's Disease","authors":"Neil R. Sims","doi":"10.1006/neur.1996.0059","DOIUrl":"10.1006/neur.1996.0059","url":null,"abstract":"<div><p>Both altered energy metabolism and oxidative stress have been proposed to contribute to tissue damage in neurogenerative diseases. Animal models and cell culture studies provide evidence for a role of these processes in several forms of neuronal death. Reductions in the activities of some key mitochondrial enzymes have been found in autopsied brain in Alzheimer's disease. However, results obtained with biopsied brain tissue as well as assessments of metabolic rates for glucose<em>in vivo</em>indicate that a reduced functional capacity of mitochondria is probably not a general feature in the brain in Alzheimer's disease. These studies do not address the possibility that short-lived changes in energy metabolism affecting a small number of cells at any one time could be contributing to cell death. Several findings point to a moderate increase in oxidative damage in those areas of brain which are most severely affected in this disease, probably resulting from an increase in production of reactive oxygen species. Whether this is a contributor to neurodegeneration or a consequence of it remains unresolved.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0059","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20065851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 46
Neurotransmitter Receptor/G-protein Mediated Signal Transduction in Alzheimer's Disease Brain 阿尔茨海默病脑神经递质受体/ g蛋白介导的信号转导
Neurodegeneration Pub Date : 1996-12-01 DOI: 10.1006/neur.1996.0067
Richard F. Cowburn , Christopher J. Fowler , Cora O'Neill
{"title":"Neurotransmitter Receptor/G-protein Mediated Signal Transduction in Alzheimer's Disease Brain","authors":"Richard F. Cowburn ,&nbsp;Christopher J. Fowler ,&nbsp;Cora O'Neill","doi":"10.1006/neur.1996.0067","DOIUrl":"10.1006/neur.1996.0067","url":null,"abstract":"<div><p>Recent evidence suggests that the neurochemical pathology of Alzheimer's disease includes severe disruptions of the neurotransmitter receptor/G-protein mediated phosphatidylinositol hydrolysis and adenylyl cyclase signal transduction pathways. The present article briefly reviews evidence from postmortem studies describing disruptions to these systems and speculates as to the importance of these changes in terms of contributing to disease pathology and limiting the success of neurotransmitter replacement strategies.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0067","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20066525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 19
Behavioural Problems in Dementia and Biochemistry: Clinical Aspects 痴呆和生物化学中的行为问题:临床方面
Neurodegeneration Pub Date : 1996-12-01 DOI: 10.1006/neur.1996.0053
Tony Hope, Janet Keene
{"title":"Behavioural Problems in Dementia and Biochemistry: Clinical Aspects","authors":"Tony Hope,&nbsp;Janet Keene","doi":"10.1006/neur.1996.0053","DOIUrl":"10.1006/neur.1996.0053","url":null,"abstract":"<div><p>Behavioural and psychiatric problems in dementia are clinically important; they are also theoretically interesting. Neurochemical factors are likely to play a causal role in some of these problems. Two approaches to investigating the biochemical basis of behavioural problems are outlined: the correlation of prospectively collected behavioural data with postmortem neurochemical measures;and the detailed analysis of behaviour allowing investigation of underlying mechanisms. These approaches are illustrated with empirical data. David Bowen's neurochemical approach to dementia provided stimulus to this work.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0053","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20065845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Pyramidal Nerve Cell Loss in Alzheimer's Disease 阿尔茨海默病的锥体神经细胞损失
Neurodegeneration Pub Date : 1996-12-01 DOI: 10.1006/neur.1996.0057
David M.A. Mann
{"title":"Pyramidal Nerve Cell Loss in Alzheimer's Disease","authors":"David M.A. Mann","doi":"10.1006/neur.1996.0057","DOIUrl":"10.1006/neur.1996.0057","url":null,"abstract":"<div><p>Loss of the large pyramidal cells of the association neocortex and hippocampus, along with plaques and tangles, is fundamental to the neuropathology of Alzheimer's disease. The extent of Alzheimer-specific cell loss, relative to controls, is age-dependent with maximal losses in younger subjects though, because of the (additive) effects of ‘normal’ ageing on such cells, the<em>absolute</em>loss remains constant at all ages. The cause of the cell loss remains unknown but probably relates to neurofibrillary degeneration through a crowding out of organelles and a disruption of intracellular transport; oxidative stress may also contribute. The degree of clinical dementia correlates well with the extent of pyramidal cell loss.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0057","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20065849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 79
Neurochemical Studies of Alzheimer's Disease 阿尔茨海默病的神经化学研究
Neurodegeneration Pub Date : 1996-12-01 DOI: 10.1006/neur.1996.0051
Alan M. Palmer
{"title":"Neurochemical Studies of Alzheimer's Disease","authors":"Alan M. Palmer","doi":"10.1006/neur.1996.0051","DOIUrl":"10.1006/neur.1996.0051","url":null,"abstract":"<div><p>Neurochemical studies of post-mortem human brain have made a major contribution to understanding the neuronal basis of neurodegenerative disease and formed the basis of rational therapies for such disorders. The application of this approach to the neurochemical pathology of Alzheimer's disease was pioneered by David Bowen. By combining assessment of post-mortem tissue (where the disease has usually run its full course) with tissue obtained ante-mortem (where the disease course is incomplete), it has been possible to (1) establish which neurones are lost in the disease, (2) determine which neurones are lost early in the course of the disease, and (3) discern which changes relate with the symptomatology of the disease. Thus, loss of cholinergic, noradrenergic and serotonergic innervation to the cortex occurs at an early stage, since markers of the neurones are lost in both post-mortem and ante-mortem tissue. By contrast, dopaminergic innervation remains intact and markers of cortical GABAergic interneurones are affected in post-mortem tissue only, suggesting that loss of GABAergic neurones occurs only at a late stage of the disease. Cholinergic markers and the number of pyramidal cell perikarya correlate with the severity of dementia, suggesting that loss of cholinergic and EAA neurones is the major contributor to the cognitive impairments of Alzheimer's disease. Loss of noradrenergic and serotonergic neurones probably contributes to the emergence of non-cognitive impairments in behaviour. Possible causes of selective neuronal loss are discussed.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0051","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20065905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 103
Glial Cell Derived Neurotrophic Factors and Alzheimer's Disease 神经胶质细胞源性神经营养因子与阿尔茨海默病
Neurodegeneration Pub Date : 1996-12-01 DOI: 10.1006/neur.1996.0068
Ambrish J. Patel, Colin Wickenden, Angela Jen, H.A.Rohan de Silva
{"title":"Glial Cell Derived Neurotrophic Factors and Alzheimer's Disease","authors":"Ambrish J. Patel,&nbsp;Colin Wickenden,&nbsp;Angela Jen,&nbsp;H.A.Rohan de Silva","doi":"10.1006/neur.1996.0068","DOIUrl":"10.1006/neur.1996.0068","url":null,"abstract":"<div><p>In Alzheimer's disease the normal balance of metabolic pathways regulating trophic factors/cytokines is disrupted; local reduction may result in neurons being deprived of neurotrophic factors while an excess may initiate a cascade of interaction between glial cells and β-amyloid precursor protein metabolism thereby facilitating plaque formation. This paper briefly discusses the findings of our group on aspects ranging from cholinergic humoral and trophic factors to mechanisms underlying amyloidogenesis in Alzheimer's disease.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0068","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20066526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 9
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