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Cellular Aspects of the Inflammatory Response in Alzheimer's Disease 阿尔茨海默病炎症反应的细胞方面
Neurodegeneration Pub Date : 1996-12-01 Epub Date: 2002-05-25 DOI: 10.1006/neur.1996.0069
Rajesh N. Kalaria, Dawn L. Cohen, Daniel R.D. Premkumar
{"title":"Cellular Aspects of the Inflammatory Response in Alzheimer's Disease","authors":"Rajesh N. Kalaria,&nbsp;Dawn L. Cohen,&nbsp;Daniel R.D. Premkumar","doi":"10.1006/neur.1996.0069","DOIUrl":"10.1006/neur.1996.0069","url":null,"abstract":"<div><p>Cerebral amyloid β protein deposition in Alzheimer's disease is associated with a predominantly local acute phase response that kindles release of various inflammatory and immune system mediators. The molecular events are accompanied by a profound cellular response which is largely orchestrated by microglia. Current evidence suggests microglia are primarily involved in phagocytic activity and may be responsible for inducing further neuronal damage by generating reactive oxygen species and proteolytic enzymes. Antiinflammatory measures that target complement activation as well as microglial-mediated oxidative damage would provide rational therapeutic strategies.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":"5 4","pages":"Pages 497-503"},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0069","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20066527","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: 38
Oxidative Mechanisms in β-Amyloid Cytotoxicity β-淀粉样蛋白细胞毒性的氧化机制
Neurodegeneration Pub Date : 1996-12-01 Epub Date: 2002-05-25 DOI: 10.1006/neur.1996.0060
John B. Davis
{"title":"Oxidative Mechanisms in β-Amyloid Cytotoxicity","authors":"John B. Davis","doi":"10.1006/neur.1996.0060","DOIUrl":"10.1006/neur.1996.0060","url":null,"abstract":"<div><p>Amyloid β-peptide has been demonstrated to be toxic for primary and clonal neuronal cell lines<em>in vitro</em>. Oxidative mechanisms have been implicated in this pathway at several points, including the aggregation of β-amyloid necessary for cytotoxic activity, generation of radicals by the peptide itself, and intracellularly in response to toxic β-amyloid peptides. Supporting an oxidative hypothesis are the observations that cells mount a stress response to β-amyloid similar to that seen in response to oxidative stress and that they may be rescued from cytotoxicity by antioxidants, inhibitors of oxidative enzyme metabolism, and overexpression of antioxidant enzymes. Although the source(s) of the oxygen radicals has not yet been identified, altered antioxidant enzyme levels and oxidative by-products in Alzheimer's disease brain samples relate the<em>in vitro</em>studies to the human disease.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":"5 4","pages":"Pages 441-444"},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/neur.1996.0060","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20065852","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: 49
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 Epub Date: 2002-05-25 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":"5 4","pages":"Pages 505-509"},"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 Epub Date: 2002-05-25 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":"5 4","pages":"Pages 409-415"},"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 Epub Date: 2002-05-25 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":"5 4","pages":"Pages 417-421"},"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 Epub Date: 2002-05-25 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":"5 4","pages":"Pages 367-377"},"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 Epub Date: 2002-05-25 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":"5 4","pages":"Pages 435-440"},"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 Epub Date: 2002-05-25 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":"5 4","pages":"Pages 483-488"},"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 Epub Date: 2002-05-25 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":"5 4","pages":"Pages 399-402"},"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 Epub Date: 2002-05-25 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":"5 4","pages":"Pages 423-427"},"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
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