Journal ArticleDOI
Alzheimer's disease and the aging brain.
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TLDR
The frequencies of each of the several types of dementia are enumerated, showing that Alzheimer’s disease is present in about 80% of cases and the strongest structural correlate with cognitive tests is synapse loss, which is probably caused by Aβ oligopeptides in the terminal axons and dendrites.Abstract:
The frequencies of each of the several types of dementia are enumerated, showing that Alzheimer's disease is present in about 80% of cases. Cerebral changes associated with cognitively normal aging include shrinkage of large cortical neurons but not a significant loss of total neuronal number. Nevertheless, the population density of synapses measured by confocal microscopy does decline significantly in normal aging. The classical lesions of Alzheimer's disease are neuritic plaques and neurofibrillary tangles, and their frequency correlates with declining cognitive measures. Although amyloid is prominent in plaques, it is probably not the agent of destruction. That role seems to be held by Abeta oligomers. The strongest structural correlate with cognitive tests is synapse loss, which is probably caused by Abeta oligopeptides in the terminal axons and dendrites.read more
Citations
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Journal ArticleDOI
Alzheimer's disease: Targeting the Cholinergic System
Talita H. Ferreira-Vieira,Isabella M. Guimaraes,Flavia Rodrigues da Silva,Fabiola M. Ribeiro +3 more
TL;DR: Synthesis of cholinergic neurons located in the basal forebrain, including the neurons that form the nucleus basalis of Meynert, are severely lost in Alzheimer’s disease, and drugs that act on the choline system represent a promising option to treat AD patients.
Journal ArticleDOI
Changes in the structural complexity of the aged brain
Dara L. Dickstein,Doron Kabaso,Anne B. Rocher,Jennifer I. Luebke,Susan L. Wearne,Patrick R. Hof +5 more
TL;DR: Findings suggest that age‐related neuronal dysfunction, which must underlie observed decline in cognitive function, probably involves a host of other subtle changes within the cortex that could include alterations in receptors, loss of dendrites, and spines and myelin dystrophy, as well as the alterations in synaptic transmission.
Journal ArticleDOI
Efficacy of a medical food in mild Alzheimer's disease: A randomized, controlled trial
Philip Scheltens,Patrick Joseph Gerardus Hendrikus Kamphuis,Frans R.J. Verhey,Marcel G. M. Olde Rikkert,Richard J. Wurtman,David Wilkinson,Jos W. R. Twisk,Alexander Kurz +7 more
TL;DR: To investigate the effect of a medical food on cognitive function in people with mild Alzheimer's disease (AD), a large number of subjects were randomly assigned to receive either a probiotic or a dummy pill.
Journal ArticleDOI
Mechanisms of Hybrid Oligomer Formation in the Pathogenesis of Combined Alzheimer's and Parkinson's Diseases
Igor F. Tsigelny,Leslie Crews,Paula Desplats,Gideon M. Shaked,Yuriy Sharikov,Hideya Mizuno,Brian Spencer,Edward Rockenstein,Margarita Trejo,Oleksandr Platoshyn,Jason X.-J. Yuan,Eliezer Masliah +11 more
TL;DR: Results support the contention that Aβ directly interacts with α-syn and stabilized the formation of hybrid nanopores that alter neuronal activity and might contribute to the mechanisms of neurodegeneration in AD and PD.
Journal ArticleDOI
Type 1 diabetes exaggerates features of Alzheimer's disease in APP transgenic mice.
Corinne G. Jolivalt,Rosemarie Hurford,Corinne A. Lee,Wilmar Dumaop,Edward Rockenstein,Eliezer Masliah +5 more
TL;DR: The results indicate that the pathologic features of AD are exaggerated in the brain of APP transgenic mice that have concurrent insulin-deficient diabetes, and underscore a possible mechanism of brain dysfunction common to AD and diabetes.
References
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Journal ArticleDOI
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Journal ArticleDOI
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Journal ArticleDOI
Physical basis of cognitive alterations in Alzheimer's disease: synapse loss is the major correlate of cognitive impairment.
Robert D. Terry,Eliezer Masliah,David P. Salmon,Nelson Butters,Richard DeTeresa,Robert Hill,Lawrence A. Hansen,Robert Katzman +7 more
TL;DR: Both linear regressions and multivariate analyses correlating three global neuropsychological tests with a number of structural and neurochemical measurements performed on a prospective series of patients with Alzheimer's disease and 9 neuropathologically normal subjects reveal very powerful correlations with all three psychological assays.
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