Journal ArticleDOI
An integrative hypothesis concerning the pathogenesis and progression of Alzheimer's disease
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TLDR
A defect in blood brain barrier function and/or structure within the cerebral cortex may be the cause of the cerebral vessel amyloidosis common in many patients with Alzheimer's disease.About:
This article is published in Neurobiology of Aging.The article was published on 1986-11-01. It has received 195 citations till now. The article focuses on the topics: Senile plaques & Alzheimer's disease.read more
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Differences in the pattern of hippocampal neuronal loss in normal ageing and Alzheimer's disease
TL;DR: It is concluded that the neurodegenerative processes associated with normal ageing and with Alzheimer's disease are qualitatively different and that Alzheimer's Disease is not accelerated by ageing but is a distinct pathological process.
Journal ArticleDOI
Widespread expression of BDNF but not NT3 by target areas of basal forebrain cholinergic neurons.
TL;DR: In human hippocampus, cells expressing BDNF mRNA are distributed in a fashion similar to that observed in the rat, which point to both basal forebrain cholinergic cells and olfactory pathways as potential central targets for BDNF.
Journal ArticleDOI
Decreased EEG synchronization in Alzheimer's disease and mild cognitive impairment.
Thomas Koenig,Leslie S. Prichep,Thomas Dierks,D. Hubl,L-O Wahlund,Erwin Roy John,Vesna Jelic +6 more
TL;DR: The hypothesis of a functional disconnection of neuro-cognitive networks in patients with mild cognitive impairment (MCI) and Alzheimer Dementia was investigated using baseline resting EEG data, and patients showed decreased GFS values in Alpha, Beta, and Gamma frequency bands, and increased GFSvalues in the Delta band, confirming the hypothesized disconnection syndrome.
Alzheimer disease models and human neuropathology: similarities and diVerences
TL;DR: In this article, a triply trans- genic model (mutated APP, PS1 and tau) was used to investigate the mechanisms of neuro-nal loss, the accumulation of A in the cell body of the neu- rons, inXammation and gliosis.
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Alzheimer disease models and human neuropathology: similarities and differences.
TL;DR: The APP transgenic mice have raised new questions concerning the mechanisms of neuronal loss, the accumulation of Aβ in the cell body of the neurons, inflammation and gliosis, and the dendritic alterations, and some insight is gained into the kinetics of the changes.
References
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Journal ArticleDOI
The Cholinergic Hypothesis of Geriatric Memory Dysfunction
Raymond T. Bartus,Raymond T. Bartus,Reginald L. Dean,Bernard Beer,Bernard Beer,Arnold S. Lippa,Arnold S. Lippa +6 more
TL;DR: Biochemical, electrophysiological, and pharmacological evidence supporting a role for cholinergic dysfunction in age-related memory disturbances is critically reviewed and an attempt has been made to identify pseudoissues, resolve certain controversies, and clarify misconceptions that have occurred in the literature.
Journal ArticleDOI
Alzheimer's disease: Initial report of the purification and characterization of a novel cerebrovascular amyloid protein
George G. Glenner,Caine W. Wong +1 more
TL;DR: A purified protein derived from the twisted beta-pleated sheet fibrils in cerebrovascular amyloidosis associated with Alzheimer's disease has been isolated and Amino acid sequence analysis and a computer search reveals this protein to have no homology with any protein sequenced thus far.
Journal ArticleDOI
Amyloid plaque core protein in Alzheimer disease and Down syndrome
Colin L. Masters,Gail Simms,Nicola A. Weinman,Gerd Multhaup,Brian L. McDonald,Konrad Beyreuther +5 more
TL;DR: The shared 4-kDa subunit indicates a common origin for the amyloids of the plaque core and of the congophilic angiopathy of Alzheimer disease and Down syndrome.
Journal ArticleDOI
The Association Between Quantitative Measures of Dementia and of Senile Change in the Cerebral Grey Matter of Elderly Subjects
TL;DR: The expectation of mental disorder shows a steep increase with advancing chronological age, and beyond 75 years a large part of this increase is accounted for by disorders associated with degenerative changes in the central nervous system for which the authors lack remedies at the present time.
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Alzheimer's disease: Initial report of the purification and characterization of a novel cerebrovascular amyloid protein
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