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Alzheimer's disease as homeostatic responses to age-related myelin breakdown

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This work delineates empirically testable mechanisms of action for genes underlying FAD and LOAD and provides "upstream" treatment targets and reframes key observations such as axonal transport disruptions, formation of axonal swellings/sphenoids and neuritic plaques, and proteinaceous deposits as by-products of homeostatic myelin repair processes.
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Dissertation

Application of anti-LRP/LR specific antibodies for the treatment of Alzheimer's disease

TL;DR: Findings indicate that LRP/LR exerts its influence on A-beta shedding via a direct interaction with the gamma-secretase and possibly an indirect interaction withThe beta- secretase.

Computerized cognitive training and physical exercise : effects on cognitive and brain function in older adults

ten Brinke, +1 more
TL;DR: In this article, the authors present a Table of Table of Contents of the Table of contents of the paper "A Table of the Contents of a Table" for the paper this article.
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Key brain cell interactions and contributions to the pathogenesis of Alzheimer’s disease

TL;DR: In this paper , the authors discuss the interactions between different brain cells, from physiological conditions to their pathological reactions in Alzheimer's disease, and how this basic knowledge can be crucial for developing new therapeutic strategies.
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Journal ArticleDOI

The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics

TL;DR: It has been more than 10 years since it was first proposed that the neurodegeneration in Alzheimer's disease (AD) may be caused by deposition of amyloid β-peptide in plaques in brain tissue and the rest of the disease process is proposed to result from an imbalance between Aβ production and Aβ clearance.
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Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families

TL;DR: The APOE-epsilon 4 allele is associated with the common late onset familial and sporadic forms of Alzheimer9s disease (AD) in 42 families with late onset AD.
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Physical basis of cognitive alterations in Alzheimer's disease: synapse loss is the major correlate of cognitive impairment.

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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Alzheimer's Disease Is a Synaptic Failure

TL;DR: Mounting evidence suggests that this syndrome begins with subtle alterations of hippocampal synaptic efficacy prior to frank neuronal degeneration, and that the synaptic dysfunction is caused by diffusible oligomeric assemblies of the amyloid β protein.
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