A Theoretical Analysis of the Synergy of Amyloid and Tau in Alzheimer's Disease

Department

neurology

Document Type

Article

Abstract

Amyloid plaques and Tau protein neurofibrillary tangles are considered the two most important pathogenic factors in Alzheimer's disease. The prevailing amyloid cascade hypothesis suggests that amyloid-β (Aβ) elevation induces downstream Tau hyperphosphorylation and aggregation, synaptic dysfunction, and neuronal loss that ultimately results in cognitive impairment. Alternatively, the dual-pathway hypothesis suggests that Aβ and abnormal Tau are two independent factors that exert synergistic effects on synaptic dysfunction and neuronal loss. We hypothesize that the intrinsic interaction of Aβ and Tau would better predict cognitive impairment. Herein, we propose an Aβ-Tau interactive model based on a review of the medical literature, mathematic modeling, and analysis of our clinicopathological data.

Medical Subject Headings

neurology

Publication Date

2016

Publication Title

Journal of Alzheimer's Disease

ISSN

1387-2877

Volume

52

Issue

4

First Page

1461

Last Page

1470

Digital Object Identifier (DOI)

10.3233/JAD-151206

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