A Theoretical Analysis of the Synergy of Amyloid and Tau in Alzheimer's Disease.
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.
Pengcheng
P
Han
Jiong
J
Shi
D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000209:etiology* / Q000378:metabolism; D000682:Amyloid / Q000378:metabolism / Q000502:physiology; D016229:Amyloid beta-Peptides / Q000378:metabolism / Q000502:physiology; D001921:Brain / Q000378:metabolism / Q000503:physiopathology; D016022:Case-Control Studies; D060825:Cognitive Dysfunction / Q000209:etiology / Q000378:metabolism; D005260:Female; D006801:Humans; D008297:Male; D008954:Models, Biological; D009474:Neurons / Q000378:metabolism / Q000502:physiology; D058225:Plaque, Amyloid / Q000378:metabolism* / Q000503:physiopathology; D013569:Synapses / Q000378:metabolism / Q000502:physiology; D016875:tau Proteins / Q000378:metabolism* / Q000502:physiology
D000682:Amyloid; D016229:Amyloid beta-Peptides; D016875:tau Proteins
Alzheimer’s disease; Tau; amyloid plaque; neurofibrillary tangle