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Updated: Mar 24, 2026

Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
Published on: December 26, 2016
Is Alzheimer's an Autoimmune Disease?
Betsi Reinoso Corrada1, Robert C Speth2
1Department of Pharmaceutical Sciences, Barry and Judy Silverman College of Pharmacy, Nova Southeastern University, Fort Lauderdale, FL, 33328, USA.
Abstract:
Alzheimer's disease is defined as a progressive neurodegenerative disorder characterized by a gradual decline in cognitive and functional abilities [1]. Although debate continues with respect to its exact pathology, several hypotheses have been proposed to explain its underlying mechanisms. The two primary pathological factors of Alzheimer's disease are the accumulation of amyloid-β plaques and neurofibrillary tangles composed of hyperphosphorylated tau and neurofilament protein [1, 2]. It should be noted that our use of the descriptor hyperphosphorylated tau is done to conform with current nomenclature; it should not be construed as indicating saturation of all the amino acids capable of being phosphorylated. Emerging clinical evidence proposes that some variants of Alzheimer's disease may be caused by an autoimmune process rather than a purely neurodegenerative one. The purpose of this paper is to review and evaluate evidence supporting and challenging the autoimmune hypothesis of Alzheimer's disease, as well as to explore its implications for future therapeutic strategies within the framework of the disease.
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