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Article type: Article Commentary
Authors: Bocti, Christian; *
Affiliations: Department of Medicine, Faculty of Medicine and Health Sciences, Division of Neurology, Memory Clinic and Research Centre on Aging, Université de Sherbrooke, Sherbrooke, QC, Canada
Correspondence: [*] Correspondence to: Christian Bocti, MD, FRCPC, Neurologist, Full Professor and Director, Department of Medicine, Faculty of Medicine and Health Sciences, Division of Neurology, Memory Clinic and Research Centre on Aging, Université de Sherbrooke, 3001, 12e Avenue Nord, room #4531, Sherbrooke, QC J1 H 5N4, Canada. Tel.: +1 819 346 1110 x 14586; Fax: +1 819 564 5395; E-mail: christian.bocti@usherbrooke.ca.
Abstract: Alzheimer’s disease (AD) research has been dominated by the single-factor amyloid hypothesis in the last decades. Several other hypotheses have been proposed and increasingly attract attention considering the limited success of amyloid-based therapeutic strategies. Surprisingly, most published alternative etiological hypotheses for AD are similarly single-factor hypotheses, such as vascular, metabolic, mitochondrial, infectious, and inflammatory hypotheses, but the existence of so many different hypotheses suggests that AD is most likely a complex, multifactorial disorder. This inventory of different etiological hypotheses will hopefully help the field to move forward with explanatory models that consider the multifaceted aspects of this devastating disorder.
Keywords: Alzheimer’s disease, amyloid hypothesis, biomarkers, dementia, diagnostic criteria, etiological hypothesis, multiple etiologies, neuropathology
DOI: 10.3233/JAD-240488
Journal: Journal of Alzheimer's Disease, vol. 100, no. 3, pp. 787-789, 2024
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