Preprint Review Version 1 This version is not peer-reviewed

Elucidating the Pathophysiological Mechanisms of Alzheimer’s Disease

Version 1 : Received: 9 September 2024 / Approved: 9 September 2024 / Online: 10 September 2024 (03:28:25 CEST)

How to cite: Saragea, P. D. Elucidating the Pathophysiological Mechanisms of Alzheimer’s Disease. Preprints 2024, 2024090687. https://doi.org/10.20944/preprints202409.0687.v1 Saragea, P. D. Elucidating the Pathophysiological Mechanisms of Alzheimer’s Disease. Preprints 2024, 2024090687. https://doi.org/10.20944/preprints202409.0687.v1

Abstract

Alzheimer’s disease (AD), the leading cause of dementia (50-70%), is a multifactorial neurodegenerative disorder characterized by progressive cognitive decline and significant neuropathological changes, including β-amyloid plaques and neurofibrillary tangles. This review synthesizes current understanding of the complex interplays that contribute to the pathogenesis of AD, while exploring the mechanisms underlying the formation of β-amyloid plaques and neurofibrillary tangles, with a focus on the amyloidogenic and non-amyloidogenic pathways, Tau protein hyperphosphorylation, and the resultant neurotoxicity. Furthermore, the study delves into mitochondrial dysfunction and oxidative stress as critical contributors to neuronal degeneration, highlighting the mitochondrial cascade hypothesis and its implications in both early (EOAD) and late-onset AD (LOAD). The study emphasizes the irreversible nature of the disease’s progression, detailing the pathological transformations from the preclinical to the severe stage, where lesions disseminate throughout the entire cortex.

Keywords

Alzheimer; neurodegeneration; dementia; β-amyloid plaques; neurofibrillary tangles

Subject

Biology and Life Sciences, Neuroscience and Neurology

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