A Detailed Analysis Of Alzheimer's Disease Pathophysiology: The Influence Of Oxidative Stress On Amyloid Precursor Protein Metabolism And Secretase Activity

Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized by cognitive decline, memory impairment, and distinct neuropathological features such as amyloid-beta (Aβ) plaques and neurofibrillary tangles. Despite extensive research, the molecular mechanisms underlying AD remain incompletely understood, posing challenges for therapeutic intervention. This review delves into the intricate processes of amyloid precursor protein (APP) processing, focusing on the roles of α-, β-, and γ-secretases in the generation of neurotoxic Aβ peptides. We explore the genetic and molecular insights into APP, emphasizing the significance of secretase-mediated cleavage and its regulation by oxidative stress, cholesterol, and mitochondrial dysfunction. The interaction between these pathological pathways offers a broader understanding of AD progression, highlighting potential targets for therapeutic strategies aimed at modulating APP processing and reducing Aβ burden.