Background: Alzheimer’s disease is the most common neurodegenerative disorder
affecting the elderly population and emerges as a leading challenge for the scientific
research community. The wide pathological aspects of AD made it a multifactorial disorder
and even after long time it’s difficult to treat due to unexplored etiological factors.
Methods: The etiogenesis of AD includes mitochondrial failure, gut dysbiosis, biochemical
alterations but deposition of amyloid-beta plaques and neurofibrillary tangles are implicated
as major hallmarks of neurodegeneration in AD. The aggregates of these proteins disrupt
neuronal signaling, enhance oxidative stress and reduce activity of various cellular enzymes
which lead to neurodegeneration in the cerebral cortex, neocortex and hippocampus.
The metals like copper, aluminum are involved in APP trafficking and promote amyloidbeta
aggregation. Similarly, disturbed ubiquitin proteasomal system, autophagy and amyloid-
beta clearance mechanisms exert toxic insult in the brain.
Results and Conclusion: The current review explored the role of oxidative stress in disruption
of amyloid homeostasis which further leads to amyloid-beta plaque formation and
subsequent neurodegeneration in AD. Presently, management of AD relies on the use of
acetylcholinesterase inhibitors, antioxidants and metal chelators but they are not specific
measures. Therefore, in this review, we have widely cited the various pathological mechanisms
of AD as well as possible therapeutic targets.