Alzheimer's disease and
Parkinson's disease are two common
neurodegenerative diseases of the elderly people that have devastating effects in terms of morbidity and mortality. The predominant form of the disease in either case is sporadic with uncertain etiology. The clinical features of
Parkinson's disease are primarily motor deficits, while the patients of
Alzheimer's disease present with
dementia and
cognitive impairment. Though neuronal death is a common
element in both the disorders, the postmortem histopathology of the brain is very characteristic in each case and different from each other. In terms of molecular pathogenesis, however, both the diseases have a significant commonality, and
proteinopathy (abnormal accumulation of misfolded
proteins), mitochondrial dysfunction and oxidative stress are the cardinal features in either case. These three damage mechanisms work in concert, reinforcing each other to drive the pathology in the aging brain for both the diseases; very interestingly, the nature of interactions among these three damage mechanisms is very similar in both the diseases, and this review attempts to highlight these aspects. In the case of
Alzheimer's disease, the
peptide amyloid beta (Aβ) is responsible for the
proteinopathy, while α-
synuclein plays a similar role in
Parkinson's disease. The expression levels of these two
proteins and their aggregation processes are modulated by reactive
oxygen radicals and transition
metal ions in a similar manner. In turn, these
proteins - as oligomers or in aggregated forms - cause mitochondrial impairment by apparently following similar mechanisms. Understanding the common nature of these interactions may, therefore, help us to identify putative neuroprotective strategies that would be beneficial in both the clinical conditions.