Population aging is an important demographic phenomenon worldwide that warrants a well organized program structure dealing with the significant impact of aging on the elderly population in particular and the society at large. Aging poses a risk for the increased incidence of neurodegenerative diseases that causes progressive loss of neuronal structure and function. Thus, identifying the risk factors associated with age-associated neurodegeneration as often seen in Alzheimer's disease (AD) or Parkinson's disease (PD) is among the greatest challenges to improve the wellbeing of the elderly population. Several environmental risk factors like pesticide exposure and dietary lifestyle choices have been implicated in the increased incidence of these diseases but the etiology remains elusive so far. There is also lack of a proper animal model system to study the effect of these environmental toxins on age-associated neurodegeneration. Why the exposure to pesticides like rotenone results in specific loss of dopaminergic neurons as often seen in sporadic cases of PD is a long standing question. Although mitochondrial dysfunction has emerged as key payers in PD it is not yet known whether they are the disease drivers. Our laboratory is currently studying the molecular mechanisms underlying age-related neurodegeneration and how aging correlates with susceptibility to environmental stress. Our research primarily focuses on the age-dependent vulnerability to low chronic exposure to the environmental toxin rotenone in a cellular as well as Drosophila model of PD.