Coffee is among the most widespread and healthiest beverages in the world. Coffee typically contains more caffeine than most other beverages, and is widely and frequently consumed. Thus, it contributes significantly to the overall caffeine consumption within the general population, particularly in adults. Controversies regarding its benefits and risks still exist as reliable evidence is becoming available supporting its health-promoting potential. Several lines of evidence have highlighted the beneficial effects towards several disease conditions including Type II diabetes, hepatitis C virus, hepatocellular carcinoma, nonalcoholic fatty liver disease and neurodegenerative disorders such as Alzheimer's disease (AD), Parkinson's disease (PD) and Amyotrophic Lateral Sclerosis (ALS). The health-promoting properties of coffee are largely attributed to its rich phytochemistry, including caffeine, chlorogenic acid, caffeic acid, and hydroxy hydroquinone. In this minireview, an attempt has been made to discuss the various evidences which are mainly derived from animal and cell models. Various mechanisms chiefly responsible for the beneficial effects of caffeine have also been briefly outlined. A short note on the undesirable effects of excessive coffee intakes is also presented.

Various nutritional components belonging to different classes of natural dietary origin display modulatory (protective) properties against age-related neurodegenerative disorders (NDD) such as Parkinson's disease (PD) and Alzheimer's disease. These compounds termed as nutraceuticals which have been shown to act at various biochemical and metabolic levels and exhibit different degree of neuroprotective properties. Present review aims to summarize the current status on the modulatory impact of some of the major nutritional compounds on the pathophysiology of PD, the second most common NDD in humans. Primarily, we have examined the data demonstrated in animal models and postulated through epidemiological studies on the compounds/molecules/life style factors which reduce the risk associated with PD and probable mechanism/s through which they elicit neuroprotection. Further we also included some of the conflicting information about the compounds which may enhance the risk associated with PD. Additionally, emphasis is also given about the new approaches to understand the impact of nutrition on the epigenome in relation to the development of NDD with a short note on emerging ideas relating to nutritional genomics.