Exposure to an aversive odor alters Caenorhabditis elegans physiology.

Perception of external cues is important for enhancing the fitness and survival of animals. However, the role of odor perception in regulation of longevity and health is incompletely defined. Here, we show that the exposure to an aversive odor 2-nonanone reduces life span, brood size, feeding rate, and increases lipid storage in worms. These effects are restored to normal levels in mutant worms lacking functional olfactory AWB neurons, suggesting a potential role of odor perception in the regulation of animal physiology and longevity.

Targeting mitochondrial dysfunction to salvage cellular senescence for managing neurodegeneration.

Aging is an inevitable phenomenon that causes a decline in bodily functions over time. One of the most important processes that play a role in aging is senescence. Senescence is characterized by accumulation of cells that are no longer functional but elude the apoptotic pathway. These cells secrete inflammatory molecules that comprise the senescence associated secretory phenotype (SASP). Several essential molecules such as p53, Rb, and p16INK4a regulate the senescence process. Mitochondrial regulation has been found to play an important role in senescence. Reactive oxygen species (ROS) generated from mitochondria can affect cellular senescence by inducing the persistent DNA damage response, thus stabilizing the senescence. Evidently, senescence plays a major contributory role to the development of age-related neurological disorders. In this chapter, we discuss the role of senescence in the progression and onset of several neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. Moreover, we also discuss the efficacy of certain molecules like MitoQ, SkQ1, and Latrepirdine that could be proven therapeutics with respect to these disorders by regulating mitochondrial activity.