About me:


My name is Amit Agrawal. I am engineer and scientist by training. I am a final year PhD student at Weizmann Institute of Science, Israel. My research interest lies understanding the aging. I am interested in finding the answers for following questions:

How increase in age is associated with vulnerability to diseases?

What is the intracellular mechanism behind the onset of aging in human? Evolutionary theory suggests that aging is an outcome of the decline in force of natural selection after the certain age. Such decline in the natural selection made an organism handicap to tackle the stochastic disorder that comes after that age.


In the absence of the repair mechanisms of these damages after that age, results in increase in damage to different cellular bodies. When these damages cross the certain threshold, it results in disrupting cellular functions.

Protein accounts for the 70% of cell mass, so in a lazy way, it can be said that protein is more prone to get disorder because there is high chance that it will encounter with reactive oxygen species or form of toxic aggregates. Certainly, the large number does not mean more prone, the higher stability of the biomolecule can make it less prone to get the disorder. Hence, an investigation to profile biomolecules with a degree of stability is required to find out the real villain behind onset of aging.


Anyway there is a lot of work done on protein damage and aging. It is observed that damage protein accumulation increases with age and people have found that protein homeostasis mechanism also declines with age. The interesting question is whether protein damage initially results in the decline of protein homeostasis that forms vicious feedback cycle, or is there some other factor that results in the decline of protein homeostasis and thus increases in protein damage.


However, it’s not only about proteostasis there are many other things those are positively correlated with aging, either they might be the cause or the outcome. Without pondering into this, I am more interested in understanding what are the starting events that trigger such intracellular disorders.