Elucidating the role of ATG8a in mediating rescue of circadian rhythm in a fly model of huntington's disease

Abstract

Neurodegenerative diseases (NDs) are incurable debilitating conditions that affect millions of people worldwide. These diseases are becoming more common because of increased life span and changing population demographics. An estimated 6.8 million people die every year because of neurological disorders (World Health Organisation, 2007, Geneva), indicating the enormity of the negative impact of these brain disorders. Some of the most prevalent NDs include Alzheimer’s disease, Parkinson’s disease, Huntington’s disease. These disorders are characterized by different morphological and pathophysiological features. The most common one includes protein aggregate formation, selective susceptibility of cells and manifestation of behavioral deficits. Different phenotypic features of neurodegenerative diseases are a combined outcome of characteristic mentioned above and cellular protein’s innate and variable response to these aggregates. This alters different cascade of events inside the cell. Which then leads to a temporal and regional pattern of neuronal dysfunction. NDs leads to disturbed cellular homeostasis which results in cellular degeneration. As an outcome of neuronal loss, multiple functions are perturbed which include memory formation, motor abilities, and many others (Jung, 2012). Even though there is extensive research on the mechanisms of neurodegenerative diseases both at molecular and phenotypic scale, very little therapeutics are available to treat these diseases. Those that are available, can only slow down the effect of the disease. Hence, in order to have better and effective therapies more detailed knowledge about the diseases is required.