Pharmacy Daily | Parkinson’s break

A NEW study published in Nature Neuroscience has uncovered how the most common genetic mutations in unfamilial Parkinson’s disease damage brain cells. These common mutations affect a gene called leucine-rich repeat kinase-2 (LRRK2), and cause the gene to code for abnormal versions of the LRRK2 protein. Thus far, it hasn't been clear how LRRK2 mutations lead to the defining microscopic sign of Parkinson's: the formation of abnormal protein aggregates inside dopamineproducing nerve cells of the brain. According to the research, the abnormal forms of LRRK2 disrupt an important garbage-disposal process in cells that normally digests and recycles unwanted proteins including one called alpha-synuclein – the main component of those protein aggregates that gunk up nerve cells in Parkinson's patients. The name for the disrupted disposal process is chaperonemediated autophagy. It involves specialised molecules that guide old and damaged proteins to enzyme-filled structures where they are digested into amino acids, which are then recycled within the cell. “We showed that when LRRK2 inhibits chaperone-mediated autophagy, alpha-synuclein doesn't get broken down and instead accumulates to toxic levels in nerve cells,” the researchers said. “We're now looking at ways to enhance the activity of this recycling system to see if we can prevent or delay neuronal death and disease," the researchers added.

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