Narrowing in on How Parkinson Disease Develops
We get yet another clue from alpha-synuclein
Posted Jan 10, 2015
Well, the holidays could distract for only so long—it took finding an article relevant to our research to compel me to sit down and share the “good news” with you. It’s been 17 years now since my team reported the PARK1 mutation in alpha-synuclein, and researchers are finally closing in on how the protein wreaks its havoc to cause Parkinson's disease (PD).
A group in California had shown that alpha-synuclein regulates the release of neurotransmitters between cells. Then, in October they showed that the protein does this by clustering the tiny vesicles containing those neurotransmitters, restricting release of their content (http://www.ncbi.nlm.nih.gov/pubmed/25264250).
We know there is a dose effect for alpha-synuclein in PD, whereby increased protein is increasingly toxic. The research suggests that abnormal elevations of alpha-synuclein sequester the neurotransmitter-containing vesicles, in essence causing a traffic jam.
Spreading from cell to cell, then, alpha-synuclein reduces the release of needed neurotransmitters and becomes toxic to certain cells. When enough cells die, we observe the symptoms of Parkinson’s.
While I find deciphering the science fascinating in its own right, is it getting down to understanding these mechanisms on the cellular level that will lead to a successful treatment for those of us who cope with the effects of Parkinson's disease on a daily basis.