A new study suggests that kinetin, a chemical frequently used in anti aging creams, could be used to develop a treatment for Parkinson’s Disease. Forget regenerating your youthful skin, this chemical could be used to reverse the cell death that causes the deadly disorder that afflicts one in every 500 people in the UK.
According to the study published Cell, researchers used kinetin to boost the activity of an enzyme called PINK1. This enzyme has been linked to brain cell death in patients with early onset Parkinson’s, and specifically, with the disorder’s hallmark symptoms.
To simplify things a bit, overwhelming evidence shows that Parkinson’s is at least partially caused by a mutation in PINK1, which causes the enzyme to malfunction. This malfunction in turn affects the cell’s mitochondria, which turns the energy that you eat into the energy that powers your cells. According to UCSF, who had a scientist on the study:
In Parkinson’s disease, poorly performing mitochondria have been associated with the death of dopamine producing nerve cells in a region of the brain called the substantia nigra, which plays a major role in control of movement. Loss of these cells is a hallmark of Parkinson’s disease and the cause of prominent symptoms including rigidity and tremor.
The study was the first to show that kinetin could be used to boost PINK1 activity to near normal levels. To keep an EXTREMELY long explanation short, kinetin can be used as replacement for one of the chemicals PINK1 usually works with. If you go back to GCSE biology, you’ll remember that enzymes are molecules which serve as catalysts for chemical reactions inside cells. Kinetin can speed up the process, so that a cell with mutated enzymes can actually work at normal levels.
That’s all that’s all a mouthful, but what’s important is that scientists have figured out how to make one of the enzymes that breaks and causes Parkinson’s Disease work like it should. This is isn’t a treatment yet, but it certainly is an encouraging first step firmly planted on solid science. [Cell via UCSF]