The Murky Depths of Parkinson's Disease

You might recall that the chemical alpha-synuclein is an aggregate that appears to be a proximate cause of Parkinson's disease (and like many biochemical aggregates, its buildup is slowed by the practice of calorie restriction). Researchers are delving deeper into the chain of mechanisms: Patients with Parkinson's disease (PD) have elevated levels of the protein called alpha-synuclein in their brains. As the protein clumps, or aggregates, the resulting toxicity causes the death of neurons that produce the brain chemical dopamine. Consequently, nerves and muscles that control movement and coordination are destroyed. The researchers discovered that the activity of three genes that control the synthesis of heme, the major component of hemoglobin that allows red blood cells to carry oxygen, precisely matched the activity of the alpha-synuclein gene, suggesting a common switch controlling both. The scientists then found that a protein called GATA-1, which turns on the blood-related genes, was also a major switch for alpha-synuclein expression, and that it induced a significant increase in alpha-synuclein protein. Finally, they demonstrated that a related protein -- GATA-2 -- was expressed in PD-vulnerable brain cells and directly controlled alpha-synuclein production. Researchers are taking a similar tack to that of mainstream Alzheimer's research now...