‘Too Much’ Brain Calcium May Cause Parkinson’s

Insights from a new study – by the University of Cambridge in the United Kingdom – about the role of calcium in brain cells’ signaling mechanisms brings us close to understanding the causes of Parkinson’s disease.

The presence of toxic protein deposits, or Lewy bodies, inside brain cells is a recognized hallmark of Parkinson’s disease. The deposits contain clusters of alpha-synuclein and other proteins that have folded into the wrong shape.

The new study – now published in the journal Nature Communications – shows that calcium affects the way in which alpha-synuclein binds to synaptic vesicles. Synaptic vesicles are small compartments in nerve terminals that hold the neurotransmitters, or chemical messengers, that carry signals between brain cells.

“There is a fine balance,” notes co-first author Dr. Amberley Stephens, a postdoctoral researcher in molecular neuroscience at the University of Cambridge, “of calcium and alpha-synuclein in the cell, and when there is too much of one or the other, the balance is tipped and aggregation begins, leading to Parkinson’s disease.”

Worldwide, there are more than 10 million people living with Parkinson’s disease, including around 1 million in the United States. In Parkinson’s disease, there is a progressive destruction of brain cells that produce a neurotransmitter called dopamine, which is important for controlling movement. Therefore, as the disease progresses, there will be a worsening of symptoms such as slowness of movement, rigidity, tremor, and impaired coordination and balance.



The authors propose that the abnormal clusters of alpha-synuclein form when the delicate balance between the protein and calcium is upset. They suggest a number of things that might causes such and imbalance: age-related slowing of the elimination of excess protein; doubling of alpha-synuclein production due to gene duplication; higher calcium levels in brain cells vulnerable to Parkinson’s; and inability to buffer calcium effectively in Parkinson’s-sensitive cells.

They also noted that a drug that blocks the calcium channel in heart disease might “prove to be a valuable candidate to act against [Parkinson’s disease] via lowering intracellular calcium load.”

My Take:
Please note that there is no mention of excess dietary calcium intake as a potential cause. This is an issue of calcium control not calcium supplementation.

I’m sure there are physicians out there that will tell their patients not to take calcium supplements because it could lead to Parkinson’s. These are the same physicians that warn patients of calcium supplementation when they have a high calcium score on a high-speed cat scan of the heart. The presence of calcium does indeed indicate “vulnerable plaque”, but the calcium is protective in nature, causing the plaque to adhere more securely to the artery wall and preventing a CVA.

Parkinsonism is a frequent side effect of calcium channel blockers and several studies have drawn as strong correlation between the use of these drugs and the onset of Parkinson’s. Just because you can alter the balance of calcium in the body doesn’t mean it will be beneficial. As Dr. Stephens said, “there is a fine balance of calcium and alpha-synuclein in the cell, and when there is too much of one or the other, the balance is tipped and aggregation begins, leading to Parkinson’s disease.”

The Bottom Line:
This is excellent basic research into the mechanisms of Parkinson’s. However, the concept that calcium channel blockers might be useful in preventing Parkinson’s has little merit. Studies already indicate these common blood pressure medications are a part of the problem.

Source: Medical News Today, February 19, 2018