‘Too much’ brain calcium may cause Parkinson’s

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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 closer to understanding the causes of Parkinson’s disease.
Having excess calcium in the brain may be a reason for why Parkinson’s disease develops. 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. Could an existing drug halt Parkinson’s disease?
Learn how a drug for a rare genetic disorder may be effective against toxic alpha-synuclein clusters in brain cells.
More recent studies have revealed that Parkinson’s also affects brain cells that do not produce dopamine, which might explain why some of the symptoms are not movement-related. Although abnormal clusters of alpha-synuclein — a small protein comprising only 140 amino acids — is a major element of the Lewy bodies that are present in Parkinson’s disease, its normal form appears to be necessary for a number of brain cell functions.
However, apart from knowing that the protein somehow interacts with synaptic vesicles to ensure the smooth transport of molecules across the synsynuclein.

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