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."
Normal vs. abnormal alpha-synuclein
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.
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