Researchers have found that excess calcium in cells of the brain may lead to Parkinson’s disease. The University of Cambridge- led team discovered that calcium can facilitate the collaboration between small membranous structures inside nerve endings (important for neuronal signalling in the brain), and alpha-synuclein, the protein associated with Parkinson’s disease. Higher levels of either calcium or alpha-synuclein could be the catalyst for the chain reaction leading to the death of brain cells.
Parkinson’s disease is a neurodegenerative disease that rises when naturally occurring proteins fold into the wrong shape and clump together with other proteins, finally forming thin filament-like structures called amyloid fibrils. These amyloid deposits of combined alpha-synuclein, also known as Lewy bodies, are the sign of Parkinson’s disease.
Calcium plays a role in the release of neurotransmitters inside neurons. The researchers saw that when calcium levels in the nerve cell rose, such as when neuronal signalling, the alpha-synuclein binds to synaptic vesicles at various points causing the vesicles to come together. This may show that the normal role of alpha-synuclein is to assist the chemical transmission of data across nerve cells.
“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,” said co-first author Dr Amberley Stephens.
The imbalance may be due to a genetic doubling of the amount of alpha-synuclein (gene duplication), by an age-related slowing of the breakdown of excess protein, by an amplified level of calcium in neurons that are sensitive to Parkinson’s, or related lack of calcium buffering volume in these neurons.
Understanding these processes may help researchers develop new treatments for Parkinson’s disease. Drugs used to block calcium, for use in heart disease for instance, may also have possibilities against Parkinson’s disease.