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Feb. 19 (UPI) -- Excess levels of calcium in the brain may lead to Parkinson's disease, according to new research in Britain. An international team of researchers, led by the University of Cambridge, is attempting to learn how and why people develop Parkinson's disease, which is the 14th leading cause of death in the United States. While drugs and surgery currently help control the symptoms, which include tremors and slowness of movement, there is no cure.
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The researchers say their findings, published today in the journal Nature Communications, can lead to better treatments. One possibility, they say, is drugs used to block calcium in heart disease, based on the new study.
"This particular study is interesting because it's the first time research has shown that there may be an important interplay between alpha-synuclein and calcium inside cells, which if disturbed, may cause the damage that ultimately leads to brain cell death," Claire Bale, head of research communications at Parkinson's UK, told the Evening Standard.
From the study, conducted with rats, researchers found that calcium can mediate interaction between small membranous structures inside nerve endings that play a role in neuronal signalling in the brain and alpha-synuclein, the protein linked to Parkinson's disease.
"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," Amberley Stephens, co-first author on the study, said in a press release.
Researchers hadn't been able to determine the effects on cells, including what is actually done, why it's there and what it's meant to do.
"Alpha-synuclein is a very small protein with very little structure, and it needs to interact with other proteins or structures in order to become functional, which has made it difficult to study," said Dr. Gabriele Kaminski Schierle, a researcher at Cambridge's Department of Chemical Engineering and Biotechnology.
Using super-resolution microscopy techniques, researchers observed the behavior of alpha-synuclein in cells. Kaminski Schierle and her colleagues isolated synaptic vesicles, part of the nerve cells that store the signals from one nerve cell to another.
When calcium levels in the nerve cell increase, the alpha-synuclein binds to synaptic vesicles, which cause the vesicles to come together at multiple points.
"This is the first time we've seen that calcium influences the way alpha-synuclein interacts with synaptic vesicles," Dr. Janin Lautenschlager, a study author, said. "We think that alpha-synuclein is almost like a calcium sensor. In the presence of calcium, it changes its structure and how it interacts with its environment, which is likely very important for its normal function."
The researchers theorized the imbalance is caused by four possibilities: genetic doubling, age-related slowing of the breakdown of excess protein, increased level of calcium in neurons sensitive to Parkinson's, or lack of calcium buffering capacity in these neurons.
"Understanding exactly how and why brain cells stop working properly and die in Parkinson's is still a mystery," Bale said. "While more research will need to be done, this important new clue could be the key to better treatments in the future."
