Calcium linked with progression of Parkinson’s disease

Excess calcium levels in brain cells lead to the formation of toxic clusters, which is a major warning sign of Parkinson’s disease. Researchers have found that calcium mediates the interaction between small membranous structures, which are present within nerve endings and are important for signaling neurons in human brain.

Alpha-synuclein is a protein associated with the development of Parkinson’s disease. When calcium or alpha-synuclein is present in excess levels, a chain reaction is triggered and it leads to the death of brain cells.

In the journal Nature, latest research studies present vividly pathogenesis of Parkinson’s disease. One in every 350 adults in the UK has Parkinson’s disease. As per global estimates, 145,000 are estimated to have developed this disease, which remains incurable till date.

Among several neurodegenerative diseases, Parkinson’s disease is the most common one that is caused under following conditions: naturally occurring proteins transform into wrongly shaped molecules, and they stick with other proteins.

They eventually form a thin structure that resembles a filament, and they are known as amyloid fibrils. Amyloid deposits of aggregated alpha-synuclein, which are also known as Lewy bodies, are warning signs of Parkinson’s disease.

The exact role of alpha-synuclein in the cell has not been understood till date. The exact role and function of alpha-synuclein is not understood till date. Alpha-synuclein is implicated in various processes, which govern smooth flow of chemical signals in human brain and flow of molecules in and out of nerve endings; however, the exact behavior of these molecules remains unclear till date.

The protein alpha-synuclein has a very small structure, and its functional capacity depends on its interaction with other proteins or structures. It is difficult to study these protein structures.

The behavior of alpha-synuclein can be determined within cells with the help of super-resolution microscopy techniques. For this purpose, researchers isolated synaptic vesicles that form a part of nerve cells, which store neurotransmitters and send signals to different nerve cells.

The release of neurotransmitters in neurons depends on the concentration of calcium levels. Calcium levels can increase in nerve cells, such as in neuronal signaling processes.

The protein alpha-synuclein would bind with synaptic vesicles at multiple points and vesicles could come into contact with each other. This indicates how alpha-synuclein is used to chemically transmit information across nerve cells.

Calcium influences the pathways of alpha-synuclein protein, which interacts with synaptic vesicles. The protein alpha-synuclein acts like a calcium sensor. In the presence of calcium, there is a change in the structure of protein alpha-synuclein and its interaction with environment. This is likely to be very important for the normal functioning of protein alpha-synuclein.

A fine balance exists between calcium and the protein alpha-synuclein in cell. Whenever there is too much of one or the other, the balance would be tipped and aggregation would begin. This leads to the development of Parkinson’s disease.

The imbalance was caused by genetically doubling the amount of alpha-synuclein, which is a protein used for duplication of genes. This is an age-related slowing mechanism involved in the breakdown of excess protein.

By increasing the level of calcium in neurons, the secretion of the protein alpha-synuclein sensitive to Parkinson’s disease can be controlled. Calcium buffering capacity is lacking in these neurons.

By understanding the role of alpha-synuclein in physiological or pathological processes, new treatments for Parkinson’s disease can be developed strategically. Calcium levels were blocked with the development of novel drug candidates, which are used in pathogenesis of heart diseases and they can also combat Parkinson’s disease.


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