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Treatment for Parkinson's might work for Alzheimer's too

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IANS New York

An effective treatment for Parkinson's disease might also work for Alzheimer's and Huntington's diseases too as researchers have found that abnormal proteins found in these neurodegenerative diseases all share a similar ability to cause damage when they invade brain cells.

The finding potentially could explain the mechanism by which Alzheimer's, Parkinson's, Huntington's and other neurodegenerative diseases spread within the brain and disrupt normal brain functions.

"A possible therapy would involve boosting a brain cell's ability to degrade a clump of proteins and damaged vesicles," said study senior author Edward Campbell from Loyola University Chicago.

"If we could do this in one disease, it's a good bet the therapy would be effective in the other two diseases," Campbell said.

 

Neurodegenerative diseases are caused by the death of neurons and other cells in the brain, with different diseases affecting different regions of the brain.

Alzheimer's destroys memory, while Parkinson's and Huntington's affect movement. All three diseases are progressive, debilitating and incurable.

Previous research has suggested that in all three diseases, proteins that are folded abnormally form clumps inside brain cells.

These clumps spread from cell to cell, eventually leading to cell deaths.

Different proteins are implicated in each disease: tau in Alzheimer's, alpha-synuclein in Parkinson's and huntingtin in Huntington's disease.

The study, published in the journal Acta Neuropathologica, focused on how these misfolded protein clumps invade a healthy brain cell.

The researchers observed that once proteins get inside the cell, they enter vesicles - small compartments that are encased in membranes.

The proteins damage or rupture the vesicle membranes, allowing the proteins to then invade the cytoplasm and cause additional dysfunction.

Thus the study showed that protein clumps associated with the three diseases cause the same type of vesicle damage.

--IANS

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First Published: May 24 2017 | 2:50 PM IST

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