Researchers uncover where and why proteins malfunction in Parkinsons disease

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Scientists at the Francis Crick Institute, UCL and the University of Edinburgh have uncovered how a build-up of harmful protein starts to happen within neurons in Parkinson’s disease, ultimately causing nerve cell death. By looking at how, where and why this build-up happens, the work provides unique insight into a key biological process driving Parkinson’s.

Parkinson’s is a progressive neurodegenerative disease that causes tremors, slowing of movements, stiffness and can progress to cause severe cognitive problems. It affects around 145,000 people in the UK, with this number expected to increase as more people live longer.

Parkinson’s is caused by a loss of neurons in specific parts of the brain. In affected nerve cells, a protein called alpha-synuclein misfolds and clumps together into harmful structures. The mechanisms behind this are not yet fully understood.

In their paper, published in Nature Neuroscience today (August 30), the researchers developed a new sensitive approach to study what happens to alpha-synuclein during the earliest stages of disease.

Using neurons derived from cells donated by people with inherited forms of Parkinson’s, as well as from healthy individuals, the team were able to visualise where, why, and how this protein starts to misfold and clump inside nerve cells.

The interdisciplinary team of neurologists, chemists and structural biologists found that alpha-synuclein contacts the membranes, or linings, of structures within nerve cells. When it contacts the membrane of the mitochondria, part of the cell responsible for generating energy, this triggers the misfolding and clumping of alpha-synuclein.

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