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June 6, 2019
The results of a study published today on a molecule targeting clusters of alpha-synuclein, an essential protein linked to Parkinson's disease, make it possible to hope that it will be possible to slow down or prevent the progression of disease in humans.
Researchers at the University of Cambridge have been able to study the effect of a molecule called anle138b by developing a new mouse model of Parkinson's.
Founded by the charity Parkinson's UK, the study examined the effect of anle138b on the accumulation of alpha-synuclein, a protein known to form sticky clumps, called Lewy bodies, in the brain. These clusters are badociated with the death of nerve cells responsible for dopamine production, which allows messages to be sent to parts of the brain that help coordinate movement. This causes the motor symptoms badociated with Parkinson's disease, including freezing, tremors and slow movements.
Anle138b has already demonstrated its ability to reduce protein clumping in neurodegenerative conditions, including other Parkinson's models. To further investigate the potential of the molecule for the treatment of the disease, researchers have created a new mouse model of Parkinson's that mimics how alpha-synuclein gradually accumulates specifically in areas of the brain typically affected by the disease. disease.
At the age of nine months, without treatment, dopamine levels in the brains of the mouse model were already reduced. This reduction was badociated with the onset of symptoms, including a subtle gait change that mimicked some of the early motor symptoms seen in people with Parkinson's disease – such as the "twitching" of feet during walking.
When mice were treated for three months with anle138b, starting at nine months, before a significant loss of nerve cells occurred, the researchers observed a reduction in alpha synuclein lumps, restoring levels of dopamine in the brain and protection against death of nerve cells. . This evolution was accompanied by an improvement in the gait of the mice, effectively suppressing several Parkinson-like motor symptoms.
These promising results published in Acta Neuropathologica Today, suggest that if anle138b is administered early before constant nerve cell death, it can reduce the dense clumping of alpha-synuclein aggregates, potentially blocking Parkinson's disease.
Principal investigator Maria Grazia Spillantini, a professor in the Department of Clinical Neuroscience at the University of Cambridge, said:
Our study demonstrates that by affecting the early aggregation of alpha-synuclein with the anle138b molecule in a new transgenic mouse model, it is possible to rescue dopaminergic dysfunction and the typical motor characteristics of Parkinson's disease.
"Using super-resolution microscopy, we could see how the compound works in the brain of the mouse to achieve this effect. This work paves the way for the development of novel mechanisms-based therapies for Parkinson's disease and related disorders. "
Dr. Beckie Port, head of research at Parkinson's UK, said:
The evidence from this early stage study is based on our understanding of how alpha-synuclein is involved in Parkinson's disease and provide a new model that could pave the way for future treatments.
In addition, the discovery that early targeting of aggregation of alpha-synuclein can restore dopamine levels and that rescue cells can prove crucial to stopping Parkinson's disease.
Today, no treatment can slow down or stop the progression of Parkinson's disease. It is essential that we continue to support leading academics, such as Cambridge, and ensure that the results achieved are transformed into future treatments, which are sorely needed for 1 out of 37 of us. will be diagnosed during our lifetime. "
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