Researchers have identified a key enzyme driving forms of parkinson’s disease, and have shown how Blocking it restores it restores normal function in animal and cell models, offering a promising a promising new drug target for the Condition.

The work is Published in the journey Neuron,

In Parkinson’s, A Protein Known as Alpha-Synuclein Builds Up in Clumps Called Lwey Bodies in NERVE CELLS in the Brain. These clumps of protein stop these cells from functioning normally, eventually leading the cells to die.

One way our Bodies rid themselves of such toxic materials is via a process know as autophagy, where cells break down and recycle unwanted components. But autophagy does not work properly in Parkinson’s, meaning cells are unable to get rid of the toxic alpha-synuclein.

The new study, LED by Dr. Sung min son and colleagues in professor david rubinsztein’s lab at the UK Dementia Research Institute (UK DRI) At the University of Cambridge, Uncovered a Pathway Involving an enzyme KNOWN EC Why they found was hyperactive in Parkinson’s.

The team first examined human cells include Brain Cells, and “Mini-Brains” Called Organoids, which contained abnormal alpha-shynuclein. Using these cells and then zebrafish and mouse models, the scientists revealed that abnormal alpha-synuclein over-activeness acaly Autophagy, leading to the accumulation of alpha-synuclein and kind of cellular stress and damage seen in parkinson’s.

The study showed that blocking the function of accepted Normal Autophagy and Reduced Levels of Toxic Alpha-Synuclein in Cells, Mini-Brains, Zebrafish and Mouse Models of Parkinsonsonsonsonsons.

By using drugs to block the function of acalya, reserchers we getting to reduce the toxicity of alpha-synuclein in brain cells and mini-brains. In zebrafish and mice that was gnetically al a carry a mutation in the alpha-ignuclein gene that causes parkinson’s in humans, blocking acalyly similery boosted autophagy, which lad to increase Alpha-Synuclein.

This reduced the disease -associated effects of this protein in these animal models. These Findings Point to a Potential Disease-Modifying Strategy Targeting a Root Cause of Cell Death in Parkinson’s.

There are Several Compounds that Block (Inhibit) Acly. One is Hydroxycitrate, a Well-KNOWN but controversial weight-level supplement. Others have been evaluated as potential anti-cancer therapeutics. However, the challenge is that these compounds do not cross the blood-brain barrier. Therefore, the next step in this research is to develop an active inhibitor which can pass into the brain from the blood.

Lead Author Prof David Rubinsztein, Group Leader at the UK Dementia Research Institute at the University of Cambridge, Said, “Our Research Shows That ACTS ACTS LIKE ACTES LIKE ACTE ACTE ACTS, Triggering A Changes Inseed Brain Cells, That We Believe are Central to Parkinson’s Progression. Also in zebrafish and mouse models.

“This sugges that problem caused by alpha-synuclein in parkinson’s aren’t just about the protein itself, but how it disrupts other processes with other processes with A Compeling Drug Target for Parkinson’s, Laying the Foundation for Future Therapies aimed at Halting or Reversing the course of the condition. “

Provided by uk dementia research institute