Parkinson’s disease, believed to be caused by a combination of genetic and environmental factors, is a chronic, progressive disease that affects the central nervous system, especially the motor system, causing tremors, stiffness and difficulty walking. . A new study finds that a gene associated with an increased risk of Parkinson’s disease also contributes to one of Parkinson’s disease hallmarks.
Some nerve cells, called axons, have presynaptic terminals at their ends. Here, nerve impulses are converted into neurotransmitters that transmit signals through synapses between two neurons or between a neuron and a muscle cell or gland.
Synapses are densely packed with proteins that facilitate the metabolic activity that takes place there. They are also fragile structures. The intensity of metabolic activity required to maintain neurotransmission can stress and damage cells. If damaged cells are not cleared by a process known as autophagy, the toxic cell debris accumulation and neuronal death seen in Parkinson’s disease can occur.
A new study by the University of Queensland, Australia, examined how dysfunctional autophagy contributes to neurodegeneration. Researchers have realized that when a cell breaks down, it signals the production of a protein called endophilin-A (EndoA) to initiate the cleanup of cellular debris in the brain.
Dr Adekunle Bademosi of the Queensland Brain Institute said: of research.
Their research led to the discovery of genetic mutations associated with an increased risk of Parkinson’s disease and the accumulation of cellular debris in the brain.
“Our team found that a Parkinson’s disease-associated mutation in a gene called endophilin-A1 blocks the process by which the body and brain recycle cellular waste,” said Bademosi. increase.
“Unfortunately, when the endophilin-A1 gene is affected in Parkinson’s disease, the endophilin A1 protein becomes insensitive to this trigger at synapses, instead accumulating debris that should be thrown away for recycling,” he said. added.
The results of this study suggest a departure from conventional treatments for Parkinson’s disease and a focus on addressing the accumulation of cellular debris that underlies the pathology.
“It may be time to shift the therapeutic focus to autophagy as a mechanism underlying the hallmarks of these diseases,” Bademosi said. This exploration could pave the way for new, more effective Parkinson’s drugs.”
The study was published in a journal neuron.
Source: University of Queensland
