New research from the University of Queensland has identified a key gene linked to Parkinson’s disease that also contributes to the build-up of toxic cell debris in the brain. The discovery could revolutionise Parkinson’s disease treatment, according to Dr Adekunle Bademosi from The Queensland Brain Institute.
“Our team has found that a Parkinson’s Disease-linked mutation in a gene called Endophilin A1 blocks the process by which the body and the brain recycle cell waste,” Dr Bademosi explained. Without this process, known as autophagy, toxic debris accumulates in the brain, causing neurons to die – a hallmark of Parkinson’s disease.
While autophagy can be induced in cells by starving them of amino acids, the discovery shows that regular signals between neurons can also initiate the recycling process. However, when the Endophilin A1 gene is affected in Parkinson’s, the protein EndoA becomes insensitive to this trigger, leading to the build-up instead.
“Now we’ve also seen that regular signals between neurons in the brain starts EndoA-induced autophagy when the electric impulses trigger the release of proteins or neurotransmitters at synapses.
“Unfortunately, when the Endophilin A1 gene is affected in Parkinson’s, the protein EndoA becomes insensitive to this trigger at the synapse and the debris that should be thrown out for recycling builds up instead,” Dr Bademosi added.
Current treatments aim to clear out the build-up and replace what is lost when too many neurons die. However, Dr Bademosi suggests that it is time to shift the focus of treatment to autophagy as the underlying mechanism of the disease.
“Exploring the use of compounds that induce or inhibit autophagy could pave the way for new, more effective Parkinson’s drugs,” Dr Bademosi said.
The study, published in Neuron, acknowledges the collaborative efforts of researchers in Professor Patrik Verstreken’s lab at the Flanders Institute of Biotechnology (VIB) in Belgium. With further research, the discovery could lead to significant advancements in Parkinson’s disease treatment.
Content from the University of Queensland. Note: Content has been edited for style and length.