Defective glial cells or cause Parkinson's disease

Spanish researchers have found that defective cells in the human brain, known as asstary glial cells, are associated with the formation of a toxic protein that is a feature of Parkinson's disease. The paper, published recently in Stem Cell Reports, suggests that glial cells play an important role in Parkinson's disease and may provide new therapeutic targets.
"We have shown that astrological glial cells play a vital role in Parkinson's disease. Our results suggest that aspartic glial cells in Parkinson's disease transfer a toxic protein to neurons that produce dopamine. The paper's co-lead author, Angelique di Domenico of the Bervitch Institute for Biomedical Research at the University of Barcelona, said.
previous autopsy study found that neurons and astrological glial cells in parkinson's patients had α-synth nucleoproteins. This is a protein that accumulates to form the Louis body and is a characteristic pathology of Parkinson's disease. It was this discovery that prompted researchers to study the role of astrological glial cells in the disease.
using cells from patients with parkinson's disease with LRRK2 mutations to produce stem cell-derived glial cells. 15% of Parkinson's cases are associated with genetic mutations, and 7% are related to a large protein complex called LRRK2. The main function of LRRK2 is not clear, but it appears to play a role in mitochondrial dynamics and autophagy.
, the researchers used CRISPR gene editing technology to track toxic α-synactactins. The results showed α accumulation of analytic-synth nucleoproteins shortened and decomposed the protruding branches (axons and dextasses) of the target neurons, leading to neuron death.
researchers used a drug to treat an abnormal build-up of toxic substances. Di Domenico said: "We are pleased to see that the process of cell degradation has resumed after treatment, with α-synthesical nucleoproteins completely removed from Parkinson's disease star glial cells. These results pave the way for new therapeutic strategies to block disease-ing interactions between neurons and glial cells. (Source: Tang Erdu, China Science Daily)