New Therapies Could Stop T Cells From Attacking Brain Cells in Parkinson’s Disease
upstart writes:
New Therapies Could Stop T Cells From Attacking Brain Cells in Parkinson's Disease:
Scientists at La Jolla Institute for Immunology (LJI) have found that people with Parkinson's disease have a clear "genetic signature" of the disease in their memory T cells. The scientists hope that targeting these genes may open the door to new Parkinson's treatments and diagnostics.
"Parkinson's disease is not usually seen as an autoimmune disease," says LJI Research Assistant Professor Cecilia Lindestam Arlehamn, Ph.D. "But all of our work points toward T cells having a role in the disease."
"Now that we can see what these T cells are doing, we think intervening with antibody therapies could have an impact on the disease progression, especially early on, " adds LJI Professor Alessandro Sette, Dr.Biol.Sci., who led the work with Lindestam Arlehamn.
[...] Parkinson's progresses as dopamine-producing neurons in the brain die. Unfortunately, scientists have been unable to pinpoint what causes this cell death-though they do have a clue: The doomed neurons contain clumps of a damaged protein called alpha-synuclein.
LJI research suggests these clumps may be the kiss of death for dopamine-producing neurons. Sette and Lindestam Arlehamn recently showed that people with Parkinson's have T cells that target alpha-synuclein early on in Parkinson's disease.
The new study offers a way to stop these T cells in their tracks. The LJI team found that people with Parkinson's disease have memory T cells with a very specific gene signature. These genes appear responsible for targeting alpha-synuclein and potentially causing ongoing inflammation in cases of Parkinson's.
Journal Reference:
Dhanwani, Rekha, Lima-Junior, Joao Rodrigues, Sethi, Ashu, et al. Transcriptional analysis of peripheral memory T cells reveals Parkinson's disease-specific gene signatures [open], npj Parkinson's Disease (DOI: 10.1038/s41531-022-00282-2)
Read more of this story at SoylentNews.