At elucidating

20-Jul-2020 03:46

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The kinase LRRK2, which has been genetically linked to development of PD and is now a hot therapeutic target by a number of labs, had much earlier been associated with Crohn’s disease and inflammatory bowel disease.According to Tansy, it could be that infection or some other assault in the gut might trigger inflammatory responses that then upregulate levels of alpha-synuclein in surrounding nerve cells that are part of the enteric system.“Maybe different strains, different conformations of alpha synuclein will lead to different diseases,” he said.Khurana also noted that lysates from the brains of MSA patients look strikingly different from the lysed cells of people with PD or Lewy body dementia.“We are trying to define what causes alpha-synuclein aggregate so it can be used as a model for developing potential drugs that modulate it,” said Tansey.

“The idea that the brain is an immune-privileged organ has gone out the window,” said Malu Tansey, Ph D, Professor of Physiology & Director of Center for Neurodysfunction & Inflammation at the Emory University School of Medicine, sponsored by Charles River Laboratories.Three years ago, researchers from the University of Virginia’s School of Medicine in Charlottesville discovered a central nervous system lymphatic pathway able to carry both fluid and immune cells from the cerebrospinal fluid.The pathways are connected to the deep cervical lymph nodes.But this rare disease—only about 1,900 cases are diagnosed yearly in the US—is quite distinct from PD, noted Vikram Khurana, MD, Ph D, Chief of the Division of Movement Disorders at Brigham & Women’s Hospital, which is developing treatments for both MSA and PD.

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One of the biological differences, says Khurana, is where alpha-synuclein accumulates. In MSA, it is primarily in oligodendrocytes, which produce the myelin sheath that electrically insulates axons.Oligodendrocytes are also glia cells, which perform a role similar to that of the peripheral immune system, and can also contribute to exaggerated pain responses.