A Role for Cellular Senescence in Medin Amyloidoisis

Medin is one of a small number of proteins that can misfold in ways that encourage other molecules of the same protein to also misfold, linking to form solid aggregates. While medin aggregation seems near ubiquitous in old people, the harms caused by this form of amyloidosis are far less well studied than is the case for, say, the amyloid-β characteristic of Alzheimer's disease. Still, evidence supports a role for medin in causing age-related dysfunction of the cerebral vasculature, and it is also suggested that this can provoke greater pathology in neurodegenerative conditions such as Alzheimer's disease. In the open access paper I'll point out today, researchers point out evidence for rising numbers of senescent cells in the aged vasculature to precede and encourage medin aggregation. These cells secrete disruptive signaling, some of which is encapsulated in extracellular vesicles. Here, the vesicles generated by senescent cells are found to contain medin in greater amounts than those generated by normal cells. This is one of many lines of research that support the use of senolytic therapies to clear senescent cells as a possible approach to the treatment of neurodegenerative conditions. Early senolytics are in clinical trials, but it remains to be seen as to whether that part of the longevity industry focused on building new senolytic therapies will pursue the rejuvenation of brain tissue with any great vigor, or any time soon. Senescence and extracellular v...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs