TDP-43 Pathology May Extend to the Vasculature and Blood-Brain Barrier

TDP-43 is one of a small number of proteins that can become altered in ways that lead to the formation of solid aggregates that, directly and indirectly, cause cell dysfunction and death in the brain. In the case of TDP-43, this proteopathy contributes to amyotrophic lateral sclerosis (ALS), frontotemporal lobar degeneration (FTLD), and what is now called limbic predominant age-related TDP-43 encephalopathy (LATE). This was a more recent discovery than other aggregates involved in neurodegenerative conditions, such as amyloid-β, tau, and α-synuclein, and so the pace of discovery for TDP-43 is a little faster; more remains to be uncovered of the biochemistry of TDP-43 pathology than is the cost for the other problematic proteins. In today's research materials, the scientists involved report on a potential role for TDP-43 in dysfunction of the vasculature and blood-brain barrier in the aging brain. Unmodified TDP-43 appears necessary for a number of processes, and depletion may be a contributing cause of some of the vascular issues seen in neurodegenerative conditions associated with TDP-43 aggregation. An important vascular issue is leakage of the blood-brain barrier, allowing unwanted cells and molecules to enter the brain to cause inflammatory reactions or other damage. That said, the usual challenges apply to the finds here, in that knowing that a mechanism exists doesn't tell us how important it is versus other mechanisms known to contribute to this problem. ...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs