Newswise — At the Keystone Symposium “New Frontiers in Neurodegenerative Disease Research,” held 4-7 February in Santa Fe, New Mexico, researchers explored the processes that lead to a variety of diseases, including Alzheimer’s and Lou Gehrig’s disease (amyotrophic lateral sclerosis, ALS). In Alzforum’s four-part series, read about the latest efforts to understand the genes and proteins that cause nerves in the brain and spinal cord to degenerate.
One top finding was that DNA in these nerves accumulates nicks and breaks as people get older, potentially contributing to disease. While young nerves can fix the damage, older ones cannot keep up, researchers suggested. In both Alzheimer’s and ALS, mutations linked to the diseases interfere with the DNA repair process. Read the story here.
In the brains of people with Alzheimer’s, the protein tau twists into tangles that are hallmarks of the disease. Researchers at the meeting reported on another protein called EF Hand 2 that mingles with tau in those tangles. EF Hand 2 also makes knots of its own. The protein might turn out to be an important player in Alzheimer’s and other dementias linked to tau tangles. As Alzforum reported, the researchers also hinted that there could be more tau partners still undiscovered.
ALS researchers have been puzzling over two other proteins associated with the disease—TDP-43 and FUS. Scientists have been using animal models to understand how these proteins cause pathology. At the meeting, one group reported that in worms, TDP-43 keeps RNAs, a kind of genetic messenger, from twisting into knots. Two other research teams reported on mice with an ALS-like version of FUS. In these animals, FUS formed unnatural globs, and apparently interfered with long tendril-like projections called dendrites that nerves use to communicate with each other. Read more about these proteins here. These animals offer clues as to what might be happening in people with ALS.
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