People with at least 16 years of education are less likely to accumulate markers of neurodegeneration in their brains, says a cross-sectional study.
Researchers identify N-terminally extended Aβ peptides that are toxic to synapses and rise after BACE1 inhibition, though whether they occur in human disease remains unclear.
The approach plays neuroinflammation against neurodegeneration. It may be too risky for people because it would instigate multiple sclerosis, but yields information on the choroid plexus.
Researchers report the highest resolution structure to date for γ-secretase, the multisubunit complex that churns out Aβ.
A NexGen prevention trial in familial Alzheimer’s mutation carriers will shoot for flexible testing of high doses and drug combinations.
A protein instigates axon degeneration by promoting destruction of the essential enzyme cofactor, NAD+.
In a Solomonic move, a prestigious prize for research in neurodegenerative disease goes to a veteran tauist and a self-professed inhabitant of “amyloid land.”
A new study suggests that tau oligomers as small as trimers enter neurons and corrupt native tau proteins inside.
In-silico modeling, quantitative pharmacology, model-based drug development ... You've heard the buzzwords and maybe balked at the mathematical equations that followed on their heels. Here’s your chance to find out what the terms really mean, and how scientists are using disease simulation tools to test concepts and predict outcomes. (No math, we promise.) Join Alzforum for a Webinar on Wednesday, May 13, at 12 p.m. U.S. Eastern time. Lilly’s Richard Mohs, CAMD’s Klaus Romero, USC’s Lon Schneider, and Merck’s Julie Stone will discuss how trial simulations can help clinicians better prepare real-world trials.
The structure of γ-secretase just got a little bit clearer. Researchers used cryo-electron microscopy to generate the highest-resolution image of the multisubunit complex to date. The 4.32Ǻ structure beat out the same group’s 4.5Ǻ structure from last year. Does the extra smidgen of clarity matter, you ask? It allowed for the assignment of each of the complex’s transmembrane domains to one of its four constituent proteins. What’s more, researchers discovered a new transmembrane domain, an unexpected location for the catalytic residues of presenilin, and unveiled how the domains interact to stabilize the giant complex within the membrane.
Last month, scientists from the DIAN Trials Unit met with funders and other stakeholders in Washington, D.C., to start planning the next phase of presymptomatic treatment trials in people who carry pathogenic mutations in the APP or presenilin genes. Now that the inaugural trial is chugging along, without safety flags thus far, the scientists have set their sights on achieving a large effect. To this end, they want to test higher doses and drug combinations in more flexibly adaptive designs starting in 2016.
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- David Bolduc, Michael Wolfe and Dennis Selkoe on Structural basis of human γ-secretase assembly.
- Lucia Chavez-Gutierrez on Structural basis of human γ-secretase assembly.
- Michal Schwartz on Astrocyte-Derived TGF-β1 Accelerates Disease Progression in ALS Mice by Interfering with the Neuroprotective Functions of Microglia and T Cells.