On Saturday, 27 October, in Los Angeles, an unusual conference marked a paradigm shift in the Alzheimer disease movement...
Flurizan has floundered in an 18-month Phase 3 clinical trial in patients with mild Alzheimer disease...
Alzheimer's disease researchers expressed sadness this week at the sudden death of Larry Sparks...
A new study finds that the cancer drug imatinib does not lower Aβ in humans, casting doubt on a previously described relationship between imatinib, γ-secretase activating protein (GSAP), and Aβ.
Two new papers rekindle acrimonious debate about exactly what “loss-of-function” means when it comes to presenilin mutations in Alzheimer’s pathogenesis.
Presenilin 2 resides almost exclusively in late endosomes, multivesicular bodies, and lysosomes, where it generates a pool of aggregation-prone Aβ. Some PS-1 mutations phenocopy this intraneuronal distribution.
The EPOCH trial of verubecestat was halted for lack of efficacy. APECS trial in prodromal AD continues.
Researchers claim this failed drug allows Aβ to accumulate inside cells, while small peptides cleaved from the C-terminal end of APP become trapped in membranes.
Recent studies have identified rare loss-of-function variants that cause Alzheimer’s with nearly 100 percent penetrance. Now there are 17 more.
Aging lymphatic vessels in the meninges hinder waste clearance from the brain and exacerbate Aβ build-up.
In the future, could Alzheimer disease treatments come as an ointment, or a skin patch?...
Binding occurs around lipid deposits in the choroid plexus, near Aβ deposits, and also in atherosclerotic plaques in blood vessels.
Big data analyses correlate viral load with clinical, molecular, and pathological features of AD. Time to consider the pathogen hypothesis anew?
Two papers advance the drive to develop an Alzheimer's vaccine, one looking at the antibody response in some of the Elan trial participants, the other using sophisticated methods to analyze the epitope recognized by antibodies generated in response to Aβ42 immunization.
Early in the course of Alzheimer disease, blockages in axonal traffic lead to sick axons swollen with the jumbled pile-up of traffic components. The blockages precede...
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