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DIAN, Roche, Lilly disclose that neither gantenerumab nor solanezumab slowed cognitive decline in the first-pass comparison of drug and placebo groups. Analyses are ongoing; dose may have been too low.
Researchers implicate PrP in the toxicity of Aβ, tau, and α-synuclein oligomers in several neurodegenerative diseases.
Vision improved in some retinitis pigmentosa patients in a Phase 1 trial.
New research presented at the HAI conference also finds links between UCB-J uptake and plaques, tangles, and cognitive decline.
Amyloid and tau PET are helping scientists pinpoint the underlying cause of specific AD symptoms. Perhaps imaging of certain brain regions will help predict an individual’s progression.
At HAI 2020, scientists more precisely quantified the relationship between plaques, tangles, and cognitive decline.
When observed over an eight-year period, people with the highest plasma concentrations were more likely to die than people with lower levels.
By engaging scientists studying every tau-based disorder, a new conference aimed to foster collaborations and research directions.
Centenarians who scored high on the MMSE stayed cognitively and physically active over the next two years, even if they carried genetic risk factors for Alzheimer’s. What protects these lucky few?
Two epigenetic proteins accelerated age-related behavioral decline in worms and in mice, at least partly by dampening mitochondrial function. Orthologs in the human brain ramped up with aging and with AD progression.
The monoclonal antibody activated TREM2 signaling on mouse microglia. It supported their survival and stimulated their clearance of amyloid plaques.
In the human brain, alpha waves fell out of sync, while delta-theta waves swelled in concert with amyloid plaques, neurofibrillary tangles. Alpha modulation correlated with cognitive decline.
Under diabetic conditions, SERP1 binds secretase subunit, cranking up cleavage of APP but not Notch. The finding offers a mechanistic link between diabetes and Alzheimer’s.
Not sure where that is? You are not alone. It is a tiny spot deep behind the nose, newly defined by the PET signal of early neurofibrillary tangle deposition. It also prompted a tau-staging scheme.
In motor neurons of TMEM106b knockout mice, swollen vacuoles piled up in axons near the soma, rendering the mice wobbly and slow to react. The finding contradicts prior reports.
