Three weeks of on-demand seminars to culminate in live Q&A.
Three young monkeys missing exon 9 of presenilin 1 seem to have an elevated Aβ42/40 ratio. It remains to be seen if they will develop plaques and tangles as they age.
The first high-resolution look at LRRK2 implies that pathogenic mutations increase binding to microtubules by biasing the kinase domain toward a closed, active conformation.
In female mice it’s the other X chromosome, not lack of a Y, that extends life and preserves memory in the face of amyloidosis. A histone demethylase gene partly explains this. It protects people, too.
In mice with defective PS1 phosphorylation, microglial autophagy falters, exacerbating Aβ burden.
Dendritic tau suppresses production of nitric oxide, which prevents blood vessels from dilating in response to neural activity.
In the mouse retina, these tender threads connect pericytes on nearby capillaries. They enable cells to coordinate constriction and dilation of blood vessels in response to neuronal activity.
Without the WD domain of Atg16L1, required for a newly discovered type of endocytosis, old mice develop hallmark pathologies of AD.
Carriers accumulate fewer tangles than noncarriers for a given amount of amyloid, explaining how the gene variant may lower a person’s Alzheimer’s risk.
Early data suggest that CT1812 and AL001 shift biomarker levels in Alzheimer’s disease and frontotemporal dementia, respectively. BI 425809 fails to improve cognition.
Subtle memory deficits resolved after volunteers stopped taking the Novartis BACE inhibitor.
New synaptic profiling and imaging techniques are enabling scientists to zero in on synaptic proteins, including phospho-tau, that make the difference between clinical Alzheimer’s and resilience.
The FDA will decide whether to approve the antibody as a treatment for Alzheimer’s disease on or before March 7, 2021.
New research pushes back the age at which dementia risk from cardiovascular and metabolic factors begins. Should protective lifestyle interventions start in youth?
Homozygous carriers of GM17—a common IgG1 variant the HSV-1 virus has evolved to evade—had quadruple the risk of developing AD. In a small Swedish cohort, that is.