Three weeks of on-demand seminars to culminate in live Q&A.
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.
A 2018 report that had spotted extra copies of APP lurking in neuronal genomes has come under scrutiny, with claims that the result is due to contamination. Does a response from the original authors bolster their claim?
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.
A C9ORF72 polydipeptide repeat induces aggregation by direct interaction with TDP-43, while progranulin mutations that trigger microglial toxicity cause TDP-43 to accumulate via complement.
Restoring proper gene editing assuaged mitochondrial defects in patient-derived neurons and organoids. Splicing errors may underlie other PD cases as well.
The antiviral protein enhances γ-secretase processing of APP. More of it is present in Alzheimer’s disease.
Learning tests may prove more informative in clinical trials of early AD. A new one claims it can spot a difference in six days.
In a career spanning four decades, Davies spearheaded the cholinergic hypothesis, unlocked secrets of tau, and readily shared antibodies in the field.
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.
A panel of experts concludes the evidence for this scary prospect is weak, but recommends neurosurgeons use separate neurosurgical instruments for young and old patients. The experts called for further studies.
The designer chimera stabilizes synapses in various mouse models of neurodegenerative disease.
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.
AMX0035, a mix of sodium phenylbutyrate and taurursodiol, slowed functional decline over six months by about as much as the approved ALS drug edaravone.
Poor coordination among grid cells in the entorhinal cortex and place cells in the hippocampus compromises navigation. Grid cells fail first.