Restoring proper gene editing assuaged mitochondrial defects in patient-derived neurons and organoids. Splicing errors may underlie other PD cases as well.
AMX0035, a mix of sodium phenylbutyrate and taurursodiol, slowed functional decline over six months by about as much as the approved ALS drug edaravone.
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.
In a career spanning four decades, Davies spearheaded the cholinergic hypothesis, unlocked secrets of tau, and readily shared antibodies in the field.
The designer chimera stabilizes synapses in various mouse models of neurodegenerative disease.
The antiviral protein enhances γ-secretase processing of APP. More of it is present in Alzheimer’s disease.
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.