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.
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.
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 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.