Imatinib, previously reported to inhibit γ-secretase, now appears to isolate APP from BACE as well.
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.
Perhaps…yes? At first blush, this is the tentative conclusion one must draw if the results of presentations yesterday on Elan's vaccine...
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.
Researchers reported negative findings from three trials at ICFTD 2016.
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.
With the buzz surrounding amyloid-targeting therapies, it is easy to lose sight of the fact that other treatments are being tested as well...
Three BACE inhibitors, a γ-secretase modulator, and a phosphodiesterase inhibitor appeared safe in Phase 1 trials.
Can genetics please parse the confusing spectrum of frontotemporal dementias? Whole genome sequences make a start.
At AAIC 2017, researchers presented new approaches to find genetic variants linked to AD risk and to understand their contributions to disease.