In astrocytes, Aβ revs up urea metabolism, spitting out the intermediate putrescine. This gets turned into the neurotransmitter GABA, which blunts synaptic transmission and memory in mice.
A spate of recent studies could not replicate the finding that knocking down the RNA-binding protein PTBP1 in astrocytes triggers their conversion to neurons. Leaky expression of the knockdown construct in endogenous neurons may be to blame.
Cognitively normal people whose PET scans showed both plaques and tangles slid toward MCI or dementia within a few years. This risk was 19 times higher than in people without these deposits.
Astrocytes react differently depending on the type of insult or injury inflicted upon the brain. Two studies identified transcriptional regulators controlling astrocyte responses.
At the Holloway Summit, scientists, regulatory, and foundation leaders discussed how to advance digital biomarkers from the idea stage into standardized, reliable tools for diagnosis and trials.
The inaugural Holloway Summit, hosted by AFTD, focused on the development of digital health technologies to track the progression of FTD’s myriad manifestations.
Digital Biomarkers of FTD: How to Move from Tech Tinkering to Trials? Digital Tools Abound, Yet Remote Biomarkers for FTD Remain Exploratory Changes in activity, speech, sleep, or the way a person moves are all examples of measurements that can be capture
A C1q antibody hit its target in a small Phase 2 Huntington’s trial, while indirect inhibition of C1q restored synaptic density in Alzheimer’s model mice.
While TMEM175 ushers potassium ions out of neutral lysosomes, it shuttles protons out of acidic ones. Sans TMEM175, lysosomes become too “tart,” and stop working. Two papers say so.
Topline results showed no statistically significant slowing of decline on either of two primary endpoints. Trends across multiple endpoints favored crenezumab.
In people with mild AD, Genentech’s anti-tau antibody, semorinemab, did not slow cognitive decline.
5xFAD mice lacking microglia develop cerebral amyloid angiopathy and amass calcium deposits. Most die by 6 months old.
Limbic-predominant age-related TDP-43 encephalopathy (LATE) most often co-occurred with AD pathology, but was detected on its own as well.
α-Synuclein prevents de-capping of transcripts, hindering their turnover. In human brain, α-synuclein accumulation correlated with slower mRNA decay.
TDP-43 inclusions in intramuscular nerve bundles, paired with clinical criteria, may enable diagnoses at early stages of ALS.
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