At the inaugural Holloway Summit hosted by AFTD, researchers, regulatory, and foundation leaders discussed how to advance digital tools from the idea stage into standardized, reliable form for diagnosis and trials.
The development of digital health technologies and biomarkers to track the progression of FTD’s myriad manifestations was the focus of the first Holloway Summit.
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.
A case-control study of half a million people nabbed the variants. Both are rare, lie in the C-terminal lipid-binding domain, and one neutralizes ApoE4.
In two Phase 1 trials, DNL201 reduced LRRK2 kinase activity in blood mononuclear cells. The inhibitor reached the same level in CSF as in blood. There were no serious side effects.
Months before mice develop plaques, faulty lysosomes swollen with Aβ commandeer plasma, ER, and Golgi membranes, creating toxic rosettes around the nucleus. The neurons eventually burst, leaving behind plaques.
Adeno-associated viruses carrying Cas9 and guide RNAs cut hexanucleotide repeats out of the C9ORF gene. RNA inclusions and poly-dipeptides became sparse.
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