Already implicated in dementia, this lysosomal receptor appears to play a role in the development of COVID-19.
In the negative Phase 2 trial of prasinezumab, populations with more rapid decline benefited; this informed the design of a new Phase 2b study.
Data from Phase 3 trials of elenbecestat show no harm to cognition, leaving open a chance that the drugs could be used safely in the future.
In early stage trials, light and sound promoted neuronal communication, calmed immune cells, and slowed brain atrophy, but cognitive benefit remains unclear.
Sensor algorithms can accurately capture patterns of resting tremor and dyskinesia. This could help clinicians manage symptoms and medication.
People who report not participating in social or cognitive activities are more likely to develop dementia within the next few years, but not after that. The findings cast nonparticipation as a consequence, not a cause, of neurodegeneration.
Transcriptomic and epigenomic data pin PD risk genes in GWAS loci; six affect splicing, five expression, four are new.
Researchers envision p-tau-based blood tests for Alzheimer’s disease within a few years, but maybe not a stand-alone test.
Two mouse models presented at AD/PD may hand scientists more translationally relevant tools to explore LOAD pathophysiology and treatment. The tricks: targeted replacement and knocking in multiple GWAS variants.
New research implicates IL-6 signaling and even Aβ42 itself as BACE targets, complicating efforts to resurrect BACE inhibitors at a low dose.
The field is shifting from targeting tau’s tips to its mid-region, especially where tau binds microtubules. Several new candidates are in the clinic; whether the strategy will work remains to be seen.
After news on “new data” they won’t see, three committee members argue against approval.
Assays will help doctors diagnose Alzheimer’s disease and amnestic mild cognitive impairment in Taiwanese clinics.
Despite plaques and tangles in the brain, this group, on average, maintains their cognitive skills over two to four years, suggesting the presence of resilience factors.
Among 14 familial Alzheimer’s APP mutations, two don’t change the Aβ42/Aβ40 ratio, but all of them yield long peptides of 45 to 49 residues that hide out in the membrane.