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.
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.
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.
Incorporation of a cryptic exon scuttles translation of UNC13A, but only in neurons lacking nuclear TDP-43. UNC13A ALS/FTD risk variants exacerbate the aberrant splicing.
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.
Merged Consortia Forge Path to Trials in Frontotemporal Dementia FTD Fluid Markers for Degeneration: Check. For Pathology: Not Yet. Imaging Exposes Hugely Heterogeneous Brain Changes Among FTDs Moving Target: Can Standardized Tests Track Symptoms of FTD?
Grappling with a rare disease whose variability is daunting, international cohort studies are charting the natural history of FTD. They have discovered biomarkers and honed physiological tests that underlie its behavioral symptoms.
The global platform trial for Alzheimer’s due to mutations in APP or presenilin will try to treat or prevent symptoms by deploying a therapeutic antibody that homes in on a piece of tau known to aggregate into neurofibrillary tangles.