In a retrospective study, people with vitiligo had 12 times the risk of developing Alzheimer’s disease than did healthy controls. Why is that?
This pathway may transmogrify microglia during neurodegeneration, without the help of TREM2.
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.
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.
In mice, polyamines boost autophagy and promote clearance of soluble Aβ species. In cells, they counteract tau aggregation. In the Alzheimer’s brain, their metabolism is ramped up. Could spermidine supplements prevent or treat AD?
After news on “new data” they won’t see, three committee members argue against approval.
Chemicals and particulates may slip across the blood-brain barrier or travel up olfactory nerves to directly affect brain cells. What are the consequences for cognition?
Growing evidence suggests exposure to air pollution increases risk of brain damage and dementia. More definitive research is needed.
Using a form of confocal microscopy and automated software, the method allows researchers to rapidly identify functional synapses within brain structures.