Researchers take first steps on road to targeting disease-causing APP mutations and amyloid processing.
The drug had no effect on any clinical measure, while there were side effects such as rashes, insomnia, and thoughts of suicide.
In an AD mouse model, a deficit in specialized mediators prevented microglia from tempering inflammation and clearing Aβ. Time to learn about resolvins?
Two enormous epidemiological studies strengthen the link between head injuries and neurodegenerative disease.
People with inflammatory bowel disease are at higher risk for Parkinson’s—but not if they take anti-inflammatory medication.
Thirty-five reviews cover two decades of Alzheimer’s research.
Three genome-wide association studies, including the largest-ever thanks to UK Biobank, reveal 13 new AD risk loci. They implicate APP processing in LOAD, and further highlight inflammation and lipid metabolism.
Transportins, methylation, and RNA all regulate LLPS and the behavior of pathogenic RNA-binding proteins.
At AAT-AD/PD, scientists said an α-synuclein PET tracer is headed into trials. And marmosets model PD behaviors better than rodents. (Spoiler alert: They kick their partners while they sleep.)
Systemic inflammation can alter the epigenome of microglia, dictating whether the cells clean up Aβ pathology, or exacerbate it.
Massive meta-analysis finds no link with AD or PD.
Volunteers kept awake all night retained more florbetaben in their hippocampi and thalami in morning-after PET scan.
In animal models, a PD risk gene revs up the immune system to fight infections, while probiotic bacteria slow α-synuclein aggregation.
Researchers at AAT-AD/PD discussed investigational PD treatments that aim to modify disease by hitting genetic risk factors.
For the first time, NIA-AA proposal bases diagnosis in living people solely on biomarkers for plaques and tangles.
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