Epidemiology study reveals 1.5-times higher risk of dementia after herpes virus infection. Short-term antiviral treatment appears to lower risk.
The first ultrasensitive plasma test for this old marker differentiates Alzheimer’s from healthy controls and non-AD dementias. It segregates people stepwise at phases of pathogenesis down to Braak stages 1 and 2 and below amyloid PET positivity.
Researchers unearthed 75 risk loci, 42 of them new, and nominated candidate genes for each. A polygenic risk score based on all variants predicted AD risk with high accuracy.
Van Leeuwen was best known for finding frameshift mutations in APP and ubiquitin B in the brains of people with tauopathies.
In mouse brain slices at least, tau shuffles in and out of protein inclusions. The tangles grew more inert as the tissue aged.
When cultured with human neurons expressing a familial Alzheimer’s gene, both microglia and astrocytes were necessary to spike complement C3 and send inflammation into overdrive.
By comparing protein changes with GWAS data, scientists identified new links to AD. This method can unearth genes that otherwise fall short of genome-wide significance.
In mouse models of Aβ toxicity and amyloidosis, inhibiting the integrated stress response restored protein production, spared synapses, and brought back memory.
Plaques abound, cytokines spike, microglia swell with lipids and send out spermine SOS signals in Denali model. Mice will be shared, allowing unrestricted use.
In mice, an anti-ApoE antibody removed plaques from the brain’s parenchyma and blood vessels better than aducanumab. Importantly, it caused no microhemorrhages.
In response to an FDA request, the drug’s sponsor submitted new data analyses. The agency moved the action date to June 7.
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.
Assays will help doctors diagnose Alzheimer’s disease and amnestic mild cognitive impairment in Taiwanese clinics.