New Smartwatch Utility Tracks Parkinson’s Symptoms
Sensor algorithms can accurately capture patterns of resting tremor and dyskinesia. This could help clinicians manage symptoms and medication.
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Sensor algorithms can accurately capture patterns of resting tremor and dyskinesia. This could help clinicians manage symptoms and medication.
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.
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.
Transcriptomic and epigenomic data pin PD risk genes in GWAS loci; six affect splicing, five expression, four are new.
Van Leeuwen was best known for finding frameshift mutations in APP and ubiquitin B in the brains of people with tauopathies.
In mice, an anti-ApoE antibody removed plaques from the brain’s parenchyma and blood vessels better than aducanumab. Importantly, it caused no microhemorrhages.
Researchers split $200,000 for their theories on the role of six microbes—one virus, four bacteria, and one parasite—in Alzheimer’s.
Epidemiology study reveals 1.5-times higher risk of dementia after herpes virus infection. Short-term antiviral treatment appears to lower risk.
Some people with severe COVID-19 have neurovascular injury and elevated markers of neural damage in their blood and CSF. What’s going on in their brains?
In people with Alzheimer’s biomarkers, the basal forebrain shrinks early, foreshadowing microglial neurotoxicity, atrophy in the medial temporal lobe, and cognitive decline.
Alector’s AL002c antibody mobilizes microglia, reduces neuronal dystrophy, and restores normal behavior—all in mice. The clinical version is in Phase 1.
The transcription factor NFATc2 mediates this response.
Researchers at the online AAT-AD/PD meeting touted therapies that target neuroinflammation, synapses, epigenetic regulation, or the cortisol stress response.
Plaques abound, cytokines spike, microglia swell with lipids and send out spermine SOS signals in Denali model. Mice will be shared, allowing unrestricted use.