Taiwan FDA Approves MagQu Plasma Aβ And Tau Tests
Assays will help doctors diagnose Alzheimer’s disease and amnestic mild cognitive impairment in Taiwanese clinics.
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Assays will help doctors diagnose Alzheimer’s disease and amnestic mild cognitive impairment in Taiwanese clinics.
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.
In mouse models of Aβ toxicity and amyloidosis, inhibiting the integrated stress response restored protein production, spared synapses, and brought back memory.
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?
Plaques abound, cytokines spike, microglia swell with lipids and send out spermine SOS signals in Denali model. Mice will be shared, allowing unrestricted use.
People who carry the ApoE4 variant are more likely to succumb to the virus. In vitro, SARS-CoV-2 infects more ApoE4 than ApoE3 brain cells. Astrocytes were activated, neurons degenerated.