‘MGWAS’ Ties Brain Metabolites to Alzheimer’s, Parkinson’s, More
Lipids, amino acids, carbohydrates, and other molecules in the CNS linked to genetic variants, some of which upped the risk for neurodegenerative disease.
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Lipids, amino acids, carbohydrates, and other molecules in the CNS linked to genetic variants, some of which upped the risk for neurodegenerative disease.
Eight proteins in blood associate with faster brain aging, five with slower. The extracellular matrix protein brevican comes with larger cortical volume, lower dementia odds.
Study correlated AD genome-wide association with concentrations of 6,000 CSF proteins to find potential disease variants.
In plaque- and tangle-laden layers of the Down’s syndrome neocortex, neuroinflammation raged, and glia sent death signals to neurons.
After symptoms of autosomal-dominant AD start, the uptick in neurofilament light chain accelerates in CSF but tapers in plasma.
Opinion leaders argue that the field’s knowledge base is now strong enough for regulators to greenlight amyloid-removing immunotherapies without evidence on cognitive/clinical outcomes.
Single-nuclei RNA-Seq of 600,000 astrocytes defined seven subtypes. One revs up metabolic support late in Alzheimer’s disease, before flagging at its end stage.
ApoE4 transports toxic lipids into lysosomes. ApoE2 and Christchurch variants do not.
Alzheimer’s Association diagnostic criteria favor the former term, International Working Group the latter, for cognitively healthy people with AD biomarkers.
In ADAD mutation carriers, blood β-synuclein crept up after their amyloid-PET scans had turned positive, but before axons degenerated. Does it reflect crumbling synapses?
Cryo-EM identifies a similar protein fold in these ependymal cell inclusions as in parenchymal TMEM106b fibrils.
By utilizing advances in parallel imaging, scientists cut the time needed for diagnostic MRI scans from 18 to 6.5 minutes, without a noticeable loss in quality.
Early stage trials hint that new therapeutics could take down APP, boost ApoE2, or fix inflammatory and metabolic dysfunction in AD.
Vendors of plasma p-tau217-based tests are filing with U.S. and European regulators for approval of fully automated, in vitro diagnostics.
The findings suggest that non-AD pathologies, driven by other comorbidities, might contribute to cognitive decline in these populations.
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