Is Your Brain Aging Fast? Plasma Proteins Might Tell
Eight proteins in blood associate with faster brain aging, five with slower. The extracellular matrix protein brevican comes with larger cortical volume and smaller dementia risk.
NEWS
‘Proteogenomics’ Ties Genes That Control 38 Proteins to Alzheimer’s
Study correlated AD genome-wide association with concentrations of 6,000 CSF proteins to find potential disease variants.
In Alzheimer’s Due to Down’s, Spatial Omics Spots Signs of Trouble
In plaque- and tangle-laden layers of the Down’s syndrome neocortex, neuroinflammation raged, and glia sent death signals to neurons.
Do CSF and Plasma NfL Diverge After Alzheimer’s Disease Onset?
After symptoms of autosomal-dominant AD start, the uptick in neurofilament light chain accelerates in CSF but tapers in plasma.
Is It Time to Approve Drugs Based on Amyloid Removal?
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.
Astrocytes Mount Complex Responses to AD. They Change Over Time
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.
Receptors and Broken Lysosomes Explain Risk from APOE Variants
ApoE4 transports toxic lipids into lysosomes. ApoE2 and Christchurch variants do not.
'Presymptomatic AD' or 'Asymptomatic at Risk'? Dx Criteria Disagree
Alzheimer’s Association diagnostic criteria favor the former term, International Working Group the latter, for cognitively healthy people with AD biomarkers.
SPOTLIGHT
Dear FDA: Is it Time to Approve Drugs Based on Amyloid Removal?
As Eisai notches wins in its campaign for lecanemab approval around the world—last month in the European Union, this week in Mexico—research and clinical leaders called on the U.S. FDA and fellow agencies elsewhere to reconceptualize their deliberations themselves. The field’s knowledge base, they argue, is strong enough for regulators to greenlight amyloid-removing immunotherapies without evidence on cognitive/clinical outcomes. Is this proposal timely? Overdue? Premature? Read the article, have a think, and share your view.
Receptors and Broken Lysosomes Explain Risk from APOE Variants
A study explains why ApoE4 increases risk for Alzheimer’s and why ApoE2 protects. The former ferries toxic lipids into cells, where they clog lysosomes with lipofuscin. ApoE2 binds too weakly to cell-surface lipoprotein receptor to do that. Ditto for protective Christchurch variants. ApoE3 also transports lipids into cells but does less damage than ApoE4, which is more likely to aggregate at the low pH found in lysosomes.
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