Stroke Severity, Recurrence Increase Dementia Risk
Dementia risk nearly doubled after each minor stroke and tripled after each major one, regardless of vascular risk factors. Risk climbed almost sevenfold after multiple major strokes.
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Amyloid Lurks in a Third of Cognitively Normal People Over 70
Large multinational meta-analysis also found that among people without dementia, CSF Aβ42 edged out PET in detecting amyloid pathology.
BDNF Val66Met Hastens Tau Phosphorylation in Familial Alzheimer’s
APP or presenilin mutation carriers who also carried the Met66 allele had more p-tau217 at presymptomatic stages, and more p-tau205 at symptomatic stages, than did Val carriers.
In Familial AD, Amyloid-PET Varies by Mutation Type; CSF Aβ42 Doesn't
A person's burden and spatial distribution of plaques, as measured by PiB-PET, varied greatly depending on his or her mutation. Their CSF Aβ42 or cognitive decline did not.
Will Insurance Cover Aducanumab? Jury Is Out
While payers public and private are deliberating whether or not to cover this first-in-class drug, the health economics group ICER re-affirms its original conclusion that aducanumab is overpriced.
In Alzheimer’s, More TREM2 Is Good for You
Longitudinal ADNI data tie higher sTREM2 in CSF to slower cognitive decline, reinforcing the idea that TREM2 activity protects the brain from AD pathology.
Are Mid-Life Depression and Anxiety Early Signs of Alzheimer’s?
CSF Aβ and tau are abnormal in older people with psychiatric problems. Are these symptoms an effect of AD pathogenesis, or risk factors for it?
Encenicline Misses Endpoints in Two Phase 3 Schizophrenia Trials
The compound had shown promise for sharpening cognition in schizophrenia and Alzheimer’s, but now faces an uncertain future.
Benzodiazepines Coax Microglia to Prune Synapses, Impair Cognition
The data, from mice, help explain how these depressants may increase a person’s risk for dementia.
Not Just Aβ—Glymphatic Flow Clears Tau, Too, Slowing Its Aggregation
Retarding glymphatic clearance in mice caused p-tau to accumulate faster, and hastened neurodegeneration.
Scientists Say LATE Worsens Cognitive Decline
Limbic predominant age-related TDP-43 encephalopathy is strikingly common among octo- and nonagenarians, and it causes their cognition to slide. LATE dramatically boosts the risk of dementia among people who also have plaques and tangles.
Sniff This: Therapeutic Peptides Through the Nose?
Peptides make lousy drugs, especially for the brain. When taken as a pill or by infusion, they either bounce off the blood-brain barrier, or get degraded within minutes...
Does LATE Subvert Alzheimer's Trials? Biomarkers, Please!
Limbic TDP-43 pathology accelerates cognitive decline in people with or without AD. Exosome and imaging biomarkers look promising.
At Tau2022: Unknown Functions Emerge for Tau, LRRK2
Neurons need LRRK2 in order to take up tau from the extracellular milieu. In ALS neurons, tau scuppers mitochondria, whereas in healthy cells it helps the nucleolus to function correctly.
11th ICFTD Meeting in Sydney Sorts Out Clinical Subtypes
Can genetics please parse the confusing spectrum of frontotemporal dementias? Whole genome sequences make a start.
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