Like GWAS, BWAS Need Thousands of Participants
To find true brain-behavior correlations, a brain-wide association study needs orders of magnitude more people than the dozens typically used in neuroimaging research.
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Field Loses GSM Developer Steven Wagner, 64
Wagner pioneered γ-secretase modulators to treat Alzheimer’s disease, with a candidate slated to enter Phase 1 trials later this year.
Robust TREM2 Expression May Delay Alzheimer’s Disease
In familial AD, the faster sTREM2 rises in a person's cerebrospinal fluid, the slower his or her amyloid grows, cortex thins, and cognition fades.
Can Preserving Vision and Hearing Prevent Dementia?
Removing cataracts cuts a person's risk of dementia. Cochlear implants stall mild cognitive impairment. Could treating sensory losses hold some dementia cases at bay?
Mild COVID Infection Can Shrink Brain, Speed Cognitive Decline
In some people who had weathered COVID at home, olfactory regions in the brain shrank and executive function slowed. Will these changes resolve or persist?
Tau Haplotypes Hint at Transcriptional Changes, Ferroptosis
In iPSC-derived cells, H1 risk haplotype is linked to noncoding, antisense variants and to a master regulator of oxidative stress
Tau Triggers Neuroinflammation, But Mechanisms Vary by Disease
In two primary tauopathies, natural killer cells invade the brain. In Alzheimer’s, a microglial antiviral response dominates, and hyperexcitability may play a role.
Tau2022 Global Conference (Virtual Meeting)
P-Tau217 Clock Predicts Alzheimer’s Progression Over 30 Years At Tau2022: Unknown Functions Emerge for Tau, LRRK2 Tau Triggers Neuroinflammation, But Mechanisms Vary by Disease Tau Haplotypes Hint at Transcriptional Changes, Ferroptosis Since Tau2020 was
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.
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.
P-Tau217 Clock Predicts Alzheimer’s Progression Over 30 Years
Once p-tau217 in cerebrospinal fluid reaches a tipping point, it rises at a constant rate in everyone and predicts the age when symptoms will begin.
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.
LATE (Limbic-predominant Age-related TDP-43 Encephalopathy) 2022
Virtual Workshop Tackles LATE, a Cause of Late-life Dementia Scientists Say LATE Worsens Cognitive Decline Does LATE Subvert Alzheimer's Trials? Biomarkers, Please! LATE (Limbic-predominant Age-related TDP-43 Encephalopathy) 2022
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.
Virtual Workshop Tackles LATE, a Cause of Late-life Dementia
At LATE 2022, researchers hashed out neuropathological and clinical characteristics of limbic predominant age-related TDP-43 encephalopathy, a major contributor to late-life cognitive decline and potential bungler of AD clinical trials.
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