Traumatic Tau: Filaments from CTE Share Distinct Structure
Atomic resolution structures of tau filaments from three people with CTE revealed a common strain of tau induced by chronic head injuries.
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Atomic resolution structures of tau filaments from three people with CTE revealed a common strain of tau induced by chronic head injuries.
Futility analysis predicts failure to reach primary endpoint.
Perturbations in the hormone correlate with memory problems. But does FGF23 act in the brain, or affect cognition indirectly via the kidneys?
Exposing AD mice to multisensory gamma therapy induced 40-Hz waves in their brains, plus effects on amyloid, tau, microglia, blood vessels, and cognitive function.
Among British civil servants, the quality of their diet did not correlate with their risk of developing dementia cognitive decline over 25 years.
IBM researchers in Australia identify a combination of four proteins in plasma that predicts amyloid positivity in cerebrospinal fluid, and correlates with progression to AD.
Deleting BACE1 with CRISPR nanocomplexes tempered Aβ pathology and boosted memory.
Liquid beads of TDP-43 form independently of stress granules and sequester proteins needed for nucleocytoplasmic transport.
When the agency sent warning letters to 17 companies that falsely advertised cures and preventions for AD, most took down exaggerated claims. But can regulations stay ahead of the market?
In people at intermediate risk for cardiovascular disease, the meds had no effect on cognitive decline over six years.
How the element relates to neurodegeneration remains unclear.
Only 16 percent of seniors report being assessed for cognition during yearly checkups. Eighty-two percent think it should be routine.
Researchers publish 14 new AD variants. This includes one near WWOX, a gene that encodes a protein linked to tau and lipid metabolism.
Using a new optogenetic model for TDP-43 phase transitions, scientists see the protein aggregate outside, not inside stress granules. The model distinguishes physiological from abnormal phase transition.
A flavonoid reportedly spices up oxidative phosphorylation in microglial mitochondria, revving up phagocytosis of amyloid plaques in mouse models. The small study needs independent replication.