Neuronal Pentraxin 2 Binds Complement Protein, Protects Synapses
NPTX2 binds complement C1q, disrupting signals to microglia to destroy synapses.
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NPTX2 binds complement C1q, disrupting signals to microglia to destroy synapses.
Scientists are refining safety and biomarker disclosure protocols, and are preparing to collect data on how well the new drugs work.
cGAS and STING initiate a type I interferon response, which weakens neurons’ resilience to tau pathology.
Transplanting a human cerebral organoid containing microglia into a mouse brain allows the cells to thrive in something close to their natural environment.
The agency reiterated its earlier decision that traditionally approved amyloid antibodies will be covered if physicians enter data into a patient registry.
In amyloidosis mice, decline of the hypothalamic melanin-concentrating hormone system jacks up neuronal activity, and contributes to sleep problems.
The more a person’s gut microbiome becomes individualized with age, the longer that person's lifespan and the better his or her health, say scientists.
Feeding taurine to mice and monkeys increased the lifespan of the former and reduced signs of aging in both.
Between basic researchers and clinicians, momentum is growing to test BACE inhibition again. This time, at low doses.
A crop of new PET tracers that bind α-synuclein aggregates shows promise in tissue samples and in animal models. Will they prove potent enough for brain imaging?
Swapping allele expression in astrocytes lowered amyloid load, lessened gliosis, and improved memory. This works even after amyloidosis is in full swing.
Six commonly used tests accurately detected dementia, even preclinical cognitive slippage, when given over video chat or face-to-face.
FTLD-causing mutations in tau turned down expression of lncRNAs including SNHG8. This goaded TIA1 to form stress granules, bringing tau along for the ride.
The oligomers beckon microglia and astrocytes to prune dendrites. This correlates with cognitive decline.
Resilient and vulnerable interneurons mark different stages of Alzheimer's. Gene regulation crumbles in late stages. Microglial states change with epigenomic shifts.
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