Breaking the Spell: Checkpoint Inhibitors Help Microglia Snap Out of It
In ApoE4 carriers, checkpoint proteins Itgb8 and TIM3 lock microglia into homeostasis. Remove the lock, and they spring into neuroprotective action.
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In ApoE4 carriers, checkpoint proteins Itgb8 and TIM3 lock microglia into homeostasis. Remove the lock, and they spring into neuroprotective action.
Scientists corroborate their recent finding that shingles vaccination reduces dementia risk in a second population.
Adding the S320F mutation to existing double-knock-in mice exacerbates tau pathology.
At AD/PD, a handful of early trials showcased approaches to counteract harmful cytotoxic T cell responses in AD and related diseases.
Antigens from the brain can tickle T cells in cervical lymph nodes, instigating a cytotoxic invasion. With ApoE4, more T cells enter.
At AD/PD, clinicians from the U.S. and Israel shared data from a few hundred patients, reporting ARIA rates equal to, or lower than, those in trials.
The marketing authorization comes after delays and reversals. It excludes APOE4 homozygotes and people taking anticoagulants, and requires a post-market study.
The cells reduced the amount of amyloid and improved downstream aspects of Alzheimer’s pathogenesis in mouse models.
The TfR-targeted, anti-Aβ antibody swiftly axed amyloid throughout the brain. It caused little ARIA, but lots of infusion reactions.
Tau fragments, alone or with other proteins, help identify people with lots of tangles. This may help select people for trials or therapy.
Real-world data hints that plasma markers can pick up Alzheimer’s pathology before people have memory complaints.
Fully automated test may be as accurate as mass spec, and more scalable.
The spatial extent of tau pathology better correlates with disease severity, and stages disease more accurately, than does tangle load.
Decreased lysosomal efficiency could result from shifts in endosomal recycling.
DIAN-TU explains how it selects APP, PSEN1, and PSEN2 genetic variants for clinical trial inclusion.
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