Could Personalizing Multimodal Interventions Give Them Oomph?
In a small pilot study, tailoring lifestyle changes to the individual boosted cognition, with an effect size three times that seen in the Finger trial.
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In a small pilot study, tailoring lifestyle changes to the individual boosted cognition, with an effect size three times that seen in the Finger trial.
In the Graduate trials, the anti-amyloid antibody gantenerumab cleared only half as much plaque as it had done in earlier studies. Is formulation or dosing to blame?
In a head-to-head comparison, donanemab banished four times as much plaque in the first six months as aducanumab did, partly due to its faster titration.
ApoE2 was detected in cerebrospinal fluid of ApoE4 carriers with Alzheimer’s disease who received a virus expressing the protective allele.
Six commonly used tests accurately detected dementia, even preclinical cognitive slippage, when given over video chat or face-to-face.
A liposomal anti-tau vaccine elicited a response against disease-linked forms of tau, outdoing a conjugated vaccine. A separate tack to vaxx against tau is waiting in the wings.
In Phase 3 trials, the drug reduced agitation more than placebo; however, both groups benefited substantially.
Scientists at CTAD found the Phase 3 trial well-done, the data consistent, and expect the drug to be approved. Priorities: grow the effect, understand the bleeding risk.
VAMP2 helps distinguish pure dementia with Lewy bodies from DLB with Alzheimer’s. A synaptic protein panel distinguished FTLD-TDP-43 from FTLD-tau.
Slow clearance of an MRI tracer offers evidence of inefficient glymph transport in the brain.
Aligning single-cell gene expression in “pseudotime” models longitudinal change. It explores how healthy cells become sick during Alzheimer's.
By pooling single-nucleus RNA-sequencing datasets, scientists found consistent changes across Alzheimer’s cohorts. Examples: hypermetabolic transcription, and a new neuron population that dies early on.
Analysis identified neuronal populations that die early in AD and glial subtypes that expand. Gliosis signaled fast memory decline.
Microglial ApoE4 hobbled these cells' protective responses against Aβ and tau. In the meninges, ApoE4 made by myeloid cells slowed lymphatic drainage; at the blood-brain barrier, ApoE4 steered aging endothelial cells and pericytes toward dysregulation.
Soluble p-tau, aggregation epicenters, and gene variants emerged as potential forces that might influence how quickly tangles propagate through the brain.