Phase 2 Data of AADvac1 in Alzheimer’s Disease Published
The tau vaccine evoked a robust anti-tau antibody response, which curbed the rise in plasma NfL and CSF p-tau over two years. Cognitive decline continued.
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The tau vaccine evoked a robust anti-tau antibody response, which curbed the rise in plasma NfL and CSF p-tau over two years. Cognitive decline continued.
Though the first two trial arms were negative on cognition, gantenerumab’s strong effect on biomarkers led to an open-label extension.
Aducanumab: Will Appropriate-Use Recommendations Speed Uptake? On Donanemab, Plaques Plummet. Off Donanemab, They Stay Away Antisense Therapy Stifles CSF Tau in Mild Alzheimer’s Disease Seeking Real-World Data on Whether Aducanumab Works Will Insurance Co
In the wake of the controversial thumbs-up for Aduhelm, the U.S. federal government is probing not only aducanumab’s price and approval history, but also the FDA’s accelerated approval pathway in general.
In an open-label Phase 2 study, fluid biomarkers suggested the anti-sortilin antibody restored lysosomal function and reduced neuroinflammation in people with symptomatic FTD. Tantalizingly, participants worsened less than historical controls.
Topline results from a Phase 2 trial of semorinemab suggest the therapeutic antibody may have eased the cognitive downturn in people with mild to moderate Alzheimer’s disease.
Markers of neuronal injury rose in plasma within a few months of severe COVID-19, then fell back to normal by six months. Some cases with brain symptoms had lower Aβ and higher tau in their blood.
North Carolina and South Texas centers to focus on risk factors and diversity.
Misfolded tau travels from a subset of neurons in the entorhinal cortex directly into CA1 neurons in the hippocampus, fouling synaptic transmission and memory in mice.
The academy elected 90 new members. Five are well-known for their contributions to the field of neurodegenerative diseases.
At a recent conference, researchers presented more evidence tying the APOE4 allele to disrupted lipid metabolism. They linked this problem to Aβ production.
In Alzheimer's mice without the AD risk gene Abi3, fewer microglia crowd around amyloid plaques. Cultured microglia without Abi3 appear stuck in a torpor, even though their phagocytosis mostly works.
The new gene JADE1 encodes an adaptor protein that sits in tangles and nonetheless appears neuroprotective. The study also turned up three AD and two PSP genes, suggesting PART overlaps with these conditions.
In a mouse model of amyloidosis, microglia carried Aβ aggregates into grafted wild-type tissue. The immune cells played a key part in the subsequent growth of plaques in the graft.
While Phase 3 trials of subcutaneous gantenerumab continue, scientists say delivering the antibody to the brain via the transferrin receptor might be twice as efficient.
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