Active Tau Vaccine: Hints of Slowing Neurodegeneration
In a Phase 2 trial, the vaccine reportedly normalized the rise in plasma NfL, and appeared to lower CSF tau and retard brain atrophy.
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In a Phase 2 trial, the vaccine reportedly normalized the rise in plasma NfL, and appeared to lower CSF tau and retard brain atrophy.
Scientists report at AAT-AD/PD that they tightened a causal connection between gut microbes, microglial function, and protein deposits. In mice, that is.
Trialists are shooting new arrows at the disease, including compounds that tweak autophagy, neuroinflammation, and glycolipid recycling.
In a mouse model of amyloidosis, human wild-type TREM2 kept Aβ deposition at bay early on, but this defense became overwhelmed as plaques grew. The R47H AD risk variant never offered protection early on, and made things worse later.
The first topline Phase 2 results from an antibody targeting Parkinson’s pathology, Roche’s prasinezumab, were a mixed bag. Next steps are unclear.
For several neurodegenerative diseases, scientists identified which cell types exert a person’s inherited risk. In Alzheimer’s, it’s microglia; in Parkinson’s, it’s dopaminergic and enteric neurons—and oligodendrocytes.
Growing evidence suggests exposure to air pollution increases risk of brain damage and dementia. More definitive research is needed.
Chemicals and particulates may slip across the blood-brain barrier or travel up olfactory nerves to directly affect brain cells. What are the consequences for cognition?
Using a form of confocal microscopy and automated software, the method allows researchers to rapidly identify functional synapses within brain structures.
Researchers at the online AAT-AD/PD meeting touted therapies that target neuroinflammation, synapses, epigenetic regulation, or the cortisol stress response.
New genes linked to early and late-onset AD offer up mechanistic insight, potential targets for treatment.
The DIAN Trials Unit is nearing the end of its first two secondary prevention trials. It has begun a cognitive run-in period for its next trial, of a tau-based drug, and for a primary prevention study in people as young as 18.
Different polymorphisms in MS4A genes up- or downregulate levels of TREM2, modulating levels of the shed ectodomain in the cerebrospinal fluid and AD risk.
In patient-derived neurons, tau mutations scupper lysosomes and SORLA shunts APP through different types of endosomes.
Changes in the composition of the cerebrospinal fluid and synapses may reveal novel insights into AD pathology.