‘Working from Home’: Do Gut Microbes Hold Sway Over Glia, Aβ?
Scientists report at AAT-AD/PD that they tightened a causal connection between gut microbes, microglial function, and protein deposits. In mice, that is.
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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.
People who lived in impoverished neighborhoods in their last year of life had greater odds of having died with AD neuropathology.
Islet amyloid protein and Aβ fibrils share similar folds.
Researchers used PET scans from 4,000 people to link RBFOX1 risk variants to amyloidosis. People with lower RBFOX1 expression in their brains had more amyloid and worse cognition.
New drug application is first for Alzheimer’s disease in the U.S. since 2003, and first based on amyloid hypothesis.
The findings hint at a liver-brain axis that transmits inflammation from periphery to brain, and could suggest therapeutic targets for preserving brain function.
The tracer distinguished people with progressive supranuclear palsy from controls with a sensitivity of 85 percent, suggesting potential as a diagnostic for 4R tauopathies.
In striatal spiny projection neurons with mutant huntingtin, mitochondria spill immunogenic RNAs into the cytosol. These touch off innate antiviral signaling inside the neurons, which may spell their demise.
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