In stark contrast to Aβ and tau fibrils, α-synuclein fibrils are asymmetric, comprising two different protofibrils.
In cell culture, slashing Aβ production by more than half harmed neuronal signaling, but a smaller cut maintained it.
New research suggests the R47H variant protects neurons from neurodegeneration, raising questions about staging and direction of future TREM2-based therapy.
By suppressing a single gene, scientists triggered the transformation of astrocytes into neurons in the mouse substantia nigra, where the converts released dopamine and connected with the striatum.
Alector’s AL002c antibody mobilizes microglia, reduces neuronal dystrophy, and restores normal behavior—all in mice. The clinical version is in Phase 1.
A mouse study claims that the small GTPase restrains pro-inflammatory responses in microglia. Aβ oligomers inhibit RhoA, promoting Aβ deposition and neurodegeneration.
Released from hippocampal neurons in response to experience, the cytokine prompted microglia to eat extracellular matrix around synapses. This facilitated growth of new spines, and sharpened memory.
This early marker distinguishes Alzheimer’s from controls and other neurodegenerative diseases more accurately than other biomarkers.
In large population datasets, people who had been vaccinated against influenza or pneumonia appeared less likely to develop AD.
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?
Growing evidence suggests exposure to air pollution increases risk of brain damage and dementia. More definitive research is needed.
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.