Microglial Transplants Reverse Age-Related Pathology in Mice
Mice missing microglia develop astrogliosis and neurodegeneration by middle age. Giving them healthy microglia prevents or reverses pathology.
6493 RESULTS
Sort By:
Mice missing microglia develop astrogliosis and neurodegeneration by middle age. Giving them healthy microglia prevents or reverses pathology.
Nixing an endosomal targeting sequence shields APP from BACE1, reducing Aβ and pathologic C-terminal fragments in mice.
Injected into the cerebrospinal fluid, a viral vector delivers the lysosomal protein into the human brain. In mice, a protein transport vehicle delivered into the blood does the same.
A panel of eight plasma proteins identified people who were on the path to Parkinson’s. Could this help select participants for prevention trials?
With limited guidance, physicians will have to navigate questions about whom to treat, when to stop, and how to manage safety.
People who sifted through piles of debris are nine times likelier to develop early onset, all-cause dementia than those exposed to little toxic dust.
C05-05 binds α-synuclein deposits in the mouse, marmoset, and human brain. Uptake in the PD midbrain correlated with motor symptom severity.
All 11 committee members voted that the antibody was effective for people with MCI or mild AD dementia, with its benefits outweighing risks.
When carrying a pathogenic tau variant, microglia were bad at phagocytosis, barely made TREM2, and spat out neurotoxic proteins.
As flies age, mitochondrial damage in their neurons somehow ages glia, which, in turn, cause lipid droplets to pile up on other, healthy glia.
The enzyme cleaves off three amino acids at a time with a twist of the substrate, and a helping hand from a β-strand.
The astrocytic receptor enforces distancing among glial cells. Free from this constraint, they better contain plaques.
A new study challenges this idea, finding that in mice, clearance of an injected dye slowed during sleep and anesthesia.
When the nuclear RNA-binding proteins NONO and SFPQ accumulate, adenosine-to-inosine editing of RNA runs amok. This spoils transcripts for axonal, synaptic, and mitochondrial proteins.
FDA qualification would streamline the use of plasma NfL to select asymptomatic carriers of pathogenic frontotemporal dementia mutations for enrollment in prevention trials.
No filters selected