G-Protein Receptor Knockout Rescues Several Models of Alzheimer’s
Ablating Gpr3 reduced amyloid burden and improved memory in various AD mouse models. Researchers propose using Gpr3 inhibitors to treat AD.
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Ablating Gpr3 reduced amyloid burden and improved memory in various AD mouse models. Researchers propose using Gpr3 inhibitors to treat AD.
The blood-brain barrier barred passage of antibodies in multiple mouse models of neurodegenerative disease, suggesting it holds up well in the face of disease.
Without the E3 ubiquitin ligase Idol, microglia readily gobble up ApoE and Aβ in a mouse model of Alzheimer’s disease.
In transgenic mice, revving up proteasome function lowered tau deposits and improved memory.
An immunotherapy drug recruits immune cells to the brain, where they help clean up amyloid plaques.
Researchers failed to confirm a high-profile, previous 10-lipid panel, but remain bullish on the potential of blood-based metabolites as biomarkers.
Caging an HDAC inhibitor in a lipid chelator raised plasma and brain concentrations of the drug and doubled the lifespan of a mouse model of Niemann-Pick type C disease.
Scientists wonder if the sodium channel blocker might also slow disease progression.
The modified protein prevents the synaptic protein KIBRA from managing plasticity.
On the heels of news that microglia mediate synaptic loss in Alzheimer’s, researchers report they may do the same in a subtype of FTD caused by progranulin deficiency.
Not exosome, not proteasome, not autophagy: Could a new pathway dubbed MAPS facilitate the spread of amyloidogenic proteins?
Claims of a positive effect in a small subgroup of patients are statistically meaningless, experts say.
Profile matches Braak staging regions, suggesting those areas are particularly susceptible to AD pathology.
The monoclonal antibody appears to remove plaques, although the small trial could not draw conclusions about cognition.
The LAG3 transmembrane protein latches onto fibrillar forms of the synaptic protein and ushers them into neurons. Researchers propose targeting LAG3 to slow toxic spread of misfolded forms of synuclein.