An FDA panel recommended the drug for approval, which would make it the first antipsychotic cleared for use in a neurodegenerative disease.
The modified protein prevents the synaptic protein KIBRA from managing plasticity.
Knocking out neuronal heparan sulfate proteoglycans slashed plaque load and facilitated Aβ clearance in AD model mice.
In several AD mouse models, Aβ caused complement proteins to move to synapses, triggering microglia to eat the structures.
Poly(GA) encoded by C9 repeats incite proteasome and nucleocytoplasmic transport problems, but no TDP43 aggregation.
Activating this endogenous protective pathway mops up protein deposits in models of movement disorders. The strategy has advanced to trials.
The compound had shown promise for sharpening cognition in schizophrenia and Alzheimer’s, but now faces an uncertain future.
Macrophages and microglia lacking the gene incite inflammation.
Fed up with slow sharing mechanisms, Sage pioneers an end run around primary investigators, and participants opt to share health data with any qualified researcher worldwide.
Studies of two new mouse models find that this mutation leads to excitotoxicity, but little protein aggregation.
Using optogenetics to multiply dendritic spines, scientists recover lost memories in young mouse models of AD.
In some people, Aβ40 in the cerebrospinal fluid correlates with plaque load in the brain.
Results raise the tentative prospect that a medical food might have possible cognitive benefit early in disease.
Tracer uptake in the brain matches autopsy data. This opens up new possibilities for in vivo disease staging and longitudinal studies.
By modifying a cation channel to respond to magnetic fields, scientists can now control neural activity quickly and noninvasively.