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.
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.
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.
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.
Despite conflicting results in the past, a large new study analyzing multiple statins in different ethnic groups suggests a protective effect from this class of medication.
Restoring normal transport of BACE1-carrying endosomes prevents synapse loss and cognitive decline in mice.
In a bizarre twist of cell biology, researchers find proteasomes in the neuronal plasma membrane. They pump signaling peptides into the extracellular space.
A new fluorescent compound labels only non-contractile cells in the capillary bed, supporting the idea that these mysterious little cells do not directly regulate brain blood flow.