Preventing these peripheral phagocytes from creeping into the brain improves memory and ameliorates pathology in mouse models of Alzheimer’s.
In a clinical trial, people who used the surgically implanted breathing-assist device died nearly a year sooner than those who used only an oxygen mask.
Researchers have generated the first atomic-level structure of γ-secretase. The new view revealed interactions between amino acid residues and the locations of familial Alzheimer’s disease mutations.
Three studies report that the C9ORF72 expansion prevents RNAs and proteins from shuttling properly between nucleus and cytosol.
The genetic relics of ancient, dormant retroviruses pepper the human genome. One such virus reanimates in about one-third of ALS cases.
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.
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.