IMAGINE that: Amyloid deposition shrinks in both treatment and placebo groups, dealing a blow to the anti-aggregation drug PBT2.
A drug candidate for Alzheimer’s aims to make cell trafficking more efficient, reduce Aβ production.
An antibody against ApoE helps clear plaques and improves cognition in AD model mice.
The same or similar molecules might treat a variety of protein-misfolding conditions.
Cellular, animal, and human studies suggest that the AD risk gene PICALM escorts Aβ through the blood-brain barrier.
The Center for Open Science published eight guidelines for journals to boost transparency and reproducibility in research. Will journals implement them?
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.