In First Phase 3 Trial, the Tau Drug LMTM Did Not Work. Period. Held July 24 to 28 in Toronto, the Alzheimer’s Association International Conference showcased a field in transformation. At the clinical level, groups from Europe, North America, and Japan ...
Claims of a positive effect in a small subgroup of patients are statistically meaningless, experts say.
Antisense oligonucleotides can flip expression of tau from the three-repeat to the four-repeat form. These ASOs triggered tau aggregation and behavioral problems.
Imaging study correlated four patterns of neurodegeneration that map to two neural networks with certain behavioral symptoms.
Four researchers received awards totaling $350,000 for their contributions to Alzheimer’s research.
Researchers may soon add another imaging agent to their tool kit—one that tracks synapse loss.
At Keystone, researchers also linked the receptor to microglial homeostasis and migration, and resolved lingering questions about TREM2’s role in plaque clearance.
A PET study comparing amyloid, tau, and volumetric imaging in preclinical AD identifies a region where local tangles correlate with brain-wide amyloid.
People who report a prior head injury have no more chance of getting Alzheimer’s than the rest of the population, but they may be at higher risk for Parkinson’s.
Researchers are discovering that microglia not only respond dramatically to their environment, but they also can quickly lose their identity.
At Keystone, researchers report the discovery of ion channels that shed light on the machinations of the brain’s microglia.
A bill approved by the U.S. House Committee on Appropriations would increase funding for Alzheimer’s by $350 million.
Could similar immune dysfunction contribute to neurodegeneration in people who carry repeat expansions in one copy of the gene?
Assessed in toto, thousands of gene alterations portend changes in cognition, brain structure, and amyloid deposition in people without dementia. A step on the way to a gene chip for AD?
Microglia and macrophages lacking the receptor consumed less amyloid in vitro, even when stimulated by anti-Aβ antibodies.