Treatments targeting the main pathological protein of Parkinson’s disease are moving toward the clinic, with two immunotherapies passing Phase 1 safety benchmarks.
Antibody against aggregated Aβ reported to clear out amyloid from brain, and perhaps slow cognitive decline, in people with prodromal Alzheimer’s disease.
Researchers at a Keystone meeting reported that a combination of protective and destructive signals target microglia to prune synapses in the brain. These signals may be altered during disease.
Researchers at a Keystone meeting proposed that quelling inflammation outside the brain could slow the progression of Alzheimer’s and other neurodegenerative diseases.
Two studies suggest that the anti-inflammatory interleukin-10 prevents efficient plaque clearance and worsens AD-like pathology in mice.
At Keystone, scientists reported that TREM2 may promote the survival of cells surrounding plaques, but where these cells come from and what they do is still up for grabs.
At an NIH conference in Washington, D.C., experts from beyond Alzheimer’s research discussed ways to beef up data collection and patient participation.
At the first NIH summit since the National Plan to Address Alzheimer’s was implemented back in 2012, scientists discussed progress made and put forth a new set of goals.
Researchers at Keystone attempted to distinguish microglia from other macrophages in the body, both in form and function, and monitor the way each behaves during disease.
Researchers at a recent Keystone symposium compared the properties of microglia with those of other macrophages in the body. The cells acquire their unique personalities through both their origins and their present environment.
Autoradiography confirms that T807/AV1451 binds tau but not TDP-43. Even so, some say the tracer will benefit from more technical work to ensure it will measure small changes robustly in multicenter settings.
At the HAI conference, scientists reported progress toward differential diagnosis of the bewildering spectrum of frontotemporal dementia and atypical Alzheimer’s variants. In some, hypometabolism overlaps with tau, not amyloid.
Researchers explored how the brain’s immune cells influence disease, and how cells and signals from outside the brain pitch in.
Early data suggest that the T807/AV1451 signal relates to cerebrospinal biomarkers of Alzheimer’s, intensifies by up to 10 percent a year, and might nail diagnoses beyond typical AD.
Data come tumbling in as more people are getting scans with the first widely used tau PET tracer. Scientists at HAI were pleased by how closely degeneration and symptoms match up in Alzheimer’s.