A revised plan of action for AD research has emerged from the Alzheimer’s Disease Research Summit 2015.
Scientists find neurodegenerative proteins squirreled away in the skin cells of patients. Could this present an untapped source of biomarkers?
Several different striatal markers may help researchers track early deterioration in Huntington's and Parkinson’s diseases.
A NexGen prevention trial in familial Alzheimer’s mutation carriers will shoot for flexible testing of high doses and drug combinations.
At AD/PD, researchers further tied TREM2 to phagocytosis and enumerated markers that may distinguish beneficial microglia from harmful ones.
Genetic and animal studies hint that B and T cells control amyloid accumulation, though the mechanisms remain unclear.
Researchers link the AD Risk gene BIN1 to tau and amyloid in different model systems, and propose a mechanism for how a PICALM variant might be protective.
Researchers no longer debate whether misfolded proteins spread through the brain in neurodegenerative disease. Now they want to know how.
New data argue that multimers of α-synuclein may protect against pathological aggregation.
At the AD/PD conference, researchers reported a protective gene variant that delays Alzheimer’s onset by 10 years, and parsed pathways to find out why particular neurons take the hit in specific diseases.
Peptides made from D-amino acids bind to Aβ oligomers and trigger their removal from the brain. Some appear poised to enter Phase 1.
The newest contender in the race for a drug to rein in the β-secretase enzyme debuted with data that reflected a methodical approach to understand a drug’s performance in cerebrospinal fluid before looking for efficacy.
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.