The 12th AD/PD conference drew some 3,100 people from across the world to the Mediterranean city of Nice. After a long day of talks—sessions ran from 8:30 a.m. to a grueling 7:15 p.m.—hungry scientists could be seen strolling to dinner across the Place Massena, with its illuminated resin statues created by the Catalan contemporary artist Jaume Plensa. The seven characters on their pedestals represent seven continents, and the changing color of their lighting is said to symbolize communication between them. At the conference, talks in four parallel sessions ran the gamut from basic to clinical science on Alzheimer's, Parkinson's, the in-between disease dementia with Lewy bodies, and even a session on the ALS-FTD spectrum.
Antibody against aggregated Aβ reported to clear out amyloid from brain, and perhaps slow cognitive decline, in people with prodromal Alzheimer’s disease.
Treatments targeting the main pathological protein of Parkinson’s disease are moving toward the clinic, with two immunotherapies passing Phase 1 safety benchmarks.
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.
Peptides made from D-amino acids bind to Aβ oligomers and trigger their removal from the brain. Some appear poised to enter Phase 1.
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.
New data argue that multimers of α-synuclein may protect against pathological aggregation.
Researchers no longer debate whether misfolded proteins spread through the brain in neurodegenerative disease. Now they want to know how.
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.
Genetic and animal studies hint that B and T cells control amyloid accumulation, though the mechanisms remain unclear.
At AD/PD, researchers further tied TREM2 to phagocytosis and enumerated markers that may distinguish beneficial microglia from harmful ones.