Large Aβ aggregates unleash smaller soluble oligomers that mess with synapses and rev up microglia.
Among older adults living in Ontario, Canada, dementia incidence crept up the closer people lived to busy roads.
People with a rapidly progressive form of Alzheimer’s have a more diverse collection of Aβ40 fibril conformations than do people whose disease progresses slowly.
As suggested by computer modelling, deep brain stimulation delivering sporadic pulses packs as much therapeutic punch as a steady rhythm, reducing need for battery replacement surgery.
Alzforum reviews the major newsmakers of the past 12 months.
A few attempts at Alzheimer’s therapy claim hints of promise in early clinical trials, though several did not include placebo controls.
Diurnal variations disappear as less Aβ42 reaches cerebrospinal fluid. Findings may improve timing of daily amyloid treatments.
Parkinsonian symptoms in welders exposed to manganese-laden fumes worsen with continued exposure.
Methods that trawl body fluids for amyloidogenic proteins are getting more sensitive and specific, and scientists are expanding the repertoire of oligomers they can detect.
At CTAD, tau-PET data from people in different stages of various neurodegenerative diseases highlighted both commonalities and peculiarities.
Biogen and Genentech rolled out more data from their Phase 1b trials, renewing hope that amyloid removal will work and shoring up dosing for Phase 3.
Sanofi Genzyme will test a compound currently in development for Gaucher’s disease in Parkinson’s patients who carry a glucocerebrosidase (GBA) mutation.
Cognitively normal people who harbor plaques in their brains are more likely to report feelings of isolation.
Scientists at SfN presented innovative ways to slow amyloid accumulation and preserve synapses.
The tau aggregation inhibitor LMTM tanks in second Phase 3 trial for Alzheimer’s. The sponsor now plans to develop the “placebo.”
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