People with moderate to severe Alzheimer’s have higher levels of orexin, a neuropeptide that keeps people awake, a study reports. The findings solidify links between orexin and sleep disturbances associated with the disease.
Aβ oligomers rapidly seed tau pathology in macaques, potentially providing a model for drug testing that better reflects human pathology.Aβ oligomers rapidly seed tau pathology in macaques, potentially providing a model for drug testing that better reflects human pathology.
Using a rarely implemented in vitro fertilization procedure, a woman whose family carries a presenilin mutation delivered twins who are virtually assured of escaping early onset Alzheimer’s disease.
Introducing a clinical trials database for ALS that encompasses nearly 9,000 patient records, the organizers tease with the first few findings.
Amyloid plaques and tau tangles sprout in human neuron cultures grown in a supportive gel. Researchers think this system may closely model human disease and aid in drug discovery.
Therapeutics that target γ-secretase produced different results in human neurons and mouse models of Alzheimer’s disease.
Results suggest the drug boosts cognition when given alongside the acetylcholinesterase inhibitor.
ALS-linked optineurin works closely with Parkinson’s-associated Pink1 and parkin in a pathway that recycles mitochondria.
Given that drugs that looked promising in Alzheimer mice have failed in human trials, is it time to find a better model? A new report claims that middle-aged macaque monkeys rapidly developed key features of AD, including neurofibrillary tangles, when A oligomers were injected into their brains. Some researchers think these primates might provide a clearer picture of how AD therapeutics will perform in people.
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To date, efforts to recapitulate Alzheimer’s disease in a dish have fallen short of recapitulating both hallmarks of the disease: plaques and tangles. Now growing cells in a three-dimensional supportive gel has made it possible, a new study reports. Using neural stem cells expressing familial AD proteins, researchers have modeled the development of amyloid plaques, and observed tau pathology form as a result. In response to secretase inhibitors, both plaques and tangles disappear, supporting the amyloid hypothesis. The new system may serve as a screening platform for drugs aiming to knock down plaques and tangles.
Researchers believe that toxic proteins, such as misfolded forms of tau and α-synuclein, can move from cell to cell throughout the brain like prions, corrupting their normal counterparts as they go. Now, they’ve developed new “biosensor” cell lines that reveal when minute amounts of seeds are present. The cells emit a fluorescent SOS when tau or α-synuclein fibrils from brain extracts promote protein aggregation within. The cell lines will soon be widely available. Researchers hope they will facilitate the tracking of neurodegenerative disease pathology in animal models and serve as diagnostics for human disease.
Imagers, get your data ready! Organizers of the ninth annual Human Amyloid Imaging meeting will review abstracts submitted between October 20 and November 14 this year. The meeting will be held January 14–16, 2015, in Miami. Registration is now open. Find further details and instructions for submitting abstracts at the conference website.
- Henrietta Nielsen on Wake Up and Smell the … Orexin? Peptide Percolates in Alzheimer’s Brain
- Brendan Lucey on Wake Up and Smell the … Orexin? Peptide Percolates in Alzheimer’s Brain
- Tara Spires-Jones on Alzheimer’s in a Dish? Aβ Stokes Tau Pathology in Third Dimension
- Sanjay Pimplikar on Alzheimer’s in a Dish? Aβ Stokes Tau Pathology in Third Dimension
- Fred Van Leuven on Alzheimer’s in a Dish? Aβ Stokes Tau Pathology in Third Dimension
- Samira Saadi on Evidence Mounts That Mitochondrial Gene Is Bona Fide ALS, FTD Risk Factor
- John Hardy on Alzheimer’s in a Dish? Aβ Stokes Tau Pathology in Third Dimension