Going from normal zzzs to sleeping longer than nine hours a night more than doubles a person’s risk of developing dementia, study says.
In AD mouse brain, transplanted human neurons develop more tau pathology and die more readily than neighboring mouse neurons.
Produced by the dreaded MRSA bacterium, PSMα3 is the first known example of a natural peptide that forms amyloid fibers made not of β-sheets, but of neatly stacked α-helices.
A well-controlled trials shows that a year of treatment offers no cognitive benefit for older men with low testosterone levels.
The extracellular fragment of TREM2, but not of its AD variants, promotes microglial survival, activation. To do that, it does not need the full-length TREM2 receptor.
Growing expansions in the C9ORF72 gene may lead to earlier onset of amyotrophic lateral sclerosis and/or frontotemporal dementia symptoms with each passing generation.
Thousands of hits on the ol’ noggin during a soccer player’s career might lead to concussive symptoms and, eventually, dementia.
The EPOCH trial of verubecestat was halted for lack of efficacy. APECS trial in prodromal AD continues.
Mutations in the profilin 1 gene cause rare cases of familial amyotrophic lateral sclerosis. We just added PFN1C71G and hPFN1G118V transgenic mice to Alzforum’s Research Model Database. These recent ALS models gradually lose motor neurons and develop progressive motor problems. Explore their full phenotypes see how they compare with other ALS research models in our interactive database.
Mouse models of Alzheimer’s develop amyloidosis but not many of the other hallmarks of the disease. Could chimeric models do better? Human neurons implanted into the brain of an AD mouse develop more tau pathology, and lose more synapses, than do neighboring mouse neurons. They also die. The findings suggest that human neurons are particularly sensitive to amyloid toxicity. Researchers believe this model may advance translational research.
As a rule, amyloid fibrils are composed of zigzag β-sheets that pile neatly atop one another. But some rules are made to be broken. A rebel bacterium that wreaks havoc on humans uses the first known natural example of an amyloid made of α-helices. Staphylococcus aureus secretes the curly PSMα3 peptide—which becomes more toxic in fibril form—to lyse membranes, incite inflammation, and build biofilms. Could fibrils rich in α-helices have something in common with intermediates of Aβ, α-synuclein, or prion fibrils, which have each been observed to contain α-helices?
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