The Microbiome and Disease—What Does Poop Have to Do With It?
Simple lifestyle factors such as alcohol consumption and stool quality alter gut flora. Research on the microbiome and disease should account for those factors, a study reports.
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Simple lifestyle factors such as alcohol consumption and stool quality alter gut flora. Research on the microbiome and disease should account for those factors, a study reports.
In a mouse model of ALS, removing mutant SOD1 from peripheral myeloid cells relieved neuroinflammation and extended lifespan.
The panel considered the evidence for efficacy to be weak, and was troubled by too-close collaboration between the sponsor and the FDA.
In mice, accumulation of tau in hilar astrocytes of the dentate gyrus spells trouble for the hippocampus and for spatial memory.
Could this forestall the amyloid cascade and the onset of Alzheimer’s disease?
At CTAD, a Phase 2 open-label extension of this anti- Aβ protofibril antibody posted data as expected, and new Phase 3 trials for people with early and preclinical Alzheimer’s were described.
The anti-Aβ biologic will be put to the test in two stages of preclinical Alzheimer’s, designated by amyloid load. The long-dormant “est” PET tracer, NAV4694, is on board to make sensitive measurements.
After years of building an online registry, designing selection algorithms, and getting sites up and running, COVID-19 nearly derailed this trial-ready cohort once again. Now, the first participants have reached the final queue.
Remote assessments on a smartphone closely matched tests taken in the clinic. They also may detect slip-ups in learning—an earlier cognitive deficit that arises in preclinical AD.
After missing primary endpoints in Alzheimer’s trials, this p38 MAPKa inhibitor gained some traction in a test in people with DLB.
In a retrospective study, people with vitiligo had 12 times the risk of developing Alzheimer’s disease than did healthy controls. Why is that?
Regulators in the U.S. and Europe have certified a mass-spectrometry-based blood test for amyloid-β. Plasma phospho-tau markers are poised to come next.
In mice lacking the recycling protein GGA3, BACE1 trafficking stalls, local Aβ production increases, and axons swell. Does this explain the neuritic dystrophies seen in early AD?
By pinpointing where tau pathology starts in a person’s brain, researchers better predicted future spread and determined small changes in tangle load.
Amyloids of AIMP2 found in Parkinson’s disease may seed α-synuclein aggregation.