Semagacestat Failure Analysis: Should γ-Secretase Remain a Target?
A debate has sprung up in response to a Cell essay arguing that the baby was thrown out with the bathwater when a γ-secretase inhibitor failed in Phase 3.
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A debate has sprung up in response to a Cell essay arguing that the baby was thrown out with the bathwater when a γ-secretase inhibitor failed in Phase 3.
Large consortium releases epigenome profiles of 111 different tissues. They are already yielding insight into the immune system’s role in Alzheimer’s disease.
A risk allele previously linked to Parkinson’s is now extended to Alzheimer’s as well, with particularly strong effects in patients who lack an ApoE4 allele.
A mouse model that was previously thought to express a transgene predominantly in the entorhinal cortex may be much leakier than previously thought. This complicates interpretation of some previous studies reporting propagation of toxic tau aggregates.
Using a viral vector, researchers created mice that express C9ORF72 hexanucleotide repeats in the brain.
In separate studies, researchers propose that high CSF ferritin and D-serine could become biomarkers to predict declining cognition in Alzheimer’s disease.
A new crystal structure shows a unique shape of Aβ in the arms of solanezumab. Exactly how this and other antibodies in the clinical pipeline grip Aβ could explain some differences in trial results.
However, once a person has ALS, diabetes does not affect how long they survive.
Levels of a neuronal protein in blood correlated with rate of decline in two U.K. cohorts.
Proper form and function of the brain’s immune cells depend on a diverse mix of “good” bacteria in the mouse intestine.
Could filling these cavities with a small molecule be therapeutic?
Neuron-derived vesicles floating in the blood carry protein signatures that flag lysosomal dysfunction. Could they detect preclinical Alzheimer’s disease?
The model provides the first functional evidence of how the ALS gene UNC13A modifies disease risk.
A behavioral variant of Alzheimer’s disease is not accompanied by shrinking of the frontal cortex. Rather, these patients have similar patterns of atrophy as those with typical AD.
Blocking a family of proteins called cytohesins helped clear toxic SOD1. Scientists speculate the inhibition just might do the same for other proteins linked to neurodegeneration.
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