There’s No Tomorrow for TOMMORROW
The trial’s sponsor announced an early end to the large Alzheimer’s prevention study based on an interim futility analysis.
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The trial’s sponsor announced an early end to the large Alzheimer’s prevention study based on an interim futility analysis.
In people with an autosomal-dominant AD mutation, Aβ and tau start accumulating long before the estimated onset of symptoms.
A CRISPR knockout screen in human cells and mouse neurons found genes that tweak C9ORF72 toxicity, zeroing in on ER stress as a potential therapeutic target.
Two new papers strengthen the evidence that TREM2 protects against amyloid pathology.
This alternative approach to Aβ immunotherapy targets unlipidated, plaque-associated ApoE.
Two papers report that the ApoE4 allele triggers both hallmarks of AD in iPSC-derived cultures, in contrast to its minimal effects in mouse neurons.
Chronic inhibition of protein synthesis, and slowing the dispersal of stress granules, contribute to neurodegeneration in C9ORF72 ALS/FTD.
Believed to be an amyloid-lowering agent, the blood pressure drug did not help people at the dementia stage of disease.
In a fly model, C9ORF72 pathology pulls TDP-43 from the nucleus, which leads to disrupted nuclear import and neurodegeneration.
Mutations that destabilize α-synuclein tetramers leave young mice with severe and progressive motor problems resembling those of PD.
In a new take on mosaicism and Alzheimer’s, scientists claim that APP mRNAs convert into DNA and reinsert into the genome. Full of mutations, these “genomic cDNAs” crop up in aging and sporadic AD.
Researchers characterize widespread cerebral amyloid angiopathy and cortical plaques found in three living people who received dural grafts as children.
Levels of irisin are lower in brain and CSF of AD patients. Upping expression in mice protected them from synaptic deficits and memory problems.
A periodontal pathogen found in human brains triggers AD pathology in mice. Will an antibiotic stave off dementia?
Building on results in AD mouse models, researchers now report that immune checkpoint inhibitors reduce pathology and improve cognition in tauopathy mice, too. Other scientists are skeptical.
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