Immunotherapy for Cerebral Small Vessel Disease?
An antibody that activates Notch 3 signaling helps keep retinal blood vessels intact in a mouse model of the small vessel disease CADASIL.
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An antibody that activates Notch 3 signaling helps keep retinal blood vessels intact in a mouse model of the small vessel disease CADASIL.
A longitudinal study identified regions in the default mode network as among the first to accumulate Aβ.
PET scans indicate no more AD pathology in PD-MCI than healthy controls, suggesting their cognitive decline results from other factors.
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.
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.
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