This alternative approach to Aβ immunotherapy targets unlipidated, plaque-associated ApoE.
Unbiased screen turns up genes expressed in immune cells, both inside and outside the CNS.
Diminishing Alzheimer’s pathology in mice appears to be as easy as shining a light in their eyes. Could it work in people?
Microglia internalize pathogenic forms of tau more robustly when anti-tau antibodies adorn the protein.
Chronic inhibition of protein synthesis, and slowing the dispersal of stress granules, contribute to neurodegeneration in C9ORF72 ALS/FTD.
Researchers have shown that the CSF goes into the brain along very specific anatomical structures...
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.
Believed to be an amyloid-lowering agent, the blood pressure drug did not help people at the dementia stage of disease.
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.
In mouse models, the Alzheimer’s risk gene TREM2 affects microglial behavior but does not lead to more amyloid deposition.
Levels of irisin are lower in brain and CSF of AD patients. Upping expression in mice protected them from synaptic deficits and memory problems.
When it seeps into the brain, fibrinogen activates innate immune responses that zap dendrites. And amyloid deposition has little to do with it.
PET scans indicate no more AD pathology in PD-MCI than healthy controls, suggesting their cognitive decline results from other factors.