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.
Researchers propose that several-fold increases of α-synuclein can trigger a slew of pathological changes leading to synaptic dysfunction...
An interim analysis predicted the antibody would not slow Alzheimer’s progression; a crenezumab trial in autosomal-dominant AD is continuing.
A newly uncovered population of astrocytes in layer V of the cortex modulate synapses by secreting a protein linked to Norrie disease, a form of blindness. Are other disease-related astroglia lurking in the brain?
In several animal models, stimulating mitophagy lowered amyloid deposits and tau phosphorylation while improving learning and memory.
Scientists know that the retina changes in people with preclinical AD; alas, there is neither consensus nor convergence in the field of retinal imaging. An upcoming initiative aims to determine which measures are most robust.
Two new papers strengthen the evidence that TREM2 protects against amyloid pathology.
The company halted its Phase 2 trial of ABBV-8E12 due to lack of efficacy.
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.
By analyzing a single MRI scan, researchers pinpointed the origin of frontotemporal dementia pathology and predicted its future progression.
DAPPD suppressed neuroinflammation and preserved cognition in mouse models of amyloidosis, suggesting potential for treating Alzheimer’s disease.