Amyloid beta, the major component of plaques in Alzheimer's disease, acutely and reversibly signals to modulate sleep as a function of oligomeric length, independently of neuronal loss.
Metabolic defects following expression of Aβ1-42 in nematode neurons are partially caused by inactivation of alpha-ketoglutarate dehydrogenase and can be rescued by Metformin.
Aβ inhibitors effectively block its aggregation, while also reducing seeding of tau aggregation from Aβ, tau, and AD derived fibrils, suggesting the two share a structurally related disease relevant interface.
Modelling beta-amyloid deposition in bioengineered human vessels represents a notable advance to further investigate the role of the vasculature in Alzheimer's disease.
By using structural methods to screen compounds for their ability to interact with amyloid beta, researchers have identified small molecules that stabilize amyloid fibers and reduce the toxic effect of smaller aggregates on cells.
Comprehensive dataset of high-level cognitive assessment in mouse models of neurodegeneration, accompanied by an open-access database/repository to change the paradigm of how cognitive studies in animal models can be shared/re-used.
Oligomeric Amyloid-β and Tau, two proteins involved in Alzheimer's disease pathogenesis, require Amyloid Precursor Protein to enter neurons and exert their detrimental effect on synaptic plasticity and memory.
