Quadri Adewale, Ahmed F Khan ... Alzheimer's Disease Neuroimaging Initiative
Identification of causal genes and their effects on other biological determinants untangles the complexities of aging and Alzheimer's and can facilitate drug discovery for sustaining healthy aging and treating Alzheimer's.
The early influence of the breakdown of both hippocampal structural network and angular gyrus-seeded default mode metabolism network on memory performance underscore the importance of early intervention in preclinical Alzheimer’s disease.
Diane M Bushman, Gwendolyn E Kaeser ... Jerold Chun
Somatically derived genomic mosaicism in the form of increased DNA content and APP copy number in single neurons plausibly has a function in sporadic Alzheimer’s disease and points to functions for single-neuron gene copy number changes.
Claudia Scheckel, Elodie Drapeau ... Robert B Darnell
Neuronal ELAV-like (nELAVL) proteins are associated with non-coding Y RNAs in stressed neurons and in the brains of Alzheimer's disease patients, suggesting a new means of regulatory protein sequestration and mRNA target regulation.
By binding to Fc gamma receptor IIb, amyloid beta induces a series of phosphorylation events that mediate the damaging effects of hyperphosphorylated tau proteins in Alzheimer's disease.
Mice modelling atherosclerosis show neurovascular breakdown in the cortex compared to healthy controls, and inducing atherosclerosis in mice modelling Alzheimer's disease increases the number of amyloid plaques in the hippocampus.
A novel neuroprotective pathway that enhances acetyl-CoA metabolism via inhibition of acetyl-CoA carboxylase 1 may prevent the contribution of the aging process in the brain to Alzheimer's disease.
Meghan E Wynne, Oluwaseun Ogunbona ... Victor Faundez
Current models of Alzheimer's disease that put mitochondria as an endpoint of disease should be reconsidered because genetic defects affecting mitochondria by themselves can also regulate Alzheimer’s disease risk factor apolipoprotein E (APOE) expression and secretion.
Laura Sebastian Monasor, Stephan A Müller ... Sabina Tahirovic
APPPS1 microglia express disease-associated proteomic signatures of Alzheimer's disease earlier, compared to the APP-KI, and these differences correlate with the levels of fibrillar Aβ and impaired microglial phagocytic function.
BADGERS, as a new powerful method for conducting polygenic score-based biobank-wide association scans, identified 48 significant associations for AD and 41 significant associations for a variety of AD endophenotypes.
