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.
A naturally occurring intracellular peptide, derived by processing the Alzheimer's protein APP, reduces synaptic transmission by acting as a dominant negative of APP.
The APP intracellular domain (AICD) physiologically regulates synaptic GluN2B-containing NMDA receptor current, a process that could contribute to pathological Alzheimer's disease-related synaptic failure upon increase of AICD levels in adult neurons.
Reducing Akt-mediated huntingtin phosphorylation decreases APP accumulation at the synapse by reducing its anterograde axonal transport and ameliorates learning and memory in a mouse model of familial Alzheimer disease.
Amyloid precursor protein expression and accumulation of its intracellular fragment are required for exuberant neurite outgrowth associated with pathological presenilin 1 loss-of-function mutations before the emergence of amyloid burden in mice.
The metalloprotease ADAM10 modulates axon and synapse function by cleaving numerous synaptic and axonal membrane proteins in the central nervous system.
A masked cryo-EM image classification approach and the structure of an inhibitor-bound complex provide insights into the molecular flexibility of the catalytic subunit of gamma-secretase.
Proteins implicated in Alzheimer’s disease, including amyloid precursor protein and ApoE receptors, interact with each other and with a signalling molecule called agrin to influence the development of the neuromuscular junction.
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.
Heparan sulfates in the vessel wall bind and regulate signaling from the megakaryocyte/platelet-specific inhibitory receptor G6b-B, a critical regulator of platelet homeostasis.
