Topic: AMPAR trafficking

Synaptic dysfunction in response to amyloid-beta (Aß) accumulation is increasingly recognized as a precursor of cognitive decline in Alzheimer's Disease (AD). AMPA receptors (AMPARs), the major neurotransmitter receptors in the brain, are implicated in the synaptic dysfunction observed in rodent models expressing amyloidogenic APP mutations. AMPARs are proposed to undergo aberrant trafficking, characterized by changes in their subunit composition and subcellular localization. The precise mechanisms underlying the dysregulation of AMPAR trafficking in AD remain poorly understood.Here, we apply

During Long Term Potentiation (LTP) AMPA receptors (AMPARs) are inserted into the plasma membrane. This form of synaptic plasticity is crucial for many aspects of brain function, including learning and memory. Protein 4.1N (EPB41L1) is a neuronally enriched member of the protein 4.1 family. In primary hippocampal cultures, 4.1N is enriched at the discrete sites of synaptic contact, co-localizing with the postsynaptic density proteins, suggesting a potential functional role for 4.1N as a component of the cytoskeletal architecture of excitatory synapses. 4.1N also directly interacts with the Glu