Sindi_2015_Neurodegener.Dis.Manag_5_137

Reference

Title : New insights into Alzheimer's disease pathogenesis: the involvement of neuroligins in synaptic malfunction - Sindi_2015_Neurodegener.Dis.Manag_5_137
Author(s) : Sindi IA , Dodd PR
Ref : Neurodegener Dis Manag , 5 :137 , 2015
Abstract :

SUMMARY Synaptic damage is a key hallmark of Alzheimer's disease and the best correlate with cognitive decline ante mortem. Signature protein combinations arrayed at tightly apposed pre- and post-synaptic sites characterize different types of synapse. Neuroligins are postsynaptic cell adhesion molecules that interact with neurexins across the synaptic cleft. These pairings recruit receptors, channels and signal transduction molecules to the synapse, and help mediate trans-synaptic transmission. Dysfunction in the neuroligin family can disrupt neuronal networks and leads to neurodegeneration and other diseases. The extracellular domain of neuroligins is homologous with acetylcholinesterase but lacks residues required for enzymatic activity. This domain may interact pathogenically with beta-amyloid. Here we summarize research over the last decade on the potential involvement of neuroligins in Alzheimer's disease.

PubMedSearch : Sindi_2015_Neurodegener.Dis.Manag_5_137
PubMedID: 25894877

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Citations formats

Sindi IA, Dodd PR (2015)
New insights into Alzheimer's disease pathogenesis: the involvement of neuroligins in synaptic malfunction
Neurodegener Dis Manag 5 :137

Sindi IA, Dodd PR (2015)
Neurodegener Dis Manag 5 :137