1,721,167 research outputs found
Synaptic localization and activity of Adam10 regulates excitatory postsynaptic compartment through N-Cadherin cleavage
No full text
Meccanismi patogenetici della malattia di Alzheimer : dalla cascata di amiloide alla sinaptopatia
No full textNew molecular mechanisms modulating NMDA receptor subunits availability at synaptic sites
No full textMAGUK proteins : new targets for pharmacological intervention in the glutamatergic synapse
No full textIn the postsynaptic density of excitatory glutamatergic synapses, membrane associated guanylate kinase (MAGUK) proteins, such as Post-Synaptic Density 95 (PSD-95), organize ionotropic glutamate receptors and their associated signalling proteins regulating the strength of synaptic activity. Modifications of MAGUK proteins function in the glutamatergic synapse such as alterations of MAGUK proteins interaction with N-Methyl-D-Aspartate (NMDA) receptors regulatory subunits are common events in several neurodegenerative disorders. Thus, a better knowledge and understanding of MAGUK structure and function as well as of the molecular events regulating MAGUK-mediated interactions in the glutamatergic synapse could lead to the identification of new targets for pharmaceutical intervention for neurodegenerative disease
Modulation of NMDA receptor at the synapse: Promising therapeutic interventions in disorders of the nervous system
No full textThere is general agreement that excessive activation of N-methyl-D-aspartate (NMDA) receptors plays a key role in mediating at least some aspects of synaptic dysfunction in several central nervous system disorders. On this view, in the last decades, research focused on the discovery of different compounds able to reduce NMDA receptor activity, such as classical and/or subunit-specific antagonists. However, the increasing body of knowledge on specific signaling pathways downstream NMDA receptors led to the identification of new pharmacological targets for NMDA receptor-related pathological conditions. Moreover, besides over-activation, several studies indicated that also abnormal NMDA receptor trafficking, resulting in the modification of the receptor subunit composition at the synapse, has a major role in the pathogenesis of several brain disorders. For this reason, the discovery of the molecular mechanisms regulating the abundance of synaptic versus extra-synaptic NMDA receptors as well as the activation of the specific signaling pathways downstream the different NMDA receptor subtypes is needed for the development of novel therapeutic approaches for NMDA receptor-dependent synaptic dysfunction
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