Modified Glutamatergic Postsynapse in Neurodegenerative Disorders.

• The postsynaptic density architecture is complex and dynamic. • In Huntington's disease, mutant huntingtin affects glutamatergic cortico-striatal synapse function. • In Parkinson's disease, striatal DA loss impairs postsynaptic morphology and function. • In Alzheimer's disease, oligomers of amyloid-beta peptide destabilize postsynaptic sites. The postsynaptic density (PSD) is a complex subcellular domain important for postsynaptic signaling, function, and plasticity. The PSD is present at excitatory synapses and specialized to allow for precise neuron-to-neuron transmission of information. The PSD is localized immediately underneath the postsynaptic membrane forming a major protein network that regulates postsynaptic signaling and synaptic plasticity. Glutamatergic synaptic dysfunction affecting PSD morphology and signaling events have been described in many neurodegenerative disorders, either sporadic or familial forms. Thus, in this review we describe the main protein players forming the PSD and their activity, as well as relevant modifications in key components of the postsynaptic architecture occurring in Huntington's, Parkinson's and Alzheimer's diseases. [ABSTRACT FROM AUTHOR]