Francesco Errico

TL;DR: D-Asp and NMDA are present endogenously in the rat and are involved in the modulation of PRL release, and experiments conducted on tissue homogenates confirm that D-AsP is the precursor of the NMDA and that the enzyme catalyzing this reaction is a methyltransferase.

TL;DR: It is found that Ras homolog enriched in striatum (Rhes), a striatal-specific protein, binds to and activates mTOR, and Rhes−/− mice showed reduced striatal mTOR signaling and diminished dyskinesia, but maintained motor improvement on L-DOPA treatment, suggesting a therapeutic benefit for Rhes-binding drugs.

TL;DR: In vivo evidence of a neuromodulatory role exerted by d-aspartate on NMDAR signaling is provided and the intriguing hypothesis that also this d-amino acid, like d-serine, could be used as a therapeutic agent in the treatment of schizophrenia-related symptoms is raised.

TL;DR: It is found that pharmacological blockade of adenosine A2A receptors (A2ARs) fully restored the impairment of synaptic plasticity observed in hMT mice, suggesting that A2AR antagonism is able to counteract the deficit in D2R-mediated transmission observed in mutant mice, opening new perspectives for the treatment of this movement disorder.

TL;DR: Interestingly, it is found that D-aspartate and NMDA are consistently decreased in schizophrenia brains compared to control brains, and this decrease is correlated with a marked downregulation of NMDAR subunits.