RETRACTED: Rett-like Severe Encephalopathy Caused by a De Novo GRIN2B Mutation Is Attenuated by D-serine Dietary Supplement (Retracted article. See vol. 83, pg. 715, 2018)


Por: Soto, D, Olivella, M, Grau, C, Armstrong, J, Alcon, C, Gasull, X, de Salazar, MG, Gratacos-Batlle, E, Ramos-Vicente, D, Fernandez-Duenas, V, Ciruela, F, Bayes, A, Sindreu, C, Lopez-Sala, A, Garcia-Cazorla, A, Altafaj, X

Publicada: 15 ene 2018
Resumen:
BACKGROUND: N-Methyl-D-aspartate receptors (NMDARs) play pivotal roles in synaptic development, plasticity, neural survival, and cognition. Despite recent reports describing the genetic association between de novo mutations of NMDAR subunits and severe psychiatric diseases, little is known about their pathogenic mechanisms and potential therapeutic interventions. Here we report a case study of a 4-year-old Rett-like patient with severe encephalopathy carrying a missense de novo mutation in GRIN2B(p. P553T) coding for the GluN2B subunit of NMDAR. METHODS: We generated a dynamic molecular model of mutant GluN2B-containing NMDARs. We expressed the mutation in cell lines and primary cultures, and we evaluated the putative morphological, electrophysiological, and synaptic plasticity alterations. Finally, we evaluated D-serine administration as a therapeutic strategy and translated it to the clinical practice. RESULTS: Structural molecular modeling predicted a reduced pore size of mutant NMDARs. Electrophysiological recordings confirmed this prediction and also showed gating alterations, a reduced glutamate affinity associated with a strong decrease of NMDA-evoked currents. Moreover, GluN2B(P553T)-expressing neurons showed decreased spine density, concomitant with reduced NMDA-evoked currents and impaired NMDAR-dependent insertion of GluA1 at stimulated synapses. Notably, the naturally occurring coagonist D-serine was able to attenuate hypofunction of GluN2B(p. P553T)-containing NMDARs. Hence, D-serine dietary supplementation was initiated. Importantly, the patient has shown remarkable motor, cognitive, and communication improvements after 17 months of D-serine dietary supplementation. CONCLUSIONS: Our data suggest that hypofunctional NMDARs containing GluN2B( p. P553T) can contribute to Rettlike encephalopathy and that their potentiation by D-serine treatment may underlie the associated clinical improvement.

Filiaciones:
Soto, D:
 Univ Barcelona, Inst Neurosci, Barcelona, Spain

 Univ Barcelona, Dept Biomed, Barcelona, Spain

 Univ Vic Cent Univ Catalonia, August Pi & Sunyer Biomed Res Inst, Barcelona, Spain

Olivella, M:
 Univ Vic Cent Univ Catalonia, Bioinfomat & Med Stat Grp, Barcelona, Spain

Grau, C:
 Univ Barcelona, Bellvitge Biomed Res Inst, Unit Neuropharmacol, Barcelona, Spain

 Univ Barcelona, Pain Grp, Barcelona, Spain

Armstrong, J:
 Hosp St Joan de Deu, Genet & Mol Med Serv, Barcelona, Spain

Alcon, C:
 Univ Barcelona, Inst Neurosci, Barcelona, Spain

 Univ Barcelona, Dept Clin Foundat, Barcelona, Spain

Gasull, X:
 Univ Barcelona, Inst Neurosci, Barcelona, Spain

 Univ Barcelona, Dept Biomed, Barcelona, Spain

 Univ Vic Cent Univ Catalonia, August Pi & Sunyer Biomed Res Inst, Barcelona, Spain

de Salazar, MG:
 Univ Barcelona, Bellvitge Biomed Res Inst, Unit Neuropharmacol, Barcelona, Spain

 Univ Barcelona, Pain Grp, Barcelona, Spain

Gratacos-Batlle, E:
 Univ Barcelona, Inst Neurosci, Barcelona, Spain

 Univ Barcelona, Dept Biomed, Barcelona, Spain

 Univ Vic Cent Univ Catalonia, August Pi & Sunyer Biomed Res Inst, Barcelona, Spain

Ramos-Vicente, D:
 Biomed Res Inst St Pau, Mol Physiol Synapse Lab, Ctr Invest Biomed Red Enfermedades Rara, Barcelona, Spain

 Autonomous Univ Barcelona, Barcelona, Spain

Fernandez-Duenas, V:
 Univ Barcelona, Dept Pathol & Expt Therapeut, Barcelona, Spain

 Univ Barcelona, Bellvitge Biomed Res Inst, Unit Neuropharmacol, Barcelona, Spain

 Univ Barcelona, Pain Grp, Barcelona, Spain

Ciruela, F:
 Univ Barcelona, Inst Neurosci, Barcelona, Spain

 Univ Barcelona, Dept Pathol & Expt Therapeut, Barcelona, Spain

 Univ Barcelona, Bellvitge Biomed Res Inst, Unit Neuropharmacol, Barcelona, Spain

 Univ Barcelona, Pain Grp, Barcelona, Spain

Bayes, A:
 Biomed Res Inst St Pau, Mol Physiol Synapse Lab, Ctr Invest Biomed Red Enfermedades Rara, Barcelona, Spain

 Autonomous Univ Barcelona, Barcelona, Spain

Sindreu, C:
 Univ Barcelona, Inst Neurosci, Barcelona, Spain

 Univ Barcelona, Dept Clin Foundat, Barcelona, Spain

Lopez-Sala, A:
 Hosp St Joan de Deu, Dept Neurol, Neurometab Unit, Barcelona, Spain

Garcia-Cazorla, A:
 Hosp St Joan de Deu, Genet & Mol Med Serv, Barcelona, Spain

 Hosp St Joan de Deu, Dept Neurol, Neurometab Unit, Barcelona, Spain

Altafaj, X:
 Univ Barcelona, Bellvitge Biomed Res Inst, Unit Neuropharmacol, Barcelona, Spain

 Univ Barcelona, Pain Grp, Barcelona, Spain
ISSN: 00063223





BIOLOGICAL PSYCHIATRY
Editorial
ELSEVIER SCIENCE INC, 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA, Estados Unidos America
Tipo de documento: Article
Volumen: 83 Número: 2
Páginas: 160-172
WOS Id: 000417608300013
ID de PubMed: 28734458
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