Giovanni Monteleone.

Giovanni Monteleone, M.D., Ph .D., Markus F. Neurath, M.D., Ph.D., Sandro Ardizzone, M.D., Antonio Di Sabatino, M.D., Massimo C. Fantini, M.D., Ph.D., Fabiana Castiglione, M.D., Maria L. Scribano, M.D., Alessandro Armuzzi, M.D., Ph.D., Flavio Caprioli, M.D., Ph.D., Giacomo C. Sturniolo, M.D., Francesca Rogai, M.D., Ph.D., Maurizio Vecchi, M.D., Raja Atreya, M.D., Ph.D., Fabrizio Bossa, M.D., Sara Onali, M.D., Ph.D., Maria Fichera, M.D., Gino R. Corazza, M.D., Livia Biancone, M.D., Ph.D., Vincenzo Savarino, M.D., Roberta Pica, M.D., Ambrogio Orlando, M.D., and Francesco Pallone, M.D.: Mongersen, an Oral SMAD7 Antisense Oligonucleotide, and Crohn?s Disease..

These mutations are pathogenic for several reasons probably. First, they bring about the production of proteins that absence domains, such QTRV and RASGAP, that have been shown to be very important to the synaptic plasticity and backbone morphogenesis that are required for learning and memory space.16,19 In addition, each of the resulting premature stop codons may possibly also destabilize the SYNGAP1 messenger RNA transcript through the nonsense-mediated mRNA decay mechanism.21 Second, mice that are heterozygous for null alleles of Syngap1 have impaired synaptic learning and plasticity, which suggests that the disruption of an individual SYNGAP1 allele is sufficient to cause cognitive dysfunction in individuals.