Pubmed du 10/06/09

Pubmed du jour

2009-06-10 12:03:50

1. Lovullo SV, Matson JL. {{Comorbid psychopathology in adults with Autism Spectrum Disorders and intellectual disabilities}}. {Res Dev Disabil};2009 (Jun 6)

There is an abundance of research investigating Autism Spectrum Disorders (ASD) in children; however, little emphasis has been placed on ASD in adults, especially in regards to comorbid psychopathology. Although scales are available that measure comorbidity in adults with ID, what is needed are scales that measure comorbidity in adults with ID and ASD. One such scale is the newly developed Autism Spectrum Disorders-Comorbidity for Adults (ASD-CA). There are two purposes of this study. The first is to further develop the ASD-CA by calculating cutoff scores for its subscales. The second is to compare the frequency of symptom endorsements on the ASD-CA among three groups: individuals with ID; individuals with ID and ASD; and individuals with ID, ASD, and additional psychopathology.

2. O’Dowd A. {{NHS must tackle its ignorance over patients with autism, says watchdog}}. {Bmj};2009;338:b2318.

3. Zhao Y, Fung C, Shin D, Shin BC, Thamotharan S, Sankar R, Ehninger D, Silva A, Devaskar SU. {{Neuronal glucose transporter isoform 3 deficient mice demonstrate features of autism spectrum disorders}}. {Mol Psychiatry};2009 (Jun 9)

Neuronal glucose transporter (GLUT) isoform 3 deficiency in null heterozygous mice led to abnormal spatial learning and working memory but normal acquisition and retrieval during contextual conditioning, abnormal cognitive flexibility with intact gross motor ability, electroencephalographic seizures, perturbed social behavior with reduced vocalization and stereotypies at low frequency. This phenotypic expression is unique as it combines the neurobehavioral with the epileptiform characteristics of autism spectrum disorders. This clinical presentation occurred despite metabolic adaptations consisting of an increase in microvascular/glial GLUT1, neuronal GLUT8 and monocarboxylate transporter isoform 2 concentrations, with minimal to no change in brain glucose uptake but an increase in lactate uptake. Neuron-specific glucose deficiency has a negative impact on neurodevelopment interfering with functional competence. This is the first description of GLUT3 deficiency that forms a possible novel genetic mechanism for pervasive developmental disorders, such as the neuropsychiatric autism spectrum disorders, requiring further investigation in humans.Molecular Psychiatry advance online publication, 9 June 2009; doi:10.1038/mp.2009.51.