Clinical and Research News
 DOI: 10.1176/appi.pn.2013.11b5
Journal Digest
Psychiatric News
Volume 48 Number 22 page 1-1

A study published in the Archives of Disease and Childhood followed 8,000 children from birth until age 12 to evaluate sleeping patterns associated with autism spectrum disorder (ASD).

The results showed that around age 3, children with ASD were more prone to sleep an average of 30 minutes less than their peers without ASD. Sleeping time lost by children with ASD was attributed to their likelihood to awaken three or more times during the night. This observation remained consistent after adjusting for factors such as birth prematurity and social class.

The authors acknowledged that the long-term impact of shortened sleep patterns in children with ASD is unknown. They pointed out that other researchers have suggested that sleep loss may have an impact on neuronal development; however, this must be confirmed through additional studies.

Humphreys J, Gringras P, Blair P. “Sleep Patterns in Children With Autistic Spectrum Disorders: A Prospective Cohort Study.” 2013. Arch Dis Child. Sep 23. [Epub ahead of Print] http://adc.bmj.com/content/early/2013/08/22/archdischild-2013-304083.


Scientists at the University of Western Ontario in Canada discovered that adjusting the levels of a protein called stress-inducible phosphoprotein 1 (STI1) can prevent neuronal toxicity through inhibiting specific protein interactions with amyloid-beta—a factor that appears to be key in the progression of Alzheimer’s disease (AD).

“When we studied the brains of people with AD, we saw that STI1 levels were increased. We think of this increase as a compensatory response that could protect against insults from amyloid-beta [interactions],” said Marco Prado, Ph.D., a study author and professor in the Department of Pharmacology.

To test their hypothesis, Prado and colleagues manipulated STI1 concentrations in mouse neurons. They observed that when STI1 levels were decreased, the neurons were more sensitive to amyloid-beta attack, whereas increased STI1 levels resulted in less sensitivity to amyloid-beta.

The researchers concluded that although AD is a very complex disorder, their findings provide additional clues about which proteins can help the brain achieve toxicity resistance during the progression of AD.

Ostapchenko, V, Beraldo, F, Mohammad, A. “The Prion Protein Ligand, Stress-Inducible Phosphoprotein 1, Regulates Amyloid-β Oligomer Toxicity.” 2013. J Neuro Sci. October 16, 33(42):i. http://www.jneurosci.org/content/33/42/16552.abstract.


Researchers at the University of California at Los Angeles AIDS Institute collected CD4 T cells—immune cells that are highly susceptible to damage during viral infections—from healthy human donors to assess the rate of HIV infection in the presence of cocaine.

After exposing immune cells to cocaine and subsequently infecting them with HIV, the researchers found that the presence of cocaine made cells more vulnerable to viral entry and new virus production than HIV-infected cells in the absence of cocaine.

“The co-epidemics of illicit drug use and infectious disease are well documented,” stated John Wherry, Ph.D., deputy editor of the Journal of Leukocyte Biology—where the study was published. Wherry said the study adds to the literature by suggesting that drugs such as cocaine “may directly help to fuel infections by altering the immune system.” He said that the study highlights the need for improved education for both HIV prevention and drug abstinence.

Kim S, Jung J, and Dixit D. “Cocaine Exposure Enhances Permissiveness of Quiescent T Cells to HIV Infection” 2013 J Leukoc Biol. Oct;94(4):835-843. http://www.jleukbio.org/content/94/4/835.abstract.


Researchers reported that individuals with autism spectrum disorder (ASD) are more likely to have gene deletions than those without the disorder.

Published in the American Journal of Human Genetics, the comparison study included genetic analyses of 431 participants with ASD and 379 people without the condition.

Results showed the ASD cohort had 803 gene deletions, compared with 583 deletions in the control group. In addition, participants with ASD were more likely to have multiple gene deletions related to autophagy—a protective process that involves degradation of excessive or dysfunctional cellular components.

Joseph Buxbaum, Ph.D., lead author and a professor of psychiatry at Mount Sinai School of Medicine, told Psychiatric News that “this is the first time that the [autophagic] pathway has been implicated in autism. Since we know that there is excess brain size early in life in individuals with autism, it may be a result of the pathway’s failure to properly prune brain connections.” Buxbaum and colleagues plan to further investigate the link between autophagy and ASD through additional research.

Poultney C, Goldberg A, Drapeau E. “Identification of Small Exonic CNV from Whole-Exome Sequence Data and Application to Autism Spectrum Disorder.” 2013 Am J Hum Genet. Oct 3;93(4):607-619. http://www.ncbi.nlm.nih.gov/pubmed/24094742.

Interactive Graphics


Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).
Related Articles