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Title: Cognitive and emotional impairments in obsessive–compulsive disorder: Evidence from functional brain alterations

Authors:
; ; ; ; ;
Publication Date:
Sponsoring Org.:
USDOE Office of Nuclear Energy (NE), Fuel Cycle Technologies (NE-5)
OSTI Identifier:
1295945
Resource Type:
Journal Article: Published Article
Journal Name:
Porto Biomedical Journal
Additional Journal Information:
Journal Volume: 1; Journal Issue: 3; Related Information: CHORUS Timestamp: 2017-06-24 16:48:24; Journal ID: ISSN 2444-8664
Publisher:
Elsevier
Country of Publication:
Country unknown/Code not available
Language:
English

Citation Formats

Gonçalves, Óscar F., Carvalho, Sandra, Leite, Jorge, Fernandes-Gonçalves, Ana, Carracedo, Angel, and Sampaio, Adriana. Cognitive and emotional impairments in obsessive–compulsive disorder: Evidence from functional brain alterations. Country unknown/Code not available: N. p., 2016. Web. doi:10.1016/j.pbj.2016.07.005.
Gonçalves, Óscar F., Carvalho, Sandra, Leite, Jorge, Fernandes-Gonçalves, Ana, Carracedo, Angel, & Sampaio, Adriana. Cognitive and emotional impairments in obsessive–compulsive disorder: Evidence from functional brain alterations. Country unknown/Code not available. doi:10.1016/j.pbj.2016.07.005.
Gonçalves, Óscar F., Carvalho, Sandra, Leite, Jorge, Fernandes-Gonçalves, Ana, Carracedo, Angel, and Sampaio, Adriana. 2016. "Cognitive and emotional impairments in obsessive–compulsive disorder: Evidence from functional brain alterations". Country unknown/Code not available. doi:10.1016/j.pbj.2016.07.005.
@article{osti_1295945,
title = {Cognitive and emotional impairments in obsessive–compulsive disorder: Evidence from functional brain alterations},
author = {Gonçalves, Óscar F. and Carvalho, Sandra and Leite, Jorge and Fernandes-Gonçalves, Ana and Carracedo, Angel and Sampaio, Adriana},
abstractNote = {},
doi = {10.1016/j.pbj.2016.07.005},
journal = {Porto Biomedical Journal},
number = 3,
volume = 1,
place = {Country unknown/Code not available},
year = 2016,
month = 7
}

Journal Article:
Free Publicly Available Full Text
Publisher's Version of Record at 10.1016/j.pbj.2016.07.005

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  • Controversial results possibly suggesting an association between Tourette`s syndrome (TS) and excess of homozygosity at an Msc I polymorphism in the Dopamine D{sub 3} receptor (DRD{sub 3}) gene have recently been reported. Since a relationship between obsessive-compulsive disorder (OCD) and Tourette`s syndrome (TS) has been suggested, in this study we assessed the frequency of this 2-allele polymorphism in a sample of 97 OCD patients and in 97 control subjects. No statistically significant differences in allele or genotype frequencies were found. Thus this mutation in the coding sequence of the DRD{sub 3} gene is unlikely to confer susceptibility to OCD. 28more » refs., 21 tabs.« less
  • Epidemiologic studies indicate that obsessive-compulsive disorder is genetically transmitted in some families, although no genetic abnormalities have been identified in individuals with this disorder. The selective response of obsessive-compulsive disorder to treatment with agents which block serotonin reuptake suggests the gene coding for the serotonin transporter as a candidate gene. The primary structure of the serotonin-transporter coding region was sequenced in 22 patients with obsessive-compulsive disorder, using direct PCR sequencing of cDNA synthesized from platelet serotonin-transporter mRNA. No variations in amino acid sequence were found among the obsessive-compulsive disorder patients or healthy controls. These results do not support a rolemore » for alteration in the primary structure of the coding region of the serotonin-transporter gene in the pathogenesis of obsessive-compulsive disorder. 27 refs.« less
  • The cerebral metabolic rate for glucose was studied in 18 adults with childhood-onset obsessive-compulsive disorder (OCD) and in age- and sex-matched controls using positron emission tomography and fludeoxyglucose F 18. Both groups were scanned during rest, with reduced auditory and visual stimulation. The group with OCD showed an increased glucose metabolism in the left orbital frontal, right sensorimotor, and bilateral prefrontal and anterior cingulate regions as compared with controls. Ratios of regional activity to mean cortical gray matter metabolism were increased for the right prefrontal and left anterior cingulate regions in the group with OCD as a whole. Correlations betweenmore » glucose metabolism and clinical assessment measures showed a significant relationship between metabolic activity and both state and trait measurements of OCD and anxiety as well as the response to clomipramine hydrochloride therapy. These results are consistent with the suggestion that OCD may result from a functional disturbance in the frontal-limbic-basal ganglia system.« less
  • Ionizing radiation causes degeneration of myelin, the insulating sheaths of neuronal axons, leading to neurological impairment. As radiation research on the central nervous system has predominantly focused on neurons, with few studies addressing the role of glial cells, we have focused our present research on identifying the latent effects of single/ fractionated -low dose of low/ high energy radiation on the role of base excision repair protein Apurinic Endonuclease-1, in the rat spinal cords oligodendrocyte progenitor cells ’ differentiation. Apurinic endonuclease-1 is predominantly upregulated in response to oxidative stress by low- energy radiation, and previous studies show significant induction ofmore » Apurinic Endonucle- ase-1 in neurons and astrocytes. Our studies show for the first time, that fractionation of pro- tons cause latent damage to spinal cord architecture while fractionation of HZE ( 28Si) induce increase in APE1 with single dose, which then decreased with fractionation. In conclusion, the oligoden- drocyte progenitor cells differentiation was skewed with increase in immature oligodendro- cytes and astrocytes, which likely cause the observed decrease in white matter, increased neuro-inflammation, together leading to the observed significant cognitive defects« less