The results of FC analysis showed weakened connectivity among the left Crus II, lobule VIII, and right striatum and between the right lobule VIII and the right striatum, and cingulate in the OCD group compared with the HC group.
Pooling the different alleles that comprised HLA-DR4 (including <i>DRB1*04:01</i>, <i>DRB1*04:04</i> and <i>DRB1*04:05</i> alleles) we observed a significantly higher frequency (X<sup>2</sup><sub>1</sub> = 5.53, <i>P</i> = 0.018; OR = 1.64, 95% CI 1.08-2.48) of these alleles in the early-onset OCD sample (10.8%) than in the reference population (6.8%).
In this study we aimed to investigate the relation of blood levels of interleukin 1-beta (IL-1ß), interleukin-6 (IL-6) and Tumor Necrosis Factor-α (TNF-α) with various neurocognitive functions in patients with OCD in comparison with its autogenous/reactive subtypes and healthy controls.
The present study is the first to verify the associations of single nucleotide polymorphisms rs1838733 of the PDE4D gene with obsessive-compulsive disorder in a Chinese Han population.
NPY is one of the most abundant neuropeptides in the human brain with emerging evidence of capacity to modulate stress response, which is of high relevance in OCD.
Pooling the different alleles that comprised HLA-DR4 (including <i>DRB1*04:01</i>, <i>DRB1*04:04</i> and <i>DRB1*04:05</i> alleles) we observed a significantly higher frequency (X<sup>2</sup><sub>1</sub> = 5.53, <i>P</i> = 0.018; OR = 1.64, 95% CI 1.08-2.48) of these alleles in the early-onset OCD sample (10.8%) than in the reference population (6.8%).
In this study we aimed to investigate the relation of blood levels of interleukin 1-beta (IL-1ß), interleukin-6 (IL-6) and Tumor Necrosis Factor-α (TNF-α) with various neurocognitive functions in patients with OCD in comparison with its autogenous/reactive subtypes and healthy controls.
Following on from previous work by our group where we showed that early onset anorexia nervosa (AN) and obsessive-compulsive disorder (OCD) shared a common genetic background, the aim of the present study is to assess genetic pleiotropy related to the serotonergic system (SLC6A4, 5HTR2A, 5HTR2C, TPH2, SLC18A1), in a common phenotype such as very-early age of onset.
The network biology data demonstrated the association of secreted protein acidic and rich in cysteine (SPARC/osteonectin) protein with Alzheimer's disease, Parkinson's disease, Huntington's disease and neurodegeneration with brain iron accumulation (NBIA) disease, whereas Coagulation factor V may have a role in Brunner Syndrome, Obsessive-Compulsive Disorder, Febrile seizures and Schizophrenia diseases.
We studied TALLYHO/JngJ (TH) mice, a model of type 2 diabetes mellitus, to (1) assess compulsive and anxious behaviors, (2) determine neuro-metabolite levels by 1 H magnetic resonance spectroscopy (MRS) and brain structural connectivity by diffusion tensor imaging (DTI), and (3) investigate plasma and brain protein levels for molecules previously associated with OCD (insulin, Igf1, Kcnq1, and Bdnf) in these subjects.
The 2017-based analysis suggested six potential common risk genes for OCD and ASD (CDH2, ADCY8, APOE, TSPO, TOR1A, and OLIG2), and the 2019-based study identified two more genes (DISP1 and SETD1A).
We implemented the preclinical quinpirole (QP) rat model for compulsive checking in OCD to analyse the behaviour and visualize the D2R, mGluR5 and GLT1 density in order to contribute to the understanding of the neuroreceptor kinetics.
Here we show that OCD-like behavior in mice is caused by deficiency of SPRED2, a protein expressed in various brain regions and a potent inhibitor of Ras/ERK-MAPK signaling.
Cortical Abnormalities Associated With Pediatric and Adult Obsessive-Compulsive Disorder: Findings From the ENIGMAObsessive-Compulsive Disorder Working Group.
Here we show that OCD-like behavior in mice is caused by deficiency of SPRED2, a protein expressed in various brain regions and a potent inhibitor of Ras/ERK-MAPK signaling.
Serum GDNF levels was higher in individuals with panic disorders (p = 0.013), generalized anxiety (p = 0.035), obsessive- compulsive disorder (p = 0.005) and social phobia (p = 0.004), when compared to individuals without ADs.
Functionally, global loss of spinophilin attenuates amphetamine-induced hyperlocomotion, a striatal behavior associated with dopamine dysregulation and OCD.