Dataset Information

Putamen gray matter volumes in neuropsychiatric and neurodegenerative disorders.

ABSTRACT: Putamen is enriched with dopamine and associated with dopamine-related phenotypes including many neuropsychiatric and neurodegenerative disorders that manifest with motor impairment, impulsive behavior, and cognitive deficits. The gray matter volume of the putamen is age-dependent and genetically controlled. In most neuropsychiatric and neurodegenerative disorders, including Parkinson's spectrum disorders, Huntington's disease, dementia with Lewy bodies, Alzheimer's disease, multiple sclerosis, attention deficit hyperactivity disorder, developmental dyslexia, and major depression, the putamen volume is significantly reduced. On the other hand, in individuals with bipolar disorder, schizophrenia spectrum disorders, especially neuroleptics-medicated patients with schizophrenia, autism spectrum disorders, obsessive-compulsive spectrum disorders, and cocaine/amphetamine dependence, the putamen volume is significantly enlarged. Therefore, the putamen volume may serve as a structural neural marker for many neuropsychiatric and neurodegenerative disorders and a predictor of treatment outcomes in individuals afflicted with these conditions. We provided an overview of the genetic bases of putamen volume and explored potential mechanisms whereby altered putamen volume manifests in these neuropsychiatric and neurodegenerative conditions, with a specific focus on dopaminergic processes.

SUBMITTER: Luo X

PROVIDER: S-EPMC6641567 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Putamen gray matter volumes in neuropsychiatric and neurodegenerative disorders.

Luo Xingguang X Mao Qiao Q Shi Jing J Wang Xiaoping X Li Chiang-Shan R CR

World journal of psychiatry and mental health research 20190530 1

Putamen is enriched with dopamine and associated with dopamine-related phenotypes including many neuropsychiatric and neurodegenerative disorders that manifest with motor impairment, impulsive behavior, and cognitive deficits. The gray matter volume of the putamen is age-dependent and genetically controlled. In most neuropsychiatric and neurodegenerative disorders, including Parkinson's spectrum disorders, Huntington's disease, dementia with Lewy bodies, Alzheimer's disease, multiple sclerosis, ...[more]

PMID: 31328186

Similar Datasets

Project description:BackgroundSelective loss of dopaminergic neurons and diminished putamen gray matter volume (GMV) represents a central feature of Parkinson's disease (PD). Recent studies have reported specific effects of kinectin 1 gene (KTN1) variants on the putamen GMV.ObjectiveTo examine the relationship of KTN1 variants, KTN1 mRNA expression in the putamen and substantia nigra pars compacta (SNc), putamen GMV, and PD.MethodsWe examined the associations between PD and a total of 1847 imputed KTN1 single nucleotide polymorphisms (SNPs) in one discovery sample [2,000 subjects with PD vs. 1,986 healthy controls (HC)], and confirmed the nominally significant associations (p < 0.05) in two replication samples (900 PD vs. 867 HC, and 940 PD vs. 801 HC, respectively). The regulatory effects of risk variants on the KTN1 mRNA expression in putamen and SNc and the putamen GMV were tested. We also quantified the expression levels of KTN1 mRNA in the putamen and/or SNc for comparison between PD and HC in five independent cohorts.ResultsSix replicable and two non-replicable KTN1-PD associations were identified (0.009 ≤ p ≤ 0.049). The major alleles of five SNPs, including rs12880292, rs8017172, rs17253792, rs945270, and rs4144657, significantly increased risk for PD (0.020 ≤ p ≤ 0.049) and putamen GMVs (19.08 ≤ β ≤ 60.38; 2.82 ≤ Z ≤ 15.03; 5.0 × 10-51 ≤ p ≤ 0.018). The risk alleles of five SNPs, including rs8017172, rs17253792, rs945270, rs4144657, and rs1188184 also significantly increased the KTN1 mRNA expression in the putamen or SNc (0.021 ≤ p ≤ 0.046). The KTN1 mRNA was abundant in the putamen and/or SNc across five independent cohorts and differentially expressed in the SNc between PD and HC in one cohort (p = 0.047).ConclusionThere was a consistent, significant, replicable, and robust positive relationship among the KTN1 variants, PD risk, KTN1 mRNA expression in putamen, and putamen volumes, and a modest relation between PD risk and KTN1 mRNA expression in SNc, suggesting that KTN1 may play a functional role in the development of PD.

Project description:Abnormal neuroanatomic brain networks have been reported in schizophrenia, but their characterization across patients with psychotic disorders, and their potential alterations in nonpsychotic relatives, remain to be clarified. Participants recruited by the Bipolar and Schizophrenia Network for Intermediate Phenotypes consortium included 326 probands with psychotic disorders (107 with schizophrenia (SZ), 87 with schizoaffective disorder (SAD), 132 with psychotic bipolar disorder (BD)), 315 of their nonpsychotic first-degree relatives and 202 healthy controls. Single-subject gray matter graphs were extracted from structural MRI scans, and whole-brain neuroanatomic organization was compared across the participant groups. Compared with healthy controls, psychotic probands showed decreased nodal efficiency mainly in bilateral superior temporal regions. These regions had altered morphological relationships primarily with frontal lobe regions, and their network-level alterations were associated with positive symptoms of psychosis. Nonpsychotic relatives showed lower nodal centrality metrics in the prefrontal cortex and subcortical regions, and higher nodal centrality metrics in the left cingulate cortex and left thalamus. Diagnosis-specific analysis indicated that individuals with SZ had lower nodal efficiency in bilateral superior temporal regions than controls, probands with SAD only exhibited lower nodal efficiency in the left superior and middle temporal gyrus, and individuals with psychotic BD did not show significant differences from healthy controls. Our findings provide novel evidence of clinically relevant disruptions in the anatomic association of the superior temporal lobe with other regions of whole-brain networks in patients with psychotic disorders, but not in their unaffected relatives, suggesting that it is a disease-related trait. Network disorganization primarily involving frontal lobe and subcortical regions in nonpsychotic relatives may be related to familial illness risk.

Dataset Information

Putamen gray matter volumes in neuropsychiatric and neurodegenerative disorders.

Publications

Putamen gray matter volumes in neuropsychiatric and neurodegenerative disorders.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure