Database : MEDLINE
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[PMID]: 29524740
[Au] Autor:Flores A; López FJ; Vervliet B; Cobos PL
[Ad] Address:Instituto de Investigación Biomédica de Málaga (IBIMA), Universidad de Málaga, Spain. Electronic address: amandafm@uma.es.
[Ti] Title:Intolerance of uncertainty as a vulnerability factor for excessive and inflexible avoidance behavior.
[So] Source:Behav Res Ther;104:34-43, 2018 Mar 01.
[Is] ISSN:1873-622X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Recent studies have shown that avoidance behavior may become excessive and inflexible (i.e., detached from its incentive value and resistant to extinction). On the other hand, prospective intolerance of uncertainty (P-IU) has been defined as a factor leading to excessive responding in uncertain situations. Thus, uncertain avoidance situations may be taken as a relevant scenario to examine the role of intolerance of uncertainty as a factor that facilitates excessive and inflexible avoidance behavior. In our experiment, we tested the hypothesis that P-IU is associated with excessive and inflexible avoidance in an outcome devaluation paradigm. Specifically, healthy participants learned in a free-operant discriminative task to avoid an aversive sound, and were tested in extinction to measure the sensitivity of avoidance responses to the devaluation of the sound aversiveness. The results showed that an increase in P-IU was positively associated to an increase in insensitivity to the devaluation. Moreover, P-IU was also related to an increase in the frequency of avoidance responses during the instrumental learning phase, and to resistance to extinction. Interestingly, these associations involving P-IU were still significant when trait anxiety was controlled for. The pattern of results suggests that P-IU may be a vulnerability factor for excessive and inflexible avoidance, which, in turn, has been found to be associated with several mental disorders.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 413890 MEDLINE  
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[PMID]: 29511121
[Au] Autor:Authement ME; Langlois LD; Shepard RD; Browne CA; Lucki I; Kassis H; Nugent FS
[Ad] Address:Department of Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.
[Ti] Title:A role for corticotropin-releasing factor signaling in the lateral habenula and its modulation by early-life stress.
[So] Source:Sci Signal;11(520), 2018 Mar 06.
[Is] ISSN:1937-9145
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Centrally released corticotropin-releasing factor or hormone (extrahypothalamic CRF or CRH) in the brain is involved in the behavioral and emotional responses to stress. The lateral habenula (LHb) is an epithalamic brain region involved in value-based decision-making and stress evasion. Through its inhibition of dopamine-mediated reward circuitry, the increased activity of the LHb is associated with addiction, depression, schizophrenia, and behavioral disorders. We found that extrahypothalamic CRF neurotransmission increased neuronal excitability in the LHb. Through its receptor CRFR1 and subsequently protein kinase A (PKA), CRF application increased the intrinsic excitability of LHb neurons by affecting changes in small-conductance SK-type and large-conductance BK-type K channels. CRF also reduced inhibitory γ-aminobutyric acid-containing (GABAergic) synaptic transmission onto LHb neurons through endocannabinoid-mediated retrograde signaling. Maternal deprivation is a severe early-life stress that alters CRF neural circuitry and is likewise associated with abnormal mental health later in life. LHb neurons from pups deprived of maternal care exhibited increased intrinsic excitability, reduced GABAergic transmission, decreased abundance of SK2 channel protein, and increased activity of PKA, without any substantial changes in or expression. Furthermore, maternal deprivation blunted the response of LHb neurons to subsequent, acute CRF exposure. Activating SK channels or inhibiting postsynaptic PKA activity prevented the effects of both CRF and maternal deprivation on LHb intrinsic excitability, thus identifying potential pharmacological targets to reverse central CRF circuit dysregulation in patients with associated disorders.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review

  3 / 413890 MEDLINE  
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[PMID]: 29510751
[Au] Autor:Baron EC; Rathod SD; Hanlon C; Prince M; Fedaku A; Kigozi F; Jordans M; Luitel NP; Medhin G; Murhar V; Nakku J; Patel V; Petersen I; Selohilwe O; Shidhaye R; Ssebunnya J; Tomlinson M; Lund C; De Silva M
[Ad] Address:Alan J Flisher Centre for Public Mental Health, Department of Psychiatry and Mental Health, University of Cape Town, 46 Sawkins Road 7700 Rondebosch, Cape Town, South Africa. emily.baron@uct.ac.za.
[Ti] Title:Impact of district mental health care plans on symptom severity and functioning of patients with priority mental health conditions: the Programme for Improving Mental Health Care (PRIME) cohort protocol.
[So] Source:BMC Psychiatry;18(1):61, 2018 Mar 06.
[Is] ISSN:1471-244X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: The Programme for Improving Mental Health Care (PRIME) sought to implement mental health care plans (MHCP) for four priority mental disorders (depression, alcohol use disorder, psychosis and epilepsy) into routine primary care in five low- and middle-income country districts. The impact of the MHCPs on disability was evaluated through establishment of priority disorder treatment cohorts. This paper describes the methodology of these PRIME cohorts. METHODS: One cohort for each disorder was recruited across some or all five districts: Sodo (Ethiopia), Sehore (India), Chitwan (Nepal), Dr. Kenneth Kaunda (South Africa) and Kamuli (Uganda), comprising 17 treatment cohorts in total (N = 2182). Participants were adults residing in the districts who were eligible to receive mental health treatment according to primary health care staff, trained by PRIME facilitators as per the district MHCP. Patients who screened positive for depression or AUD and who were not given a diagnosis by their clinicians (N = 709) were also recruited into comparison cohorts in Ethiopia, India, Nepal and South Africa. Caregivers of patients with epilepsy or psychosis were also recruited (N = 953), together with or on behalf of the person with a mental disorder, depending on the district. The target sample size was 200 (depression and AUD), or 150 (psychosis and epilepsy) patients initiating treatment in each recruiting district. Data collection activities were conducted by PRIME research teams. Participants completed follow-up assessments after 3 months (AUD and depression) or 6 months (psychosis and epilepsy), and after 12 months. Primary outcomes were impaired functioning, using the 12-item World Health Organization Disability Assessment Schedule 2.0 (WHODAS), and symptom severity, assessed using the Patient Health Questionnaire (depression), the Alcohol Use Disorder Identification Test (AUD), and number of seizures (epilepsy). DISCUSSION: Cohort recruitment was a function of the clinical detection rate by primary health care staff, and did not meet all planned targets. The cross-country methodology reflected the pragmatic nature of the PRIME cohorts: while the heterogeneity in methods of recruitment was a consequence of differences in health systems and MHCPs, the use of the WHODAS as primary outcome measure will allow for comparison of functioning recovery across sites and disorders.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1186/s12888-018-1642-x

  4 / 413890 MEDLINE  
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[PMID]: 29506557
[Au] Autor:Sundby A; Boolsen MW; Burgdorf KS; Ullum H; Hansen TF; Mors O
[Ad] Address:Department of Clinical Medicine, Psychosis Research Unit, Aarhus University Hospital, Skovagervej 2, 8240, Risskov, Denmark. anna.sundby@regionh.dk.
[Ti] Title:Attitudes of stakeholders in psychiatry towards the inclusion of children in genomic research.
[So] Source:Hum Genomics;12(1):12, 2018 Mar 05.
[Is] ISSN:1479-7364
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Genomic sequencing of children in research raises complex ethical issues. This study aims to gain more knowledge on the attitudes towards the inclusion of children as research subjects in genomic research and towards the disclosure of pertinent and incidental findings to the parents and the child. METHODS: Qualitative data were collected from interviews with a wide range of informants: experts engaged in genomic research, clinical geneticists, persons with mental disorders, relatives, and blood donors. Quantitative data were collected from a cross-sectional web-based survey among 1227 parents and 1406 non-parents who were potential stakeholders in psychiatric genomic research. RESULTS: Participants generally expressed positive views on children's participation in genomic research. The informants in the qualitative interviews highlighted the age of the child as a critical aspect when disclosing genetic information. Other important aspects were the child's right to an autonomous choice, the emotional burden of knowing imposed on both the child and the parents, and the possibility of receiving beneficial clinical information regarding the future health of the child. Nevertheless, there was no consensus whether the parent or the child should receive the findings. A majority of survey stakeholders agreed that children should be able to participate in genomic research. The majority agreed that both pertinent and incidental findings should be returned to the parents and to the child when of legal age. Having children does not affect the stakeholder's attitudes towards the inclusion of children as research subjects in genomic research. CONCLUSION: Our findings illustrate that both the child's right to autonomy and the parents' interest to be informed are important factors that are found valuable by the participants. In future guidelines governing children as subjects in genomic research, it would thus be essential to incorporate the child's right to an open future, including the right to receive information on adult-onset genetic disorders.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1186/s40246-018-0144-8

  5 / 413890 MEDLINE  
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[PMID]: 29285652
[Au] Autor:Åberg M; Nyberg J; Robertson J; Kuhn G; Schiöler L; Nissbrandt H; Waern M; Torén K
[Ad] Address:Department of Public Health and Community Medicine/Primary Health Care, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Box 454, 405 30, Gothenburg, Sweden. maria.aberg@gu.se.
[Ti] Title:Risk factors in Swedish young men for amyotrophic lateral sclerosis in adulthood.
[So] Source:J Neurol;265(3):460-470, 2018 Mar.
[Is] ISSN:1432-1459
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Recent research suggests that the incidence of amyotrophic lateral sclerosis (ALS) may be on the rise. Since ALS becomes predominant in later life, most studies on causal factors are conducted in middle-aged or older populations where potentially important influences from early life can usually not be adequately captured. We aimed to investigate predictors in young Swedish men for ALS in adulthood. Therefore, we performed a prospective cohort study of young men (aged 16-25, n = 1,819,817) who enlisted 1968-2005 and took part in comprehensive conscription examinations. Incident cases of ALS (n = 526) during up to 46 years of follow-up were identified in the National Hospital Register and Swedish Cause of Death Register. Those who developed ALS had lower BMI (body mass index) at conscription than their peers (p = 0.03). The risk of ALS during follow-up was calculated with Cox proportional hazards models. No associations were found with physical fitness, erythrocyte sedimentation rate, or non-psychotic mental disorders. Low overall muscle strength compared to high overall muscle strength [hazard ratio (HR) 1.36; 95% confidence interval (CI) 1.01-1.83] and low BMI (a one-unit increase HR 0.96; 95% CI 0.93-0.99) and lower erythrocyte volume fraction (a one-unit increase HR 0.96; 95% CI 0.92-0.998) were the statistically significant predictors for ALS in adjusted models. These findings provide novel epidemiologic evidence of a prospective association between low overall muscle strength and erythrocyte volume fraction in young men and ALS risk.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1007/s00415-017-8719-1

  6 / 413890 MEDLINE  
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[PMID]: 29206893
[Au] Autor:Hoche F; Guell X; Vangel MG; Sherman JC; Schmahmann JD
[Ad] Address:Ataxia Unit, Cognitive Behavioral Neurology Unit, Laboratory for Neuroanatomy and Cerebellar Neurobiology, Department of Neurology Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
[Ti] Title:The cerebellar cognitive affective/Schmahmann syndrome scale.
[So] Source:Brain;141(1):248-270, 2018 Jan 01.
[Is] ISSN:1460-2156
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Cerebellar cognitive affective syndrome (CCAS; Schmahmann's syndrome) is characterized by deficits in executive function, linguistic processing, spatial cognition, and affect regulation. Diagnosis currently relies on detailed neuropsychological testing. The aim of this study was to develop an office or bedside cognitive screen to help identify CCAS in cerebellar patients. Secondary objectives were to evaluate whether available brief tests of mental function detect cognitive impairment in cerebellar patients, whether cognitive performance is different in patients with isolated cerebellar lesions versus complex cerebrocerebellar pathology, and whether there are cognitive deficits that should raise red flags about extra-cerebellar pathology. Comprehensive standard neuropsychological tests, experimental measures and clinical rating scales were administered to 77 patients with cerebellar disease-36 isolated cerebellar degeneration or injury, and 41 complex cerebrocerebellar pathology-and to healthy matched controls. Tests that differentiated patients from controls were used to develop a screening instrument that includes the cardinal elements of CCAS. We validated this new scale in a new cohort of 39 cerebellar patients and 55 healthy controls. We confirm the defining features of CCAS using neuropsychological measures. Deficits in executive function were most pronounced for working memory, mental flexibility, and abstract reasoning. Language deficits included verb for noun generation and phonemic > semantic fluency. Visual spatial function was degraded in performance and interpretation of visual stimuli. Neuropsychiatric features included impairments in attentional control, emotional control, psychosis spectrum disorders and social skill set. From these results, we derived a 10-item scale providing total raw score, cut-offs for each test, and pass/fail criteria that determined 'possible' (one test failed), 'probable' (two tests failed), and 'definite' CCAS (three tests failed). When applied to the exploratory cohort, and administered to the validation cohort, the CCAS/Schmahmann scale identified sensitivity and selectivity, respectively as possible exploratory cohort: 85%/74%, validation cohort: 95%/78%; probable exploratory cohort: 58%/94%, validation cohort: 82%/93%; and definite exploratory cohort: 48%/100%, validation cohort: 46%/100%. In patients in the exploratory cohort, Mini-Mental State Examination and Montreal Cognitive Assessment scores were within normal range. Complex cerebrocerebellar disease patients were impaired on similarities in comparison to isolated cerebellar disease. Inability to recall words from multiple choice occurred only in patients with extra-cerebellar disease. The CCAS/Schmahmann syndrome scale is useful for expedited clinical assessment of CCAS in patients with cerebellar disorders.awx317media15678692096001.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1093/brain/awx317

  7 / 413890 MEDLINE  
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[PMID]: 29188292
[Au] Autor:Santavirta T; Santavirta N; Gilman SE
[Ad] Address:Institute for Housing and Urban Research, Uppsala University and Swedish Institute for Social Research, Stockholm University, Uppsala, Sweden.
[Ti] Title:Association of the World War II Finnish Evacuation of Children With Psychiatric Hospitalization in the Next Generation.
[So] Source:JAMA Psychiatry;75(1):21-27, 2018 Jan 01.
[Is] ISSN:2168-6238
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Importance: Although there is evidence that adverse childhood experiences are associated with worse mental health in adulthood, scarce evidence is available regarding an emerging concern that the next generation might also be affected. Objective: To compare the risk of psychiatric hospitalization in cousins whose parents were vs were not exposed to the Finnish evacuation policy that involved a mean 2-year stay with a Swedish foster family. Design, Setting, and Participants: This multigenerational, population-based cohort study of Finnish individuals and their siblings born between January 1, 1933, and December 31, 1944, analyzed the association of evacuee status as a child during World War II in the first generation with the risk of psychiatric hospitalization among offspring in the second generation. Evacuee status during World War II was determined using the Finnish National Archive's registry of participants in the Finnish evacuation. Data on evacuee status were linked to the psychiatric diagnoses in the Finnish Hospital Discharge Register from January 1, 1971, through December 31, 2012, for offspring (n = 93 391) born between January 1, 1950, and December 31, 2010. Sex-specific Cox proportional hazards regression models were used to estimate hazard ratios for risk of psychiatric hospitalization during the follow-up period. Because offspring of evacuees and their nonevacuated siblings are cousins, the Cox proportional hazards regression models included fixed effects to adjust for confounding factors in families. Data analysis was performed from June 15, 2016, to August 26, 2017. Exposures: Parental participation in the evacuation during World War II (coded 1 for parents who were evacuated and placed in foster care and 0 for those not evacuated). Main Outcomes and Measures: Offspring's initial admission to the hospital for a psychiatric disorder, obtained from the Finnish Hospital Discharge Register from January 1, 1971, through December 31, 2012. Results: Of the 93 391 study persons, 45 955 (49.2%) were women and 47 436 (50.8) were men; mean (SD) age in 2012 among survivors was 45.4 (6.58) years. Female offspring of mothers evacuated to Sweden during childhood had an elevated risk of psychiatric hospitalization (hazard ratio for any type of psychiatric disorder: 2.04 [95% CI, 1.04-4.01]; hazard ratio for mood disorder: 4.68 [95% CI, 1.92-11.42]). There was no excess risk of being hospitalized for a psychiatric disorder among women whose fathers were exposed to the Finnish evacuation policy during World War II or among men whose mothers or fathers were exposed. Conclusions and Relevance: In a prior follow-up study of the Finnish evacuees, girls evacuated to Swedish foster families during World War II were more likely to be hospitalized for a psychiatric disorder-in particular, a mood disorder-in adulthood than their nonevacuated sisters. The present study found that the offspring of these individuals were also at risk for mental health problems that required hospitalization and suggests that early-life adversities, including war-related exposures, may be associated with mental health disorders that persist across generations.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1001/jamapsychiatry.2017.3511

  8 / 413890 MEDLINE  
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[PMID]: 29524078
[Au] Autor:Wolitzky-Taylor K; Fenwick K; Lengnick-Hall R; Grossman J; Bearman SK; Arch J; Miranda J; Chung B
[Ad] Address:Department of Psychiatry and Biobehavioral Sciences, University of California-Los Angeles, Los Angeles, USA. kbtaylor@mednet.ucla.edu.
[Ti] Title:A Preliminary Exploration of the Barriers to Delivering (and Receiving) Exposure-Based Cognitive Behavioral Therapy for Anxiety Disorders in Adult Community Mental Health Settings.
[So] Source:Community Ment Health J;, 2018 Mar 09.
[Is] ISSN:1573-2789
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Despite the effectiveness of exposure-based cognitive behavioral therapy (CBT) for anxiety disorders, few individuals in need receive this treatment, particularly in community mental health settings serving low-income adults. The present study took a preliminary step to understand these barriers by conducting a series of key informant interviews and focus groups among patients, providers, clinical administrators, and policy makers. Several themes emerged as barriers to the delivery of exposure-based CBT in these settings, including therapist training and compentency issues, logistical issues, and funding stream issues. Clinical implications and future research that can build from these data are discussed.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1007/s10597-018-0252-x

  9 / 413890 MEDLINE  
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[PMID]: 29524018
[Au] Autor:Becker SP; Willcutt EG
[Ad] Address:Division of Behavioral Medicine and Clinical Psychology, Cincinnati Children's Hospital Medical Center, Cincinnati, USA. stephen.becker@cchmc.org.
[Ti] Title:Advancing the study of sluggish cognitive tempo via DSM, RDoC, and hierarchical models of psychopathology.
[So] Source:Eur Child Adolesc Psychiatry;, 2018 Mar 10.
[Is] ISSN:1435-165X
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Sluggish cognitive tempo (SCT) is separable from attention-deficit/hyperactivity disorder (ADHD) and other psychopathologies, and growing evidence demonstrates SCT to be associated with impairment in both children and adults. However, it remains unclear how SCT should optimally be conceptualized. In this article, we argue that multiple models of psychopathology should be leveraged to make substantive advances to our understanding of SCT. Both categorical and dimensional approaches should be used, including the Diagnostic and Statistical Manual of Mental Disorders (DSM) nosology, the Research Domain Criteria (RDoC) initiative, and hierarchical models of psychopathology. Studies are needed to determine whether individuals categorized with SCT can be reliably identified and differentiated from individuals without SCT in pathophysiological, neuropsychological, behavioral, and daily life functioning. Studies are also needed to evaluate the validity and utility of SCT as a transdiagnostic and dimensional construct. In considering SCT as a dimensional and potentially transdiagnostic construct, we describe ways in which SCT might be examined within the RDoC framework, including negative valence systems, cognitive systems, and arousal/regulatory systems, as well as within hierarchical models of psychopathology. Conceptualizing SCT within both categorical and dimensional models of psychopathology will help to better understand the causes, developmental pathways, and clinical implications of SCT, both as a construct in its own right and also in relation to other psychopathologies.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1007/s00787-018-1136-x

  10 / 413890 MEDLINE  
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[PMID]: 29523295
[Au] Autor:Peter-Ross EM
[Ad] Address:Department of Psychiatry and Mental Health, University of Cape Town, Neurogenetic Psychiatric Outpatients Clinic, Groote Schuur Hospital, Main Road, Observatory 7935, Cape Town, South Africa; Life Vincent Pallotti Hospital, Suite 116, Alexandra Road, Pinelands 7405, Cape Town, South Africa. Electronic address: peterem@mweb.co.za.
[Ti] Title:Molecular hypotheses to explain the shared pathways and underlying pathobiological causes in catatonia and in catatonic presentations in neuropsychiatric disorders.
[So] Source:Med Hypotheses;113:54-64, 2018 Apr.
[Is] ISSN:1532-2777
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The pathobiological causes, the shared cellular and molecular pathways in catatonia and in catatonic presentation in neuropsychiatric disorders are yet to be determined. The hypotheses in this paper have been deduced from the latest scientific research findings and clinical observations of patients with genetic disorders, behavioral phenotypes and other family members suffering mental disorders. The first hypothesis postulates that catatonia and the heterogeneity of catatonic signs and symptoms involve nucleolar dysfunction arising from abnormalities of the brain-specific, non-coding micro-RNA, SNORD115 genes (either duplications or deletions) which result in pathobiological dysfunction of various combinations in the downstream pathways (possibly along with other genes in these shared pathways). SNORD115 controls five genes CRHR1, PBRM1, TAF1, DPM2, and RALGPS1 as well as the alternative splicing of serotonin 2C receptor. SNORD115 abnormalities with varying downstream multigene involvement would account for catatonia across the life span within some subtypes of autism spectrum disorders, schizophrenia, bipolar and major depressive disorder, psychosis, genetic disorders, and in immune disorders such as anti-N-methyl-d-aspartate receptor (NMDAR) antibody encephalitis as well as the susceptibility to the neuroleptic malignant syndrome (NMS) if environmentally triggered. Furthermore, SNORD115 genes may underlie a genetic vulnerability when environmental triggers result in excess serotonin producing the serotonin syndrome, a condition similar to NMS in which catatonia may occur. Dysfunction of SNORD115-PBRM1 connecting with SMARCA2 as well as other proven schizophrenia-associated genes might explain why traditionally catatonia has been classified with schizophrenia. SNORD115-TAF1 and SNORD-DPM2 dysfunction introduce possible clues to the parkinsonism and increased creatinine phosphokinase in NMS, while abnormalities of SNORD115-RALGPS1 suggest links to both anti-NMDAR encephalitis and the proven predisposing catatonic SHANK3 gene. The second hypothesis postulates that periodic catatonia (PC) on 15q15 involves abnormalities of vacuolar protein sorting 39 (VPS39), a proven de novo schizophrenic gene in this chromosomal locus and part of the HOPS complex. These will impact the autophagic and endocytic pathways, thereby lowering lysosomal degradation. VPS39 mutations may be considered also to disrupt lysosome-mitochondria tethering and transport of lipids and calcium through membrane contact sites (MCSs). To account for the periodicity in PC it is speculated that the mammalian equivalent of the vacuole and mitochondria patch (vCLAMP) would be altered by VPS39 mutations and subsequently followed by the mammalian equivalent of endoplasmic reticulum mitochondria encounter structure (ERMES) restoring mitochondrial homeostasis. Future precision psychiatry will require accurate pathophysiologically-defined psychiatric diagnoses to accelerate the discovery of specific molecular-targeted medications to improve therapeutic outcomes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Process


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