Diagnostic Interview for Genetic Studies

Nürnberger, John I.; Blehar, Mary C.; Kaufmann, Charles A.; York-Cooler, Carolyn; Simpson, Sylvia G.; Harkavy‐Friedman, Jill; Severe, Joanne B.; Malaspina, Dolores; Reich, Theodore

doi:10.1001/archpsyc.1994.03950110009002

Cited by 1,880 publications

(485 citation statements)

References 47 publications

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“…The relationship between depression and hippocampal size, however, is controversial. While some MRI studies (Nurnberger et al 1994;Sheline et al 1996) reported significantly reduced hippocampal volumes in major depression, other studies found no reduction (Axelson et al 1993b;Vakili et al 2000), although depression severity and treatment response correlated with hippocampal size (Vakili et al 2000). In conclusion, there remain questions concerning the role of potential confounding variables in the previously reported MRI data in PTSD.…”

Section: Discussionmentioning

confidence: 90%

Decreased hippocampal N-acetylaspartate in the absence of atrophy in posttraumatic stress disorder

Schuff

Neylan

Lenoci

et al. 2001

Biological Psychiatry

226

155

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Background-Previous magnetic resonance imaging studies of posttraumatic stress disorder reported hippocampal volume loss. The goals of this study were 1) to determine the relationship between hippocampal atrophy and posttraumatic stress disorder in the absence of alcohol abuse, and 2) to test if loss of N-acetylaspartate (a neuron marker) in the hippocampus of posttraumatic stress disorder occurs separate from atrophy. In addition, volume changes in the entorhinal cortex were also explored.

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Section: Discussionmentioning

confidence: 90%

Decreased hippocampal N-acetylaspartate in the absence of atrophy in posttraumatic stress disorder

Schuff

Neylan

Lenoci

et al. 2001

Biological Psychiatry

226

155

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“…For the at‐risk cohort, proband consensus DSM‐IV diagnoses were determined by two independent psychiatrists using best estimate methodology [Leckman et al, 1982], using information from an adapted version of the Schedule for Affective Disorders and Schizophrenia for School‐Age Children—Present and Lifetime Version (K‐SADS‐BP) [Kaufman et al, 1997; Geller et al, 2001], the Diagnostic Interview for Genetic Studies (DIGS) Version 4 [Nurnberger et al, 1994], the Family Interview for Genetic Studies (FIGS) [Maxwell, 1992], and medical records (where available). For participants under the age of 22, the K‐SADS‐BP was administered as the diagnostic instrument.…”

Section: Methodsmentioning

confidence: 99%

Assessment of first and second degree relatives of individuals with bipolar disorder shows increased genetic risk scores in both affected relatives and young At‐Risk Individuals

Fullerton

Koller

Edenberg

et al. 2015

American J of Med Genetics Pt B

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Recent studies have revealed the polygenic nature of bipolar disorder (BP), and identified common risk variants associated with illness. However, the role of common polygenic risk in multiplex families has not previously been examined. The present study examined 249 European‐ancestry families from the NIMH Genetics Initiative sample, comparing subjects with narrowly defined BP (excluding bipolar II and recurrent unipolar depression; n = 601) and their adult relatives without BP (n = 695). Unrelated adult controls (n = 266) were from the NIMH TGEN control dataset. We also examined a prospective cohort of young (12–30 years) offspring and siblings of individuals with BPI and BPII disorder (at risk; n = 367) and psychiatrically screened controls (n = 229), ascertained from five sites in the US and Australia and assessed with standardized clinical protocols. Thirty‐two disease‐associated SNPs from the PGC‐BP Working Group report (2011) were genotyped and additive polygenic risk scores (PRS) derived. We show increased PRS in adult cases compared to unrelated controls (P = 3.4 × 10−5, AUC = 0.60). In families with a high‐polygenic load (PRS score ≥32 in two or more subjects), PRS distinguished cases with BPI/SAB from other relatives (P = 0.014, RR = 1.32). Secondly, a higher PRS was observed in at‐risk youth, regardless of affected status, compared to unrelated controls (GEE‐χ2 = 5.15, P = 0.012). This report is the first to explore common polygenic risk in multiplex families, albeit using only a small number of robustly associated risk variants. We show that individuals with BP have a higher load of common disease‐associated variants than unrelated controls and first‐degree relatives, and illustrate the potential utility of PRS assessment in a family context. © 2015 The Authors. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics Published by Wiley Periodicals, Inc.

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“…In addition, there is a lower threshold for NMDA receptor antagonist mediated neurotoxicity in female rats (Olney et al 1989) and this study sought a maximum safety margin (see Ketamine Dosing and Safety Considerations below). Sub-jects were interviewed using the Diagnostic Instrument for Genetic Studies (Nurnberger et al 1994). A senior clinician reviewed all data to determine whether subjects met criteria for any DSM-IV diagnoses.…”

Section: Subjectsmentioning

confidence: 99%

“…A senior clinician reviewed all data to determine whether subjects met criteria for any DSM-IV diagnoses. Subjects were also interviewed with the Family Instrument for Genetic Studies (Nurnberger et al 1994) in order to identify relevant psychopathology within first degree relatives; none was detected in this sample.…”

Section: Subjectsmentioning

confidence: 99%

Ketamine-Induced NMDA Receptor Hypofunction as a Model of Memory Impairment and Psychosis

Newcomer

Farber

Jevtović-Todorović

et al. 1999

Neuropsychopharmacology

546

350

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Considerable research interest has recently been focused on the role of glutamate and related neural circuitry in the neurobiology of schizophrenia. The results of these investigations have emphasized hypofunction of glutamatergic neurons and/or the N-methyl-D-aspartate (NMDA) glutamate receptor (Tsai et al. 1995;Kim et al. 1980aKim et al. , 1980bSherman et al. 1991;Deutsch et al. 1989;Javitt and Zukin 1991;Olney 1988a;Olney 1988b;Olney and Farber 1995). An important element of several of these theoretical positions is that NMDA receptor hypofunction (NRH) produced by any mechanism can be psychotogenic. This has renewed interest in the clinical effects of NMDA glutamate receptor antagonists.Ketamine and phencyclidine (PCP) are non-competitive NMDA glutamate receptor antagonists (Zukin and Zukin 1979;Vincent et al. 1979;Lodge and Anis 1982;Lodge et al. 1987) which can produce a transient state of NRH in the brain. Early investigators characterized a PCP-induced clinical syndrome of schizophrenia-like Received March 18, 1998; revised June 19, 1998; accepted June 29, 1998. N EUROPSYCHOPHARMACOLOGY 1999 -VOL . 20 , NO . 2 NMDA Receptor Hypofunction Induced Memory Decrease 107 symptoms, including hallucinations, delusions, idiosyncratic and illogical thinking, poverty of speech and thought, agitation, disturbances of emotion, affect, withdrawal, decreased motivation, and dissociation (Johnstone et al. 1959;Luby et al. 1959;Rosenbaum et al. 1959;Luby et al. 1962;Corssen and Domino 1966;Bakker and Amini 1961;Davies and Beech 1960;Domino and Luby 1981). This PCP-induced syndrome can be indistinguishable from acute presentations of schizophrenia (Yesavage and Freeman 1978;Erard et al. 1980). Ketamine, a PCP analog still used in human anesthesia, has been reported to cause reactions similar to but not as severe as those caused by PCP, including brief, reversible "positive" and "negative" schizophrenia-like symptoms (Krystal et al. 1994;Malhotra et al. 1996). Both PCP and ketamine can exacerbate psychosis in schizophrenia Luby et al. 1962;Lahti et al. 1995a;Lahti et al. 1995b;Malhotra et al. 1997).Declarative, explicit or secondary memory and learning deficits in patients with schizophrenia occur early in the course of the illness and are quantitatively large compared with deficits in other differentiated elements of cognitive performance, showing stability "on" versus "off" antipsychotic medication and over repeated testing (Gruzelier et al. 1988;Saykin et al. 1991Saykin et al. , 1994Cannon et al. 1994). Clinical and preclinical investigations suggest the hypothesis that changes in NMDA glutamate receptor activity in patients with schizophrenia may be causally related to memory impairments found in this disorder. Relevant to this hypothesis, the activation of post-synaptic NMDA receptors is important for the induction of the activity-dependent synaptic modification called long-term potentiation (LTP) (Bliss and Collingridge 1993;Collingridge and Bliss 1995), and hippocampal LTP has been postulated to underlie cert...

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Diagnostic Interview for Genetic Studies

Cited by 1,880 publications

References 47 publications

Decreased hippocampal N-acetylaspartate in the absence of atrophy in posttraumatic stress disorder

Decreased hippocampal N-acetylaspartate in the absence of atrophy in posttraumatic stress disorder

Assessment of first and second degree relatives of individuals with bipolar disorder shows increased genetic risk scores in both affected relatives and young At‐Risk Individuals

Ketamine-Induced NMDA Receptor Hypofunction as a Model of Memory Impairment and Psychosis

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