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R R Crowe

Publications and source records attributed to R R Crowe.

At least 19 recordsLinked to original sources
PubMed1992

Alpha 2 adrenergic receptor subtypes in depression: a candidate gene study.

Alpha 2 adrenergic receptors play an important role in regulating the neuronal release of norepinephrine through presynaptic feedback inhibition in the locus ceruleus. Therefore, alpha 2 adrenergic autoreceptors may underlie some aspects of the pathogenesis and symptomatic expression of depressive illness. We studied two brain-expressed alpha 2 adrenergic receptor genes as genetic markers in linkage analyses in 17 multiplex pedigrees of unipolar depression. Neither of the genes was supportive of linkage to depression. Lod scores of less than -2 were found in both familial pure depressive disease pedigrees and in depression spectrum disease pedigrees. Therefore, we conclude that depression in our pedigrees is not related to mutations in the two alpha 2 adrenergic receptor genes tested.

Adult↗
PubMed1992

Alcoholism and the D2 receptor gene.

The allelic association of the human dopamine D2 receptor gene and alcoholism was evaluated in 20 male alcoholics and 20 controls (sex, race, and geographic place of birth matched). This study further examines the issue of alcoholism severity and A1 allele frequency. No difference in A1 allele frequency was observed between these two groups. Similarly, no relationship between alcoholism severity and A1 frequency within the alcoholics was demonstrated.

Adult↗
PubMed1992

Adrenergic receptor genes as candidate genes for panic disorder: a linkage study.

OBJECTIVE: Several lines of investigation suggest that the noradrenergic neurotransmitter system may be involved in the pathogenesis of panic disorder. Since a mutation in a gene coding for one of the adrenergic receptors could account for both the familial nature and autonomic dysfunction of panic disorder, the authors performed analyses of the linkage between panic disorder and five adrenergic receptor loci. METHOD: The subjects were 14 multiplex pedigrees with DSM-III panic disorder or agoraphobia with panic attacks. The loci tested were the alpha 1/beta 2 pair on chromosome 5q32-q34, the alpha 2/beta 1 pair on chromosome 10q24-q26, and a second alpha 2 locus on chromosome 4. Flanking loci were included in the analysis on chromosomes 5 and 10 to increase the informativeness of the adrenergic receptor loci. RESULTS: Lod scores less than -2.0 were found at all five receptor loci. CONCLUSIONS: These findings provide strong evidence against the possibility that genetic mutation at any of these loci is responsible for panic disorder in these pedigrees.

Adolescent↗
PubMed1991

Lack of linkage to chromosome 5q11-q13 markers in six schizophrenia pedigrees.

We examined linkage between schizophrenia and five genetic markers on chromosome 5 in six pedigrees. Analyses were run considering the affected phenotype to be schizophrenia, schizophrenia plus a spectrum of related disorders, and these disorders plus any axis I diagnosis. None of the analyses were suggestive of linkage at any of the markers, either considering the pedigrees individually or in the aggregate. In our pedigrees, multipoint linkage analyses excluded much of the region that had supported linkage in an earlier study. These findings are consistent with other attempts to replicate the chromosome 5 linkage finding.

Chromosome Mapping↗
PubMed1991

Close linkage of esterase-D to unipolar depression and alcoholism is ruled out in eight pedigrees.

Unipolar depression and alcoholism were tested for genetic linkage to esterase-D at 13q14.1. Tight linkage to esterase-D was ruled out for three phenotypes using three models of penetrance: (1) unipolar depression and alcoholism taken together as affected, (2) unipolar depression alone as affected with alcoholism considered unaffected and (3) alcoholism alone as affected with unipolar depression considered unaffected. This study does not support an earlier finding of possible linkage between the esterase-D locus at 13q14.1 and alcoholism.

Adolescent↗
PubMed1990

Close linkage between panic disorder and alpha-haptoglobin excluded in 10 families.

We previously reported a lod score of 2.3 suggesting linkage between panic disorder and the alpha-haptoglobin locus on chromosome 16q22 in 26 pedigrees. In the present study we tested for linkage between alpha-haptoglobin and panic disorder in 10 new pedigrees and excluded a gene for panic disorder from 6 centimorgans (recombination fraction, 0.06) surrounding the alpha-haptoglobin locus. The data were analyzed under a variety of assumptions about the transmission of panic disorder, and linkage was excluded by all genetic models but one. When lod scores from the present set of 10 pedigrees were pooled with those from the first 26, no evidence of genetic heterogeneity was found, and the maximum lod score was 0.67 at a recombination fraction of 0.17. Taken as a whole, the present findings do not support the presence of a disease gene for panic disorder closely linked to the alpha-haptoglobin locus on chromosome 16q22.

Adult↗
PubMed1990

Linkage of c-Harvey-ras-1 and INS DNA markers to unipolar depression and alcoholism is ruled out in 18 families.

Eighteen families informative for c-Harvey-ras-1 and INS DNA markers were tested for linkage to unipolar depression and alcoholism. No evidence of linkage was found between these DNA markers and the disorders observed in the families. This study fails to replicate the Old Order Amish Study and suggests that a significant degree of genetic heterogeneity may be present among psychiatric disorders.

Adolescent↗
PubMed1990

The Iowa multiplex family study of schizophrenia: linkage analyses on chromosome 5.

We analysed six multiplex pedigrees of schizophrenia for linkage to two DNA probes mapping to the chromosome 5q11-q13 region where linkage to a gene for schizophrenia was recently reported. Analyses were conducted using three penetrance models and considering the affected state to be schizophrenia, the schizophrenia spectrum, and all psychiatric diagnoses. All analyses gave consistently negative lod scores. Although the region was not formally excluded, no evidence for linkage was found.

Chromosomes, Human, Pair 5↗
PubMed1990

Panic disorder: genetic considerations.

Panic disorder is a common illness that can have serious consequences, including increased long-term mortality. Family and twin studies suggest that it is a genetic disorder and transmission patterns within families are compatible with a hypothesis of a disease gene predisposing to the condition. Recently, it has become possible to locate disease genes causing familial disorders through linkage analysis. A preliminary linkage analysis of panic disorder at the University of Iowa found suggestive but inconclusive evidence of linkage to the alpha-haptoglobin locus on chromosome 16q22. Future strategies for identifying disease genes in anxiety disorders are described.

Anxiety Disorders↗
PubMed1990

The application of genetic methods to the study of disease associations in psychiatry.

The problem of multiple diagnoses in the same patient is a very real one in psychiatry. Theoretical causes of disease associations are reviewed and illustrated with examples from a variety of psychiatric conditions. These include Huntington's disease and depression, mitroprolapse and panic attacks, anxiety disorder and depression, and others.

Agoraphobia↗
PubMed1988

Reliability of the telephone interview in diagnosing anxiety disorders.

The reliability of psychiatric diagnosis using the Schedule of Affective Disorders and Schizophrenia-Lifetime Version in personal and telephone interviews with 39 subjects was assessed using a 12- to 19-month test-retest design. Interrater reliability was high (kappa, .69 to .84) for the diagnosis of panic disorder, agoraphobia with panic attacks, probable panic disorder, major depression, and alcohol abuse. We conclude that it is possible to reliably make these lifetime diagnoses in a family study using the telephone interview.

Agoraphobia↗
PubMed1988

Delusional disorder: jealous and nonjealous types.

We studied the records of 101 patients with delusional disorder admitted to the Psychiatric Hospital between 1920 and 1980 and divided the sample into those with jealous (43) and those with nonjealous (58) delusions. Patients and relatives were located by telephone and follow-up information was collected. Compared with the nonjealous patients, the jealous ones were more likely to have had a single delusion, and to have experienced a more benign course as indicated by a lower rate of hospitalization and outpatient treatment. The original delusion tended to remain and the illness did not develop into another form of delusional disorder or other psychiatric illness.

Adult↗
PubMed1988

Chromosomal localization of the human diazepam binding inhibitor gene.

We have used in situ chromosome hybridization and human-mouse somatic cell hybrids to map the gene(s) for human diazepam binding inhibitor (DBI), an endogenous putative modulator of the gamma-aminobutyric acid receptor acting at the allosteric regulatory center of this receptor that includes the benzodiazepine recognition site. In 784 chromosome spreads hybridized with human DBI cDNA, the distribution of 1476 labeled sites revealed a significant clustering of autoradiographic grains (11.3% of total label) on the long arm of chromosome 2 (2q). Furthermore, 63.5% of the grains found on 2q were located on 2q12-21, suggesting regional mapping of DBI gene(s) to this segment. Secondary hybridization signals were frequently observed on other chromosomes and they were statistically significant mainly for chromosomes 5, 6, 11, and 14. In addition, DNA from 32 human-mouse cell hybrids was digested with BamHI and probed with human DBI cDNA. A 3.5-kilobase band, which probably represents the human DBI gene, was assigned to chromosome 2. Four higher molecular weight bands, also detected in BamHI digests, could not be unequivocally assigned. A chromosome 2 location was excluded for the 27-, 13-, and 10-kilobase bands. These results assign a human DBI gene to chromosome 2 (2q12-21) and indicate that three of the four homologous sequences detected by the human DBI probe are located on three other chromosomes.

Animals↗
PubMed1987

A linkage study of panic disorder.

We tested for linkage between panic disorder and a battery of 29 genetic markers in 26 families. Linkage between panic disorder and 18 of the marker loci could be excluded at a recombination fraction of 0.00, nine at a recombination fraction of 0.05, and four at a recombination fraction of 0.10. The 18 loci are distributed over ten chromosomes. One locus was suggestive of linkage. The maximum lod score for alpha-haptoglobin was 2.27 at a recombination fraction of 0.0, representing odds in favor of linkage of 186.1. alpha-Haptoglobin has been mapped to chromosome 16q22. The results demonstrate that linkage studies of psychiatric disorders can yield informative results by identifying tentative linkages that merit further investigation and by excluding regions of the genome from future linkage searches.

Adult↗