Angiotensin‐Converting Enzyme Modulates Dopamine Turnover in the Striatum

Jenkins, Trisha A.; Mendelsohn, Frederick A.O.; Chai, Siew Yeen

doi:10.1046/j.1471-4159.1997.68031304.x

Cited by 92 publications

(47 citation statements)

References 43 publications

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“…Central ACE plays an important role in catalyzing the release of dipeptide from a variety of substrates and can modulate dopamine activity [1,2]. It has long been considered a pathogenetic candidate for schizophrenic disorders; however, previous reports investigating ACE levels for schizophrenia have been inconsistent.…”

Section: Discussionmentioning

confidence: 99%

“…Renin catalyzes the formation of angiotensin I, which is further converted into angiotensin II by angiotensin-converting enzyme (ACE) [1], which also catalyzes the degradation of substance P and other peptides. In addition, animal study has demonstrated that ACE mod- Ouyang/Wang/Hong/Cheng/Tsai ulates dopamine turnover in the midbrain [2]. Thus, the ACE gene may have pleitrophic effects within the central nervous system.…”

Section: Introductionmentioning

confidence: 99%

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Association Study of Angiotensin-Converting Enzyme Gene Polymorphism with Schizophrenia and Polydipsia

Ouyang¹,

Wang

Cheng

et al. 2001

Neuropsychobiology

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Angiotensin-converting enzyme (ACE) is a key enzyme in the renin-angiotensin system and can modulate dopamine turnover in the midbrain. Previous studies have revealed changes in the central ACE levels for schizophrenic patients, possibly related to the polydipsia commonly demonstrated for chronic schizophrenia. An insertion (I)/deletion (D) polymorphism of the ACE gene has been associated with ACE levels. Therefore, we elected to investigate the ACE I/D polymorphism for 124 schizophrenic patients and 117 control subjects. No significant differences for the genotype distribution or the allele frequency were revealed comparing controls and schizophrenic patients. The ACE genotypes were not associated with onset age or psychiatric symptoms for the schizophrenic cases. A modest association was revealed for this ACE polymorphism and polydipsia diagnosis for these patients. Using bearers of the D allele as baseline, the ratio for I/I homozygote was 2.31 (95% CI 0.95–5.65). This association needs further replication as it may have implications for the pathogenesis and the treatment of polydipsia for schizophrenic patients.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Association Study of Angiotensin-Converting Enzyme Gene Polymorphism with Schizophrenia and Polydipsia

Ouyang¹,

Wang

Cheng

et al. 2001

Neuropsychobiology

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“…This system has previously been thought to be involved in schizophrenia as well as other disorders [40,54,55]. Angiotensin II is a neurotransmitter that communicates with dopaminergic systems in the brain and is hypothesized to be important for normal thought processes [56,57].…”

Section: The Unbiased Screening Of the Genomementioning

confidence: 99%

The Sex Chromosome Hypothesis of Schizophrenia: Alive, Dead, or Forgotten? A Commentary and Review

Bache

DeLisi

2018

Complex Psychiatry

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The X chromosome has long been an intriguing site for harboring genes that have importance in brain development and function. It has received the most attention for having specific genes underlying the X-linked inherited intellectual disabilities, but has also been associated with schizophrenia in a number of early studies. An X chromosome hypothesis for a genetic predisposition for schizophrenia initially came from the X chromosome anomaly population data showing an excess of schizophrenia in Klinefelter’s (XXY) males and triple X (XXX) females. Crow and colleagues later expanded the X chromosome hypothesis to include the possibility of a locus on the Y chromosome and, specifically, genes on X that escaped inactivation and are X-Y homologous loci. Some new information about possible risk loci on these chromosomes has come from the current large genetic consortia genome-wide association studies, suggesting that perhaps this hypothesis needs to be revisited for some schizophrenias. The following commentary reviews the early and more recent literature supporting or refuting this dormant hypothesis and emphasizes the possible candidate genes still of interest that could be explored in further studies.

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“…11 The evidence about an involvement of the brain renin-angiotensin system in regulation of mood is based on several observations, as eg the co-localisation of angiotensin with dopamine synthesising neurones, 12 the fact that angiotensin converting enzyme (ACE) is involved in the metabolism of the neuropeptide substance P, which in turn is supposed to play a role in depression, 13 as well as the clinical observation that the application of ACE inhibitors in hypertensives might induce euphoric or depressive states. 14,15 Further, an animal study with angiotensinogen-deficient mice showed a reduction in depressive-like behaviour.…”

mentioning

confidence: 99%

Combined action of the ACE D- and the G-protein β3 T-allele in major depression: a possible link to cardiovascular disease?

Bondy¹,

Baghai²,

Zill³

et al. 2002

Mol Psychiatry

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Although it is well established that depression is a major risk factor for the development of coronary artery disease and that cerebrovascular disease can be a major contributing factor for the development of depression, the information about the interplay between the central nervous system and cardiovascular disease is still limited. We investigated the angiotensin I converting enzyme (ACE) ID and the G-protein ␤3-subunit (G␤3) C825T polymorphism in 201 patients with unipolar major depression and 161 ethnically and age-matched controls. Both gene variants have earlier been associated with either cardiovascular disease or affective disorders, making them good candidates for a combined analysis. We found a significant increase in the G␤3 T allele (OR = 1.61, 95% CI 1.17-2.2, P = 0.0035) and a marginal altered genotype distribution of the ACE ID polymorphism with decrease in the II genotypes ( 2 = 6.43, df=3, P = 0.04) in the patients' group. Analysing the data for both genes we found that the combined actions of ACE and G␤3 genotypes accumulate in carriers of the ACE D allele (ID and DD) and G␤3 TT homozygotes with ID/DD-TT carriers showing a more than five-fold increase in risk for major depression (crude OR = 5.83, 95% CI 1.99-17.08, P = 0.0002). As our study was carried out with depressive patients without serious cardiac impairment at the time of the investigation, we are presently unable to predict whether this combined action of the ACE ID/DD-G␤3 TT genotype is increasing the risk for both disorders. Nevertheless our study reports for the first time that the same allelic combination of two genes that have been shown to increase the risk for myocardial infarction (Naber et al, 2000) increase the vulnerability for depressive disorder.

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Angiotensin‐Converting Enzyme Modulates Dopamine Turnover in the Striatum

Cited by 92 publications

References 43 publications

Association Study of Angiotensin-Converting Enzyme Gene Polymorphism with Schizophrenia and Polydipsia

Association Study of Angiotensin-Converting Enzyme Gene Polymorphism with Schizophrenia and Polydipsia

The Sex Chromosome Hypothesis of Schizophrenia: Alive, Dead, or Forgotten? A Commentary and Review

Combined action of the ACE D- and the G-protein β3 T-allele in major depression: a possible link to cardiovascular disease?

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