Increased serum adenosine deaminase activity in schizophrenic receiving antipsychotic treatment

Brunstein, Miriam Garcia; Silveira, Elza Maria Santos da; Chaves, Leticia Santos; Machado, H. A.; Schenkel, O.; Belmonte-de-Abreu, Paulo; Souza, Diogo O.; Lara, Diogo R.

doi:10.1016/j.neulet.2006.11.071

Cited by 30 publications

(32 citation statements)

References 22 publications

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“…By contrast, plasma reelin [94] , which is involved in the migration of neurons; and adenosine deaminase activity [95] , a homeostatic modulator that affects brain DA and glutamate activities, were higher in people with Sz. It is also of note that acute metabolic stress in the brain, induced by pharmacological doses of 2-deoxyglucose (2DG), a glucoprivic agent transported across the bloodbrain barrier into brain tissue where it inhibits intracellular glucose metabolism and produces a clinical state similar to hypoglycaemia [96] , appears to affect the peripheral vesopressinergic system via the pituitaryadrenal axis [96,97] .…”

Section: Other Neurochemicalsmentioning

confidence: 80%

“…In light of the tendency of people with psychiatric disorders, particularly Sz, to develop metabolic syn drome, several studies have examined molecules involved in glucose homeostasis [95,108113] . In a study where PBMC were stimulated ex vivo with staphylococcal enterotoxin B, eight out of total of 18 proteins examined were differentially expressed in cells from people with Sz who were first onset and drugnaive Sz compared to controls.…”

Section: Metabolismmentioning

confidence: 99%

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Biomarkers in schizophrenia: A focus on blood based diagnostics and theranostics

Lai

Scarr

Udawela

et al. 2016

WJP

140

108

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Identifying biomarkers that can be used as diagnostics or predictors of treatment response (theranostics) in people with schizophrenia (Sz) will be an important step towards being able to provide personalized treatment. Findings from the studies in brain tissue have not yet been translated into biomarkers that are practical in clinical use because brain biopsies are not acceptable and neuroimaging techniques are expensive and the results are inconclusive. Thus, in recent years, there has been search for blood-based biomarkers for Sz as a valid alternative. Although there are some encouraging preliminary data to support the notion of peripheral biomarkers for Sz, it must be acknowledged that Sz is a complex and heterogeneous disorder which needs to be further dissected into subtype using biological based and clinical markers. The scope of this review is to critically examine published blood-based biomarker of Sz, focusing on possible uses for diagnosis, treatment response, or their relationship with schizophreniaassociated phenotype. We sorted the studies into six categories which include: (1) brain-derived neurotrophic factor; (2) inflammation and immune function; (3) neurochemistry; (4) oxidative stress response and metabolism; (5) epigenetics and microRNA; and (6) transcriptome and proteome studies. This review also summarized the molecules which have been conclusively reported as potential blood-based biomarkers for Sz in different blood cell types. Finally, we further discusses the pitfall of current blood-based studies and suggest that a prediction model-based, Sz specific, blood World Journal of Psychiatry W J P oriented study design as well as standardize blood collection conditions would be useful for Sz biomarker development.

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Section: Other Neurochemicalsmentioning

confidence: 80%

Section: Metabolismmentioning

confidence: 99%

Biomarkers in schizophrenia: A focus on blood based diagnostics and theranostics

Lai

Scarr

Udawela

et al. 2016

WJP

140

108

View full text Add to dashboard Cite

show abstract

“…Therefore it is conceivable that the mechanisms regulating extracellular adenosine levels are impaired. In line with this, increased serum adenosine deaminase (ADA) activity, which converts extracellular adenosine into inosine, as well as low frequency of the low activity ADA allelic variant, has been reported in SZ patients [9,10]. Moreover, transgenic mice overexpressing adenosine kinase, a cytosolic ribokinase that phosphorylates the re-uptaken adenosine into 5′-adenosine monophosphate (AMP), show attention impairments linked to SZ, while adenosine augmentation exerts antipsychotic-like activity in mice [11].…”

Section: Introductionmentioning

confidence: 77%

Reduced striatal ecto-nucleotidase activity in schizophrenia patients supports the “adenosine hypothesis”

Aliagas

Villar-Menéndez

Sévigny

et al. 2013

Purinergic Signalling

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Schizophrenia (SZ) is a major chronic neuropsychiatric disorder characterized by a hyperdopaminergic state. The hypoadenosinergic hypothesis proposes that reduced extracellular adenosine levels contribute to dopamine D 2 receptor hyperactivity. ATP, through the action of ecto-nucleotidases, constitutes a main source of extracellular adenosine. In the present study, we examined the activity of ecto-nucleotidases (NTPDases, ecto-5′-nucleotidase, and alkaline phosphatase) in the postmortem putamen of SZ patients (n=13) compared with aged-matched controls (n=10). We firstly demonstrated, by means of artificial postmortem delay experiments, that ectonucleotidase activity in human brains was stable up to 24 h, indicating the reliability of this tissue for these enzyme determinations. Remarkably, NTPDase-attributable activity (both ATPase and ADPase) was found to be reduced in SZ patients, while ecto-5′-nucleotidase and alkaline phosphatase activity remained unchanged. In the present study, we also describe the localization of these ecto-enzymes in human putamen control samples, showing differential expression in blood vessels, neurons, and glial cells. In conclusion, reduced striatal NTPDase activity may contribute to the pathophysiology of SZ, and it represents a potential mechanism of adenosine signalling impairment in this illness.

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“…11 Our results showed that the G/A genotype with low activity was less frequent in schizophrenic patients (GG 95.4% and GA 4.6%) than in the general population (GG 88.3% and GA 11.7%). Interestingly, serum adenosine deaminase activity is increased in medicated schizophrenic patients, 14 but it remains to be established if this increase in related to the phenotype or to medication.…”

Section: Discussionmentioning

confidence: 99%

Lower frequency of the low activity adenosine deaminase allelic variant (ADA1*2) in schizophrenic patients

Dutra

Ottoni

Lara

et al. 2010

Rev. Bras. Psiquiatr.

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Objective: Adenosine may play a role in the pathophysiology of schizophrenia, since it modulates the release of several neurotransmitters such as glutamate, dopamine, serotonin and acetylcholine, decreases neuronal activity by pos-synaptic hyperpolarization and inhibits dopaminergic activity. Adenosine deaminase participates in purine metabolism by converting adenosine into inosine. The most frequent functional polymorphism of adenosine deaminase (22G→A) (ADA1*2) exhibits 20-30% lower enzymatic activity in individuals with the G/A genotype than individuals with the G/G genotype. The aim of this study was to evaluate the ADA polymorphism 22G→A (ADA1*2) in schizophrenic patients and healthy controls. Method: The genotypes of the ADA 22G→A were identified with allele-specific PCR strategy in 152 schizophrenic patients and 111 healthy individuals. Results: A significant decrease in the frequency of the G/A genotype was seen in schizophrenic patients (7/152 -4.6%) relative to controls (13/111 -11.7%, p = 0.032, OR = 2.6). Conclusion: These results suggest that the G/A genotype associated with low adenosine deaminase activity and, supposingly, with higher adenosine levels is less frequent among schizophrenic patients. 7%, p = 0,032,OR = 2,6 Descriptors

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Increased serum adenosine deaminase activity in schizophrenic receiving antipsychotic treatment

Cited by 30 publications

References 22 publications

Biomarkers in schizophrenia: A focus on blood based diagnostics and theranostics

Biomarkers in schizophrenia: A focus on blood based diagnostics and theranostics

Reduced striatal ecto-nucleotidase activity in schizophrenia patients supports the “adenosine hypothesis”

Lower frequency of the low activity adenosine deaminase allelic variant (ADA1*2) in schizophrenic patients

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