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The neurodevelopmental hypothesis defends the existance of factors that would cause an early impairment on the normal brain development. The neurodegenerative hypothesis proposes the existance of later and progressive pathological phenomena, responsible of the appearance of clinical manifestations and changes on neuroimaging. Both hypotheses would be complementary. Neurodevelopment is completed during adolescence. Within this period, these deficts on executive functions would become apparent, reflecting a neurodevelopmental impairment. Glutamate is the main excitatory neurotransmitter, present throughout the normal postnatal brain development and maduration. In schizophrenic patients and unaffected relatives, a glutamatergic hypofunction has been found and so, an alteration of the dopaminergic mesocortical limbic and nigrostriatal pathways.
Usage of molecules that are capable of reversing the glutamatergic hypofunction would be potentially benefitial for either positive or negative symptomathology in schizophrenia.
We have performed a review of several clinical trials (on humans and animals) using glutamatergic drugs alone and combined with neuroleptics to diminish behavioural disturbances related to NMDA blockage.
Usage of glycine binding site agonists (glycine, D- cicloserine, D-serine) has been proposed. D-serine is effective both as monotherapy and combined with neuroleptics. D-cicloserine is not effective on negative symptoms. Usage of high doses of oral glycine (30–60 mg a day) on its own has not shown any clinical change but there is an improvement on negative and positive symptoms if combined with neuroleptics.
Nowadays, there is no glutamatergic agonist used in schizophrenia treatment. Out of the three previously mentioned drugs, only D-serine has shown some efficacy.
Natural polyamines (putrescine, spermidine and spermine) are low molecular weight highly protonated aliphatic molecules that physiologically modulate NMDA, AMPA/kainate glutamatergic receptors and limbic dopaminergic neurotransmission. Previous studies had demonstrated that polyamine metabolism might be disrupted in schizophrenia, what could potentially be linked to glutamatergic dysfunction. In particular, polyamine levels in blood and fibroblast cultures from patients with schizophrenia had previously been found to be higher than in healthy controls. Indeed, a significant positive correlation between blood polyamine levels and severity of illness may exist.
In order to test potential differences in blood polyamine levels between drug-free schizophrenia in-patients (n = 12), and healthy controls (n = 26, blood donors), spermidine (spd), spermine (spm), and spermidine/spermine index (spd/spm) were determined using HPLC after dansylation.
No significant differences were found between groups (t = 0,974; df = 36; P = 0,337 for spd, t = l0, 52; df = 36; P = 0,959 for Spm, and, t = 0, 662; df = 36; P = 0,512 for spd/spm).
Though we couldn’t replicate previous findings suggesting disturbances in blood polyamine levels in schizophrenia, this issue may be a promising target. Future research should take into account possible factors such as sex, nutritional state, and stress.
A growing interest in the potential role of polyamines in stress, mood disorders and suicidal behavior has recently emerged. In particular, the expression of polyamine's rate-limiting catabolic enzyme (SAT-1, Spermidine/spermine N1-acetyltransferase-1) may be reduced in ventral prefrontal cortex and posterior cyngulate gyrus of patients who committed suicide. However, there is some controversy regarding the involvement of potential cis-acting loci controlling SAT-1 gene expression (rs6526342 or rs17286006) in suicidal behavior. Moreover, a significant association between SAT-1 rs1960264 SNP and anxiety disorders has been found in a male caucasian spanish sample.
In order to test the potential association of SAT-1 -1415T/C SNP (rs1960264) with suicidal behavior, genotype frequencies for that SNP were compared between 193 suicidal attempters (126 female and 67 male) and 650 non-suicidal patients (314 female and 336 male) from an in-patient sample.
We could not find a significant difference in the distribution of the genotypes for rs1960264 SNP between suicide attempters versus non-suicidal individuals (Linear-by-Linear association X2 = 0,203; df = 1; P = 0,652, females; Linear-by-Linear association X2 = 0,000; df = 1; P = 0,990, males). Neither could we demonstrate a relationship between rs1960264 genotype and past history of suicidal attempts (Linear-by-Linear association X2 = 2,966 ; df = 1; P = 0,085, females; Linear-by-Linear association X2 = 1,171; df = 1; P = 0,279, males).
Although we did not find a link between rs1960264 genotype and suicidal behavior, SAT-1 may be an interesting target to investigate the biology of this phenotype. Future studies should take into account other genetic polymorphisms at SAT-1, and definitively evaluate whether or not rs6526342 and rs1960264 have any functional implications.
Ramón y Cajal Hospital is the reference centre for Madrid-Barajas airport. Passengers at the airport who need medical assistance are brought to this hospital. A percentage of these passengers require psychiatric evaluation and frequently need to stay inward for a certain term.
Calculate the approximate costs derived from the inward stay at the Psychiatry ward of patients referred from Madrid-Barajas airport.
Revise retrospectively clinical histories of inward psychiatric patients referred from Barajas airport in the last 5 years. The Department of Economic management of the hospital has provided the costs of stay at the Psychiatry ward for the year 2007 (395 euros per day). Data is analyzed using the SPSS software 15.0 version.
The average stay of these patients is 13.96 days. Then, the average cost is 5514.2 euros. Extrapolating these data to our sample, we notice that being the reference centre for an international airport supposes an estimated cost of 545.905.8 euros (109181.16 per year) due to inward stay of psychiatric patients.
The psychiatric attention to the airport population represents an economic extra charge that has an impact on the hospital and the National Health System. We only expose the charge derived from inward stay. To obtain a more realistic overall result we should add the costs of the attention at the emergency room to the result above.
N-acetil-aspartate (NAA) is located inside the soma and dendrites. Its believed to be an indirect indicator of the metabolic activity of these cells. Phosphomonoesters (PME) are involved in synthesis of neuronal membranes and phosphodiesters (PDE) in its degradation. Glutamine, an aminoacid produced by glial cells, is transported into the neurone for its transformation into glutamate and gamma aminobutyric acid.
Review clinical trials performed on schizophrenic patients with SF-MRI, with 31P y 1H, to measure concentration of NAA, PME, PDE and glutamine.
Detecting chemichal alterations that could be used as indicators in schizophrenia.
NAA concentration in temporal and frontal cortex of schizophrenic patients, are significantly lower than in healthy controls. In other trials, differences in NAA concentration (measured in prefrontal cortex) have not been found, comparing patients during their first psychotic episode and healthy controls. Lowered concentrations of PME and increased ones of PDE in prefrontal cortex of schizophrenic patients have been found. Glutamine levels are increased in schizophrenic patients, being directely correlated with the duration of the process. These levels are reduced when antipsychotic drugs are used.
The decrease on NAA levels at schizophrenia onset and on healthy relatives remark its value as an endophenotypical indicator, but not as an illness indicator. Changes on PME and PDE concentrations cannot be used as illness indicators. The increase on glutamine synthesis could be due to glutamatergic hypofunction in schizophrenic patients, but there are other factors that may cause it, so it cannot be used as an indicator.
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