Elevated Serum Levels of Homocysteine as an Early Prognostic Factor of Psychiatric Disorders in Children and Adolescents

Abstract

Background and Goal. The aim was to examine the serum levels of homocysteine (Hcy) and their associations with the methylenetetrahydrofolate reductase (MTHFR) gene C677T polymorphism in patients with schizophrenia and mood disorders as well as controls. Materials and Methods. There were 198 patients: 82 with schizophrenia spectrum disorders, 22 with mood disorders, and 94 controls. The level of Hcy was determined by an isocratic high-performance liquid chromatography system. MTHFR C677T polymorphism was analysed using the restriction fragment length polymorphism-polymerase chain reaction method. Results. The average level of Hcy was 11.94 ± 5.6 μmol/L for patients with schizophrenia, 11.65 ± 3.3 μmol/L for patients with affective disorders, versus 6.80 ± 2.93 μmol/L in a control. The highest level of Hcy has been observed in patients with episodic-recurrent course of schizophrenia (11.30 ± 7.74 μmol/L), paranoid schizophrenia continuous (12.76 ± 5.25 μmol/L), and in patients with affective disorders (11.65 ± 3.26 μmol/L). An association between the MTHFR gene C677T polymorphism and Hcy level was found by linear regression analysis (r = 1.41, P = 0.029). Conclusions. The data indicate a link between Hcy levels and schizophrenia and mood disorders. No associations between the level of Hcy in patients with schizophrenia and mood disorders and the MTHFR C677T polymorphism were found.

Homocysteine levels in schizophrenia patients newly admitted to an acute psychiatric ward

“…The polymorphic variant of the methylenetetrahydrofolate reductase gene (C677T) is responsible for hyperhomocysteinaemia due to a 70% reduction of enzyme activity (4). Some authors have hypothesised that this condition may represent a risk factor for schizophrenia (5)(6)(7), although others have not confirmed this (8)(9)(10). According to Vares et al (11), the C677T genetic variant could be responsible for an earlier onset of schizophrenia in selected populations.…”

Current and Emergent Treatments for Symptoms and Neurocognitive Impairment in Schizophrenia

“…Although management of diet and lifestyle is not sufficient of itself to control schizophrenia, nevertheless, attention to these aspects may optimize brain function, improve quality of life and reduce excess mortality [1, 2] commonly associated with schizophrenia. Efficacy of exercise in schizophrenia is supported by randomized, controlled clinical trials [3]Exercise-induced increases in hippocampal volume in schizophrenia are linked to improved short-term memory [4]Genetically based disturbances in folate metabolism may also be linked to negative symptoms [5], age of onset [6], and risk for weight gain [7]; metabolic syndrome [8]Elevated homocysteine levels [9, 10] may increase oxidative stress [11] and lead to inhibition of NMDAR-mediated neurotransmission [12]Genetic dysregulation of glutathione synthesis may also lead to increased brain oxidative stress [13]Treatment with folic acid + vitamin B12 may lead to improved negative symptoms in individuals with genetic alterations in folate absorption [14, 15] …”

“…Elevated homocysteine levels [9, 10] may increase oxidative stress [11] and lead to inhibition of NMDAR-mediated neurotransmission [12]…”

Serum Level of Homocysteine and Perinatal CNS Lesions in Infants

“…(3) Elevated Hcy is associated with an increased risk of occlusive vascular disease, birth defects (neural tube defects), complications during pregnancy, and psychiatric disorders. (4,5) Hcy influences the fetus in the early stages, through disordered brain structure development and function, and/or through placenta vascularization disorders, which reduces the oxygen feed to the fetus. (6) Hyperhomocysteinemia may arise from genetic defects of enzymes involved in homocysteine metabolism.…”