N-Terminal pro-Brain Natriuretic Peptide, Homocysteine and Methylenetetrahydrofolate Reductase Gene Polymorphism in Elderly Depressed and Mild Cognitive Impairment Patients | ||||
Bulletin of Egyptian Society for Physiological Sciences | ||||
Article 5, Volume 28, Issue 2, December 2008, Page 61-80 PDF (245.44 K) | ||||
Document Type: Original Article | ||||
DOI: 10.21608/besps.2008.37030 | ||||
![]() | ||||
Authors | ||||
Manal El-Batch* 1; Mai Eissa2; Gihan Farouk3; Mohamed Attia3 | ||||
1Medical Biochemistry Department, Faculty of Medicine , Tanta University | ||||
2Neuropsychiatry Department, Faculty of Medicine , Tanta University | ||||
3Clinical Pathology Department, Faculty of Medicine , Tanta University | ||||
Abstract | ||||
There is increasing evidence that vascular disease contributes to cognitive impairment and depression. Secretion of N-Terminal pro-Brain Natriuretic Peptide (NT-proBNP) increases in several cardiac illnesses, mak ing this neurohormone a reliable diagnostic and prognostic biomark er of cardiovascular risk . Homocysteine (Hcy) is harmful to neurons and blood vessels, including the cerebral microvasculature. It is possible that such effects contribute to the cascade of events that leads to cognitive decline, dementia, and depression in later life. Hcy is produced during the metabolism of the essential amino-acid methionine, its plasma level can be influenced by factors such as vitamin deficiency, renal function, and a common mutation in the methylenetetrahydrofolate reductase (MTHFR) gene, where cytosine is replaced by thymine (C→T) at nucleotide position 677. The aim of the present study was to evaluate the role of NT-proBNP, Hcy, folate , and MTHFR gene polymorphism in late life mild cognitive impairment (MCI) and depression, and to determine the association between homozygous carriers of the TT genotype and Hcy and NT-proBNP on one-hand and depressive and cognitive scores on other-hand. T he study included 60 elderly patients, they attended the Outpatient Clinic for treatment of depression (group I, n=32) and/or MCI (group II, n=28). In addition to a control group (group III, n=20) which matched to the patients with respect to age and gender with no previous history of psychiatric diseases. Both plasma NT-proBNP and Hcy levels were assayed by ELISA and folate levels were assayed by electrochemiluminescene immunoassay, in addition MTHFR C677T gene polymorphism was evaluated using PCR and restriction fragment length polymorphism (RFLP) using HinfI restriction enzyme. Both NT-proBNP and Hcy were significantly increased but folate was significantly decreased in the patients groups as compared to the control subjects. Both Hcy and NT-proBNP were significantly positively correlated with depression scores assessed by Hamilton Rating Scale of Depression (HRSD), but significantly negatively correlated with cognitive impairment assessed by Mini-mental state examination (MMSE) score. The carriers of MTHFR, TT genotypes had an increased risk of developing depression and had significantly higher plasma level of both and NT-proBNP and Hcy than CT or CC patients genotypes (p<0.001). In conclusion: the MTHFR C677T gene variation may play an important role in the modulation of mood but does not contribute to genetic susceptibility to cognitive performance in later life. The MTHFR C677T mutation is associated with plasma Hcy and NT-proBNP levels. Elevated NT-proBNP and Hcy levels may play a role in link ing depression and /or MCI with increased cerebrovascular and/or cardio-vascular risk . | ||||
Statistics Article View: 144 PDF Download: 96 |
||||