Nevin F W Zaki1, Elsayed Saleh2, Mahmoud Elwasify2, Elhasanein Mahmoud2, John Zaki3, David Warren Spence4, Ahmed S BaHammam5, Seithikurippu R Pandi-Perumal6. 1. Sleep Research Unit, Mansoura University, Egypt; Department of Psychiatry, Mansoura University, Egypt. Electronic address: mernakero@mans.edu.eg. 2. Department of Psychiatry, Mansoura University, Egypt. 3. Department 0f Mechanical Engineering, Statistical Consultation Office, Mansoura University, Egypt. 4. Dufferin Street, Toronto, Canada. 5. University Sleep Disorders Center, College of Medicine, King Saud University, Riyadh, Saudi Arabia. 6. Somnogen Canada Inc., Toronto, Canada.
Abstract
BACKGROUND: Reductions in BDNF activity have shown associations with depressed mood. Other evidence has demonstrated that the BDNF Val66Met polymorphism (rs6265) appears to reduce neural plasticity. A limited number of studies have investigated the influence of these genetic polymorphisms in insomnia. The present study sought to confirm the presence of associations between BDNF Val66Met polymorphism (rs6265) occurrence in normal sleepers and those with insomnia. METHOD: The study subjects consisted of a patient group (n = 199) complaining of insomnia and a control group (n = 51). Each subject was clinically interviewed using questions taken from the Brief Insomnia Questionnaire. After the interview, the subjects were asked to complete the Insomnia Severity Index, The Hamilton Depression Rating Scale, and the Montreal Cognitive Assessment Test. An overnight polysomnography test was also administered. Blood samples were collected for genetic study. RESULTS: The insomnia patients showed a greater prevalence of heterozygous (A/G) VAL/MET polymorphism than the normal controls (p = ≤ 0.0001). This finding confirmed that this genetic polymorphism, which impairs BDNF activity, is an important correlate of disturbed sleep. Further, the finding of significantly greater (p = ≤ 0.0001) depression scores among the insomnia group suggested that BDNF is an important factor in the development of depressive symptoms. CLINICAL IMPLICATIONS: The results of the present study indicate that BDNF gene polymorphism plays a prominent role in the variation of symptoms among insomnia patients and, further, that this polymorphism is strongly related to the severity of depression.
BACKGROUND: Reductions in BDNF activity have shown associations with depressed mood. Other evidence has demonstrated that the BDNF Val66Met polymorphism (rs6265) appears to reduce neural plasticity. A limited number of studies have investigated the influence of these genetic polymorphisms in insomnia. The present study sought to confirm the presence of associations between BDNF Val66Met polymorphism (rs6265) occurrence in normal sleepers and those with insomnia. METHOD: The study subjects consisted of a patient group (n = 199) complaining of insomnia and a control group (n = 51). Each subject was clinically interviewed using questions taken from the Brief Insomnia Questionnaire. After the interview, the subjects were asked to complete the Insomnia Severity Index, The Hamilton Depression Rating Scale, and the Montreal Cognitive Assessment Test. An overnight polysomnography test was also administered. Blood samples were collected for genetic study. RESULTS: The insomniapatients showed a greater prevalence of heterozygous (A/G) VAL/MET polymorphism than the normal controls (p = ≤ 0.0001). This finding confirmed that this genetic polymorphism, which impairs BDNF activity, is an important correlate of disturbed sleep. Further, the finding of significantly greater (p = ≤ 0.0001) depression scores among the insomnia group suggested that BDNF is an important factor in the development of depressive symptoms. CLINICAL IMPLICATIONS: The results of the present study indicate that BDNF gene polymorphism plays a prominent role in the variation of symptoms among insomniapatients and, further, that this polymorphism is strongly related to the severity of depression.