Isabel Cubero-Millán1, María-José Ruiz-Ramos1, Antonio Molina-Carballo2,3, Sylvia Martínez-Serrano1, Luisa Fernández-López1, Irene Machado-Casas1,4, Pilar Tortosa-Pinto1, Aida Ruiz-López1, Juan-de-Dios Luna-Del-Castillo5, José Uberos1,4, Antonio Muñoz-Hoyos6,7. 1. Departamento de Pediatría, Facultad de Medicina, Universidad de Granada, Avda de Madrid 12, 18012, Granada, Spain. 2. Departamento de Pediatría, Facultad de Medicina, Universidad de Granada, Avda de Madrid 12, 18012, Granada, Spain. amolinac@ugr.es. 3. Servicio de Neuropediatría, Neuropsicología y Atención Temprana, Unidad de Gestión Clínica de Pediatría, Complejo Hospitalario Granada, Hospital Clínico San Cecilio, Avda Dr. Olóriz 16, Granada, Spain. amolinac@ugr.es. 4. Servicio de Neuropediatría, Neuropsicología y Atención Temprana, Unidad de Gestión Clínica de Pediatría, Complejo Hospitalario Granada, Hospital Clínico San Cecilio, Avda Dr. Olóriz 16, Granada, Spain. 5. Departamento de BioEstadística, Facultad de Medicina, Universidad de Granada, Granada, Spain. 6. Departamento de Pediatría, Facultad de Medicina, Universidad de Granada, Avda de Madrid 12, 18012, Granada, Spain. amunozh@ugr.es. 7. Servicio de Neuropediatría, Neuropsicología y Atención Temprana, Unidad de Gestión Clínica de Pediatría, Complejo Hospitalario Granada, Hospital Clínico San Cecilio, Avda Dr. Olóriz 16, Granada, Spain. amunozh@ugr.es.
Abstract
RATIONALE: Brain-derived neurotrophic factor (BDNF) enhances the growth and maintenance of several monoamine neuronal systems, serves as a neurotransmitter modulator and participates in the mechanisms of neuronal plasticity. Therefore, BDNF is a good candidate for interventions in the pathogenesis and/or treatment response of attention deficit hyperactivity disorder (ADHD). OBJECTIVE: We quantified the basal concentration and daily fluctuation of serum BDNF, as well as changes after methylphenidate treatment. METHOD: A total of 148 children, 4-5 years old, were classified into groups as follows: ADHD group (n = 107, DSM-IV-TR criteria) and a control group (CG, n = 41). Blood samples were drawn at 2000 and 0900 hours from both groups, and after 4.63 ± 2.3 months of treatment, blood was drawn only from the ADHD group for BDNF measurements. Factorial analysis was performed (Stata software, version 12.0). RESULTS: Morning BDNF (36.36 ± 11.62 ng/ml) in the CG was very similar to that in the predominantly inattentive children (PAD), although the evening concentration in the CG was higher (CG 31.78 ± 11.92 vs PAD 26.41 ± 11.55 ng/ml). The hyperactive-impulsive group, including patients with comorbid conduct disorder (PHI/CD), had lower concentrations. Methylphenidate (MPH) did not modify the concentration or the absence of daily BDNF fluctuations in the PHI/CD children; however, MPH induced a significant decrease in BDNF in PAD and basal day/night fluctuations disappeared in this ADHD subtype. This profile was not altered by the presence of depressive symptoms. CONCLUSIONS: Our data support a reduction in BDNF in untreated ADHD due to the lower concentrations in PHI/CD children, which is similar to other psychopathologic and cognitive disorders. MPH decreased BDNF only in the PAD group, which might indicate that BDNF is not directly implicated in the methylphenidate-induced amelioration of the neuropsychological and organic immaturity of ADHD patients.
RATIONALE: Brain-derived neurotrophic factor (BDNF) enhances the growth and maintenance of several monoamine neuronal systems, serves as a neurotransmitter modulator and participates in the mechanisms of neuronal plasticity. Therefore, BDNF is a good candidate for interventions in the pathogenesis and/or treatment response of attention deficit hyperactivity disorder (ADHD). OBJECTIVE: We quantified the basal concentration and daily fluctuation of serum BDNF, as well as changes after methylphenidate treatment. METHOD: A total of 148 children, 4-5 years old, were classified into groups as follows: ADHD group (n = 107, DSM-IV-TR criteria) and a control group (CG, n = 41). Blood samples were drawn at 2000 and 0900 hours from both groups, and after 4.63 ± 2.3 months of treatment, blood was drawn only from the ADHD group for BDNF measurements. Factorial analysis was performed (Stata software, version 12.0). RESULTS: Morning BDNF (36.36 ± 11.62 ng/ml) in the CG was very similar to that in the predominantly inattentive children (PAD), although the evening concentration in the CG was higher (CG 31.78 ± 11.92 vs PAD 26.41 ± 11.55 ng/ml). The hyperactive-impulsive group, including patients with comorbid conduct disorder (PHI/CD), had lower concentrations. Methylphenidate (MPH) did not modify the concentration or the absence of daily BDNF fluctuations in the PHI/CD children; however, MPH induced a significant decrease in BDNF in PAD and basal day/night fluctuations disappeared in this ADHD subtype. This profile was not altered by the presence of depressive symptoms. CONCLUSIONS: Our data support a reduction in BDNF in untreated ADHD due to the lower concentrations in PHI/CD children, which is similar to other psychopathologic and cognitive disorders. MPH decreased BDNF only in the PAD group, which might indicate that BDNF is not directly implicated in the methylphenidate-induced amelioration of the neuropsychological and organic immaturity of ADHDpatients.
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