Peripheral brain-derived neurotrophic factor (BDNF) and salivary cortisol levels in college students with different levels of academic stress. Study protocol.

INTRODUCTION: Brain-derived neurotrophic factor (BDNF) is essential for brain physiological processes influencing memory and learning. BDNF levels can be affected by many factors, including stress. Stress increase serum and salivary cortisol levels. Academic stress is of the chronic type. BDNF levels can be measure from serum, plasma or platelets, and there is still no standard methodology, which is relevant to ensure reproducibility and comparability between studies. HYPOTHESIS: (i) BDNF concentrations in serum show greater variability than in plasma. (ii) In college students with academic stress, peripheral BDNF decreases and salivary cortisol increases. GENERAL OBJECTIVE: To standardize plasma and serum collection for BDNF levels and to determine whether academic stress affects peripheral BDNF and salivary cortisol levels. DESIGN: Quantitative research, with a non-experimental cross-sectional descriptive design. PARTICIPANTS: Student volunteers. Under convenience sampling, 20 individuals will be included for standardization of plasma and serum collection and between 70 and 80 individuals to determine the effect of academic stress on BDNF and salivary cortisol. PERIPHERAL BLOOD AND SALIVARY CORTISOL SAMPLING, MEASUREMENTS: 12 mL of peripheral blood (with and without anticoagulant) will be drawn per participant, separated from plasma or serum and cryopreserved at -80°C. Additionally, they will be instructed in the collection of 1 mL of saliva samples, which will be centrifuged. Val66Met polymorphism will be performed by allele-specific PCR, while BDNF and salivary cortisol levels will be determined by ELISA. STATISTICAL ANALYSIS: (i) descriptive analysis of the variables, through measures of central tendency and dispersion, and the categorical variables through their frequency and percentage. (ii) Then a bivariate analysis will be performed comparing groups using each variable separately. EXPECTED RESULTS: We expect to (i) determine the analytical factors that allow a better reproducibility in the measurement of peripheral BDNF, and (ii) the effect of academic stress on BDNF and salivary cortisol levels.

Deterioro de la memoria visuoespacial en estadios 2 y 3 de la enfermedad de Parkinson / Impairment of visuospatial memory in stages 2 and 3 of Parkinson's disease

Objetivo: la enfermedad de Parkinson no solo suele relacionarse con dificultades motoras sino también con deterioro cognitivo. En este sentido, cabe preguntarse si las funciones cognitivas relacionadas con información visuoespacial se ven afectadas a medida que aumenta la severidad de la enfermedad. Método: a partir de la evaluación y análisis del procesamiento y la memoria visuoespacial mediante el test Figura compleja de Rey-Osterrieth en 27 sujetos con enfermedad de Parkinson en estadios 2 y 3 se pretenden establecer diferencias según el estadio. Resultados: los resultados evidencian diferencias significativas en la memoria visuoespacial, lo que podría indicar que la evolución de la enfermedad parece determinar la severidad de la alteración cognitiva, principalmente en lo que respecta a memoria visuoespacial. Conclusión: a partir de los resultados, se sugiere incorporar evaluaciones fonoaudiológicas de la información visuoespacial en esta población con el fin de diseñar planes terapéuticos enfocados en el déficit neuropsicológico

Objective: Parkinson's disease is not only related to motor difficulties but also to cognitive impairmet. Hence, it is worth knowing if the cognitive functions related to visuospatial information are affected as the severity of the disease increases. Method: this study intends to establish differences according to the Parkinson's disease stage from evaluation and analysis of visuospatial information in 27 patients using the Complex figure of Rey-Osterrieth test. Results: the results show significant differences in the visuospatial memory between both groups, which could indicates that the evolution of the disease seems to determine the severity of the cognitive alteration, mainly with regard to visuospatial memory. Conclusion: the results suggest to incorporate visuospatial information in speech-language evaluations of Parkinson's disease patients in order to design therapeutic plans focused on the neuropsychological deficit

[Association between serotonin transporter and monoamine oxidase A gene polymorphisms and depression]. / Asociación entre los polimorfismos 5HTTLPR, uMAOA y depresión en una cohorte de pacientes de atención primaria.

BACKGROUND: Serotonin plays a central role regulating mood and on the development of depressive disorders. AIM: To study whether 5HTTLPR functional polymorphisms in the serotonin transporter gene or the Monoamine oxidase A gene (uMAOA) were risk markers for depression. MATERIAL AND METHODS: The Composite International Diagnostic Interview (CIDI) was applied to 1,062 consultants in primary health care centers aged between 18 and 75 years to establish the diagnosis of depression. A sample of saliva was obtained for DNA extraction and genetic analyses. RESULTS: No association between the presence of depressive disorders and 5HTTLPR (ss) or uMAOA (3/3) risk genotypes was found. Psychological abuse and the presence of two or more life events were found to be predictors of depression in the studied sample. CONCLUSIONS: In this study, 5HTTLPR and uMAOA polymorphisms were not risk factors for depression. However, psychological abuse and the presence of two or more life events were risk factors for depressive disorders.

Asociación entre los polimorfismos 5HTTLPR, uMAOA y depresión en una cohorte de pacientes de atención primaria / Association between serotonin transporter and monoamine oxidase A gene polymorphisms and depression

Background: Serotonin plays a central role regulating mood and on the development of depressive disorders. Aim: To study whether 5HTTLPR functional polymorphisms in the serotonin transporter gene or the Monoamine oxidase A gene (uMAOA) were risk markers for depression. Material and Methods: The Composite International Diagnostic Interview (CIDI) was applied to 1,062 consultants in primary health care centers aged between 18 and 75 years to establish the diagnosis of depression. A sample of saliva was obtained for DNA extraction and genetic analyses. Results: No association between the presence of depressive disorders and 5HTTLPR (ss) or uMAOA (3/3) risk genotypes was found. Psychological abuse and the presence of two or more life events were found to be predictors of depression in the studied sample. Conclusions: In this study, 5HTTLPR and uMAOA polymorphisms were not risk factors for depression. However, psychological abuse and the presence of two or more life events were risk factors for depressive disorders.

Serum brain-derived neurotrophic factor and glucocorticoid receptor levels in lymphocytes as markers of antidepressant response in major depressive patients: a pilot study.

Depressive patients often have altered cortisol secretion, an effect that likely derives from impaired activity of the glucocorticoid receptor (GR), the main regulator of the hypothalamus-pituitary-adrenal (HPA) axis. Glucocorticoids reduce the levels of brain-derived neurotrophic factor (BDNF), a downstream target of antidepressants. Antidepressants promote the transcriptional activity of cyclic adenosine monophosphate (cAMP) response element binding protein (CREB), a regulator of BDNF expression. To identify potential biomarkers for the onset of antidepressant action in depressive patients, GR and phospho-CREB (pCREB) levels in lymphocytes and serum BDNF levels were repeatedly measured during the course of antidepressant treatment. Thirty-four depressed outpatients (10 male and 24 female) were treated with venlafaxine (75mg/day), and individuals exhibiting a 50% reduction in their baseline 17-Item Hamilton Depression Rating Scale score by the 6th week of treatment were considered responders. Responders showed an early improvement in parallel with a rise in BDNF levels during the first two weeks of treatment. Non-responders showed increased GR levels by the third week and reduced serum BDNF by the sixth week of treatment. In contrast, venlafaxine did not affect levels of pCREB. We conclude that levels of BDNF in serum and GR levels in lymphocytes may represent biomarkers that could be used to predict responses to venlafaxine treatment.

Hyperglycaemia inhibits thymidine incorporation and cell growth via protein kinase C, mitogen-activated protein kinases and nitric oxide in human umbilical vein endothelium.

An elevated extracellular concentration of D-glucose (i.e. hyperglycaemia) inhibits cell proliferation and incorporation of the endogenous nucleoside thymidine into DNA in human umbilical vein endothelial cells (HUVECs). Cells in their log-phase of growth (3.7 +/- 0.3 days, n = 27) incubated for 30 min with 25 mM D-glucose, but not with equimolar concentrations of L-glucose or D-mannitol, exhibited reduced [3H]thymidine incorporation and cell growth rate, with no change in cell viability (> 98 %), total DNA, protein content or cell volume. Incubation with D-glucose activated protein kinase C (PKC), endothelial NO synthase (eNOS), p42 and p44 mitogen-activated protein kinases (p42/44(mapk)), but inhibited superoxide dismutase (SOD). Incubation with D-glucose also increased cGMP and cAMP levels. The effect of D-glucose was blocked by the PKC inhibitor calphostin C, the MAP kinase kinase 1/2 (MEK1/2) inhibitor PD-98059, the eNOS inhibitor L-NAME, the protein kinase G (PKG) inhibitor KT-5823 and the protein kinase A (PKA) inhibitor KT-5720. In the presence of 5 mM D-glucose, [3H]thymidine incorporation and cell growth were reduced by the PKC activator phorbol 12-myristate 13-acetate (PMA), the NO donor S-nitroso-N-acetyl-L,D-penicillamine (SNAP), dibutyryl cGMP, dibutyryl cAMP and the Ca2+ ionophore A-23187. The effect of A-23187 was blocked by calphostin C and PD-98059. D-Glucose-dependent inhibition of thymidine incorporation and cell proliferation is associated with increased PKC, eNOS, and MEK1/2, but decreased SOD activity, and higher intracellular levels of cGMP, cAMP and Ca2+ in HUVECs. These are cellular mechanisms which may reduce endothelial cell growth in pathological conditions such as in diabetes mellitus or hyperglycaemia.