Person:
Rubio Valladolid, Gabriel

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First Name
Gabriel
Last Name
Rubio Valladolid
URI
https://hdl.handle.net/20.500.14352/79052
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Medicina
Department
Medicina Legal, Psiquiatría y Patología
Area
Psiquiatría
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2017 - 20192
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    Alcohol-induced cognitive deficits are associated with decreased circulating levels of the neurotrophin BDNF in humans and rats
    (Addiction Biology, 2019) Silva Peña, Daniel; Martín Velasco, Ana Isabel; Villanúa Bernués, María Ángeles; Rubio Valladolid, Gabriel; Rodríguez De Fonseca, Fernando Antonio; Suárez Pérez, Juan
    Chronic alcohol consumption is associated with neurocognitive and memory deficits, dramatically affecting plasticityand connectivity, with maximal expression as dementia. Neurotrophic factors may contribute to alcohol-related cogni-tive decline. For further investigation, a cross-sectional study was performed to evaluate the association of cognitiveimpairment, by using frontal assessment battery, and memory loss, using memory failures everyday, with the circulat-ing levels of the neurotrophin brain-derived neurotrophic factor (BDNF) and neurotrophin 3 (NT-3) in abstinent sub-jects with alcohol use disorders (AUDs,N= 58, average of 17.9 years of problematic use and 4.3 months of abstinence)compared with healthy control subjects (N= 22). This association was also explored in a pre-clinical model of adoles-cent rats chronically exposed to alcohol up to adulthood (~77 days old) in a three-bottle free-choice (5–10–20 per-cent), repeated abstinence and relapse paradigm. AUD subjects had low educational level and cognitive impairmentassociated with teenage consumption and lower circulating levels of BDNF and NT-3. Only BDNF concentrationshowed a positive correlation with frontal assessment battery in AUD patients. In the ethanol-exposed rats, the plasmalevels of BDNF and NT-3 were also decreased, and a negative correlation between hippocampalBdnfmRNA levels andrecognition memory was found. The ethanol-exposed rat hippocampus showed a decrease in the mRNA levels of neu-rotrophic (BdnfandNtf-3) and neurogenic (Mki67,Sox2,Dcx,Ncam1andCalb1) factors, associated to a deactivation ofthe neurogenic regulator mitogen-activated protein kinase extracellular signal-regulated kinase. Results suggest a rel-evant role of BDNF/extracellular signal-regulated kinase 2 signaling in alcohol-induced cognitive impairment and sug-gest that early alcohol exposure-derived effects on cognition are associated with neurotrophin signaling deficits.
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    Decreased plasma concentrations of BDNF and IGF-1 in abstinent patients with alcohol use disorders
    (Plos One, 2017) García Marchena, Nuria; Martín Velasco, Ana Isabel; Villanúa Bernués, María Ángeles; Rubio Valladolid, Gabriel; Pavón Moron, Francisco José
    The identification of growth factors as potential biomarkers in alcohol addiction may help to understand underlying mechanisms associated with the pathogenesis of alcohol use disorders (AUDs). Previous studies have linked growth factors to neural plasticity in neurocognitive impairment and mental disorders. In order to further clarify the impact of chronic alcohol consumption on circulating growth factors, a cross-sectional study was performed in abstinent AUD patients (alcohol group, N = 91) and healthy control subjects (control group, N = 55) to examine plasma concentrations of brain-derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1) and IGF-1 binding protein-3 (IGFBP-3). The association of these plasma peptides with relevant AUD-related variables and psychiatric comorbidity was explored. The alcohol group was diagnosed with severe AUD and showed an average of 13 years of problematic use and 10 months of abstinence at the moment of participating in the study. Regarding common medical conditions associated with AUD, we observed an elevated incidence of alcohol-induced liver and pancreas diseases (18.7%) and psychiatric comorbidity (76.9%). Thus, AUD patients displayed a high prevalence of dual diagnosis (39.3%) [mainly depression (19.9%)] and comorbid substance use disorders (40.7%). Plasma BDNF and IGF-1 concentrations were significantly lower in the alcohol group than in the control group (p<0.001). Remarkably, there was a negative association between IGF-1 concentrations and age in the control group (r = -0.52, p<0.001) that was not found in the alcohol group. Concerning AUD-related variables, AUD patients with liver and pancreas diseases showed even lower concentrations of BDNF (p<0.05). In contrast, the changes in plasma concentrations of these peptides were not associated with abstinence, problematic use, AUD severity or lifetime psychiatric comorbidity. These results suggest that further research is necessary to elucidate the role of BDNF in alcohol-induced toxicity and the biological significance of the lack of correlation between age and plasma IGF-1 levels in abstinent AUD patients.