Rubén Antonio Vázquez‐Roque

Benemérita Universidad Autónoma de Puebla

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Gonzalo Flores

Benemérita Universidad Autónoma de Puebla

Alfonso Díaz

Benemérita Universidad Autónoma de Puebla

Samuel Treviño

Benemérita Universidad Autónoma de Puebla

Fernando García‐Dolores

Instituto de Salud del Estado de México

Jorge Guevara

Universidad Nacional Autónoma de México

Brenda Cabrera‐Mendoza

Connecticut Health Foundation

Humberto Nicolini

National Institute of Genomic Medicine

Alma Delia Genis‐Mendoza

National Institute of Genomic Medicine

Hiram Tendilla‐Beltrán

Benemérita Universidad Autónoma de Puebla

José Jaime Martínez‐Magaña

National Institute of Genomic Medicine

Cooperative Institutions

Benemérita Universidad Autónoma de Puebla

Universidad Nacional Autónoma de México

Instituto Politécnico Nacional

University of California, San Diego

National Institute of Genomic Medicine

Center for Research and Advanced Studies of the National Polytechnic Institute

Autonomous University of Tlaxcala

Universidad Autónoma de la Ciudad de México

Tecnológico Nacional de México

Universidad Complutense de Madrid

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

PGC-1α Rescues Huntington’s Disease Proteotoxicity by Preventing Oxidative Stress and Promoting TFEB Function

Science Translational Medicine (2012)

Taiji Tsunemi Travis D. Ashe Brad E. Morrison Kathryn Soriano Jonathan Au

Huntington's disease (HD) is caused by CAG repeat expansions in the huntingtin (htt) gene, yielding proteins containing polyglutamine repeats that become misfolded and resist degradation. Previous studies demonstrated that mutant htt interferes with transcriptional programs coordinated by the peroxisome proliferator-activated receptor γ (PPARγ) coactivator 1α (PGC-1α), a regulator of mitochondrial biogenesis and oxidative stress. We tested whether restoration of PGC-1α could ameliorate the symptoms of HD in a mouse model. We found that PGC-1α induction virtually eliminated htt protein aggregation and ameliorated HD neurodegeneration in part by attenuating oxidative stress. PGC-1α promoted htt turnover and the elimination of protein aggregates by activating transcription factor EB (TFEB), a master regulator of the autophagy-lysosome pathway. TFEB alone was capable of reducing htt aggregation and neurotoxicity, placing PGC-1α upstream of TFEB and identifying these two molecules as important therapeutic targets in HD and potentially other neurodegenerative disorders caused by protein misfolding.

TFEB

Proteotoxicity

Huntingtin Protein

10.1126/scitranslmed.3003799

Cite

Citations (408)

Brain Gene Expression- DNA Methylation Correlation in Suicide Completers

Biological Psychiatry (2021)

Brenda Cabrera‐Mendoza José Jaime Martínez‐Magaña Alma Delia Genis‐Mendoza Nancy Monroy‐Jaramillo Consuelo Walss‐Bass

10.1016/j.biopsych.2021.02.366

Cite

Citations (0)

Metabolic syndrome causes recognition impairments and reduced hippocampal neuronal plasticity in rats

Journal of Chemical Neuroanatomy (2017)

Samuel Treviño Rubén Antonio Vázquez‐Roque Gustavo López‐López Claudia Pérez-Cruz Carolina Morán

Synaptophysin

Environmental Enrichment

10.1016/j.jchemneu.2017.02.007

Cite

Citations (31)

Chronic cerebrolysin administration attenuates neuronal abnormalities in the basolateral amygdala induced by neonatal ventral hippocampus lesion in the rat

Synapse (2013)

Rubén Antonio Vázquez‐Roque Kiren Ubhi Eliezer Masliah Gonzalo Flores

The neonatal ventral hippocampal lesion (nVHL) has emerged as a model of schizophrenia-related behavior in the rat. Our previous report demonstrated that cerebrolysin (Cbl), a neuropeptide preparation which mimics the action of endogenous neurotrophic factors on brain protection and repair, promoted recovery of dendritic and neuronal damage of the prefrontal cortex and nucleus accumbens and behavioral improvements in postpubertal nVHL rats. We recently demonstrated that nVHL animals exhibit dendritic atrophy and spine loss in the basolateral amygdala (BLA). This study aimed to determine whether Cbl treatment was capable of reducing BLA neuronal alterations observed in nVHL rats. The morphological evaluation included examination of dendrites using the Golgi-Cox procedure and stereology to quantify the total cell number in BLA. Golgi-Cox staining revealed that nVHL induced dendritic retraction and spine loss in BLA pyramidal neurons. Stereological analysis demonstrated nVHL also produced a reduction in cells in BLA. Interestingly, repeated Cbl treatment ameliorated dendritic pathology and neuronal loss in the BLA of the nVHL rats. Our data show that Cbl may foster recovery of BLA damage in postpubertal nVHL rats and suggests that the use of neurotrophic agents for the management of some schizophrenia-related symptoms may present an alternative therapeutic pathway in these disorders. Synapse, 68:31–38, 2014. © 2013 Wiley Periodicals, Inc.

Cerebrolysin

Basolateral amygdala

10.1002/syn.21718

Cite

Citations (28)

M93. BRAIN GENE EXPRESSION PROFILING OF INDIVIDUALS WITH DUAL DIAGNOSIS WHO DIED BY SUICIDE

Schizophrenia Bulletin (2020)

Brenda Cabrera‐Mendoza Cristóbal Fresno Nancy Monroy‐Jaramillo Consuelo Walss‐Bass Gabriel R. Fries

Abstract Background Dual diagnosis is the co-occurrence of at least one substance use disorder (SUD) and one or more mental disorders in a given individual. Despite this comorbidity is highly prevalent and associated with adverse clinical outcomes, its neurobiology remains unclear. Furthermore, patients with dual diagnosis are at higher risk for suicidal behavior in comparison with single disorder patients. Our objective was to evaluate brain gene expression patterns in individuals with dual diagnosis who died by suicide. Methods We compared the gene expression profile in the dorsolateral prefrontal cortex of suicides with DD (n= 10) to the transcriptome of suicides with SUD alone (n=10), suicides with mood disorders alone (n=13), and suicides without mental comorbidities (n=5). Gene expression profiles were assessed by microarrays. Microarray data quality control was performed. Then, microarray data were background corrected and quantile normalized. Differentially expressed genes among the conditions were identified by a linear model implemented in the limma package. Results When comparing the transcriptome of suicides with dual diagnosis to suicides with SUD alone and suicides with mood disorders alone, we identified 255 and 172 differentially expressed genes, respectively. When comparing suicides with DD to suicides without mental comorbidities, we identified 330 differentially expressed genes, mainly enriched in neurogenesis. Discussion Our results suggest that suicides with dual diagnosis present a gene expression profile distinct from that of suicides with a single disorder and suicides without mental disorders. Also, suicides with dual diagnosis, SUD and mood disorders exhibited alterations in the expression of synaptic genes. However, suicides with each condition (dual diagnosis, SUD or mood disorders) exhibited unique gene expression changes at different levels within synaptic signaling. These gene expression differences might contribute to the phenotypical and clinical discrepancies observed in patients with dual diagnosis and patients with a single disorder

Dual diagnosis

10.1093/schbul/sbaa030.405

Cite

Citations (1)

High-carbohydrate and fat diet consumption causes metabolic deterioration, neuronal damage, and loss of recognition memory in rats

Journal of Chemical Neuroanatomy (2023)

Estefania Fuentes Berenice Venegas Guadalupe Muñoz‐Arenas Carolina Morán Rubén Antonio Vázquez‐Roque

Chronic Stress

10.1016/j.jchemneu.2023.102237

Cite

Citations (18)

Correction to: Hyper-response to Novelty Increases c-Fos Expression in the Hippocampus and Prefrontal Cortex in a Rat Model of Schizophrenia

Neurochemical Research (2018)

Tomás Monfil Rubén Antonio Vázquez‐Roque Israel Camacho‐Abrego Hiram Tendilla‐Beltrán Tommaso Iannitti

Mistake

Spelling

Neurochemistry

Expression (computer science)

10.1007/s11064-018-2468-0

Cite

Citations (0)

Histological correlates of N40 auditory evoked potentials in adult rats after neonatal ventral hippocampal lesion: animal model of schizophrenia

Schizophrenia Research (2014)

Ana Luisa Romero-Pimentel Rubén Antonio Vázquez‐Roque Israel Camacho‐Abrego Kurt L. Hoffman P. Linares

Neurophysiology

10.1016/j.schres.2014.09.009

Cite

Citations (11)

Risperidone Ameliorates Prefrontal Cortex Neural Atrophy and Oxidative/Nitrosative Stress in Brain and Peripheral Blood of Rats with Neonatal Ventral Hippocampus Lesion

Journal of Neuroscience (2019)

Hiram Tendilla‐Beltrán Silvia Meneses-Prado Rubén Antonio Vázquez‐Roque Miguel Tapia‐Rodríguez Andrea Judith Vázquez-Hernández

Reduction of the dendritic arbor length and the lack of dendritic spines in the pyramidal cells of the prefrontal cortex (PFC) are prevalent pathological features in schizophrenia (SZ). Neonatal ventral hippocampus lesion (NVHL) in male rats reproduces these neuronal characteristics and here we describe how this is a consequence of BDNF/TrkB pathway disruption. Moreover, COX-2 proinflammatory state, as well as Nrf-2 antioxidant impairment, triggers oxidative/nitrosative stress, which also contributes to dendritic spine impairments in the PFC. Interestingly, oxidative/nitrosative stress was also detected in the periphery of NVHL animals. Furthermore, risperidone treatment had a neurotrophic effect on the PFC and antioxidant effects on the brain and periphery of NVHL animals; these cellular effects were related to behavioral improvement. Our data highlight the link between brain development and immune response, as well as several other factors to understand mechanisms related to the pathophysiology of SZ.SIGNIFICANCE STATEMENT Prefrontal cortex dysfunction in schizophrenia can be a consequence of morphological abnormalities and oxidative/nitrosative stress, among others. Here, we detailed how impaired plasticity-related pathways and oxidative/nitrosative stress are part of the dendritic spine pathology and their modulation by atypical antipsychotic risperidone treatment in rats with neonatal ventral hippocampus lesion. Moreover, we found that animals with neonatal ventral hippocampus lesion had oxidative/nitrosative stress in the brain as well as in the peripheral blood, an important issue for the translational approaches of this model. Then, risperidone restored plasticity and reduced oxidative/nitrosative stress of prefrontal cortex pyramidal cells, and ultimately improved the behavior of lesioned animals. Moreover, risperidone had differential effects than the brain on peripheral blood oxidative/nitrosative stress.

10.1523/jneurosci.1249-19.2019

Cite

Citations (38)

Memory and dendritic spines loss, and dynamic dendritic spines changes are age-dependent in the rat

Journal of Chemical Neuroanatomy (2020)

Leonardo Aguilar‐Hernández Andrea Judith Vázquez-Hernández Diana Frida de-Lima-Mar Rubén Antonio Vázquez‐Roque Hiram Tendilla‐Beltrán

Dendrite (mathematics)

Dendritic filopodia

Apical dendrite

10.1016/j.jchemneu.2020.101858

Cite

Citations (15)