Jorge Guevara

ORCID: 0000-0003-3428-3179
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About
Contact & Profiles
Research Areas
  • Alzheimer's disease research and treatments
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Glycosylation and Glycoproteins Research
  • Neuroscience and Neuropharmacology Research
  • Medicinal Plants and Neuroprotection
  • Trace Elements in Health
  • Neurological Disease Mechanisms and Treatments
  • Regulation of Appetite and Obesity
  • Biochemical effects in animals
  • Prion Diseases and Protein Misfolding
  • Galectins and Cancer Biology
  • Tryptophan and brain disorders
  • Parkinson's Disease Mechanisms and Treatments
  • Ecology and Vegetation Dynamics Studies
  • Plant Diversity and Evolution
  • Neurological diseases and metabolism
  • Gastrointestinal disorders and treatments
  • Anesthesia and Neurotoxicity Research
  • Heavy Metal Exposure and Toxicity
  • Plant and animal studies
  • Biliary and Gastrointestinal Fistulas
  • Diet and metabolism studies
  • Advanced Glycation End Products research
  • Heat shock proteins research
  • Memory and Neural Mechanisms

Universidad Nacional Autónoma de México
2016-2025

Vall d'Hebron Hospital Universitari
2023

University of Edinburgh
2016

Universidad Autónoma de la Ciudad de México
2014

Instituto Nacional de Neurología y Neurocirugía
2001-2009

Université de Montréal
2005

Instituto Nacional de Enfermedades Respiratorias
2003

École Nationale Supérieure de Chimie de Lille
2003

Universidad de Oriente
2003

Center for Research and Advanced Studies of the National Polytechnic Institute
1998-2001

A high calorie intake can induce the appearance of metabolic syndrome (MS), which is a serious public health problem because it affects glucose levels and triglycerides in blood. Recently, has been suggested that MS cause complications brain, since chronic hyperglycemia insulin resistance are risk factors for triggering neuronal death by inducing state oxidative stress inflammatory response affect cognitive processes. This process, however, not clear. In this study, we evaluated effect...

10.1002/syn.21832 article EN Synapse 2015-06-13

Amyloid-β (Aβ)25-35 is able to cause memory impairment and neurodegenerative events. Recent evidence has shown that the injection of Aβ25-35 into temporal cortex (TCx) rats increases inflammatory response; however, it unclear how in

10.3233/jad-2012-111979 article EN Journal of Alzheimer s Disease 2012-06-04

Abstract Metabolic syndrome (MS) results from excessive consumption of high‐calorie foods and sedentary lifestyles. Clinically, insulin resistance, abdominal obesity, hyperglycemia, dyslipidemia, hypertension are observed. MS has been considered a risk factor in the development dementia. In brain, metabolically impaired environment generates oxidative stress production pro‐inflammatory cytokines that deteriorate morphology neuronal function hippocampus, leading to cognitive impairment....

10.1002/syn.22186 article EN Synapse 2020-08-12

The cognitive functions of people over 60 years age have been diminished, due to the structural and functional changes that brain has during aging. most evident are at behavioral level, with decreased learning capacity, recognition memory, motor incoordination. use exogenous antioxidants implemented as a potential pharmacological option delay onset aging by attenuating oxidative stress neurodegeneration. Resveratrol (RSVL) is polyphenol present in various foods, such red fruits, drinks,...

10.1002/syn.22271 article EN Synapse 2023-05-02

ABSTRACT Brain aging is a multifactorial process that includes reduction in the biological and metabolic activity of individuals. Oxidative stress inflammatory processes are characteristic brain aging. Given current problems, need arises to implement new therapeutic approaches. Polyoxidovanadates (POV), as well curcumin, have stood out for their participation variety activities. This work aimed evaluate coupling metavanadate curcumin (Cuma‐MV) on learning, memory, redox balance,...

10.1002/syn.70008 article EN Synapse 2025-01-01

Alcohol use disorder (AUD) involves excessive and chronic ethanol consumption, leading to various health issues, including cerebellar atrophy. The cerebellum is particularly susceptible ethanol-induced damage through neuroinflammation, oxidative stress excitotoxicity. This has been documented predominantly in the anterior lobe, primarily due its role motor function, which often impaired patients with AUD. However, less known about impact of AUD on posterior lobes. In contrast, alterations...

10.1111/nan.70011 article EN Neuropathology and Applied Neurobiology 2025-03-26

Energy drinks (EDs) are often consumed in combination with alcohol because they reduce the depressant effects of alcohol. However, different researches suggest that chronic use these psychoactive substances can trigger an oxidative and inflammatory response. These processes regulated by both a reactive astrogliosis increase proinflammatory cytokines such as IL‐1 β , TNF‐ α iNOS, causing cell death (apoptosis) at central peripheral nervous systems. Currently, mechanisms toxicity caused mixing...

10.1155/2016/8725354 article EN cc-by Oxidative Medicine and Cellular Longevity 2016-01-01

Galectin-3 has been implicated in tumor progression. We demonstrated immunohistochemically that was negative normal breast tissue, but it highly increased cancer and metastatic tissues to brain. Similarly, histochemistry with mucin-specific lectins showed recognition metastasis Machaerocereus eruca agglutinin (Fuα 1,2 (GalNAcα 1,3) Galß1,4 complex mucin) not for Amaranthus leucocarpus (Galß1,3-GalNAc-α 1,0-Ser/Thr) Arachis hypogaea (Galß1,3GalNAc/Galß1,4GlcNAc). Mucin-type glycans...

10.1080/07357900701837051 article EN Cancer Investigation 2008-01-01

Abstract Metabolic syndrome (MS) is a health problem that characterized by body fat accumulation, hypertension, dyslipidemia, and hyperglycemia; recently, it has been demonstrated MS also damages memory processes. The first‐line drug in the treatment of type 2 diabetes mellitus metformin, which an antihyperglycemic agent. This shown to produce neuroprotection improve However, mechanism involved this unknown. A 90‐day administration metformin improved cognitive processes rats with as...

10.1002/syn.22153 article EN Synapse 2020-03-19

Post-translational modifications due to glycosylation of proteins in human brains from patients with Alzheimer disease (AD) were analyzed using lectin histochemistry. Results indicate a significant increase the production O-glycosylated (containing Galβ1,3GalNAcα1,0 Ser/Thr or GalNAcα1.0 Ser/Thr) neuritic plaques and neurofibrillary tangles which are major histopathological hallmarks AD brains. These alterations determined by positive labelling lectins obtained Amaranthus leucocarpus (ALL)...

10.1097/00005072-199810000-00003 article EN Journal of Neuropathology & Experimental Neurology 1998-10-01
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