Marı́a E. Jiménez-Capdeville

ORCID: 0000-0002-8342-7063
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About
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Research Areas
  • Heavy Metal Exposure and Toxicity
  • Parkinson's Disease Mechanisms and Treatments
  • Electrochemical Analysis and Applications
  • Neuroscience and Neuropharmacology Research
  • Alzheimer's disease research and treatments
  • Neurological disorders and treatments
  • Arsenic contamination and mitigation
  • Genomics and Chromatin Dynamics
  • Nuclear Structure and Function
  • Memory and Neural Mechanisms
  • Cholinesterase and Neurodegenerative Diseases
  • Botulinum Toxin and Related Neurological Disorders
  • Neurological diseases and metabolism
  • Aluminum toxicity and tolerance in plants and animals
  • Pesticide Exposure and Toxicity
  • Genetic Neurodegenerative Diseases
  • Olfactory and Sensory Function Studies
  • Immune Cell Function and Interaction
  • Neurotransmitter Receptor Influence on Behavior
  • Neurogenesis and neuroplasticity mechanisms
  • Neurological and metabolic disorders
  • Stress Responses and Cortisol
  • Molecular Sensors and Ion Detection
  • Birth, Development, and Health
  • Ion channel regulation and function

Autonomous University of San Luis Potosí
2014-2025

Polytechnic University of San Luis Potosí
2002-2020

Universidad Mexicana
2019

Asociación Mexicana de Psicología y Desarrollo Comunitario
2019

Instituto Nacional de Neurología y Neurocirugía
2003

Université de Montréal
1993-1996

Deposition of the pathological α-synuclein (αSynP) in brain is hallmark synucleinopathies, including Parkinson disease (PD), Lewy body dementia (LBD), and multiple system atrophy (MSA). Whether real-time quaking-induced conversion (RT-QuIC) protein misfolding cyclic amplification (PMCA) assays can sensitively detect skin biomarkers for PD non-PD synucleinopathies remains unknown.

10.1001/jamaneurol.2020.3311 article EN cc-by JAMA Neurology 2020-09-28

We studied the effect of an acute infusion quinolinic acid (QUIN) on in vivo hydroxyl radical (.OH) formation striatum awake rats. Using microdialysis technique, generation .OH was assessed through electrochemical detection salicylate hydroxylation product 2,3-dihydroxybenzoic (2,3-DHBA). The extracellular levels increased up to 30 times over basal after QUIN (240 nmol/μl), returning baseline 2 h later. This response attenuated, but not abolished, by pretreatment with NMDA receptor...

10.1097/00001756-200108280-00020 article EN Neuroreport 2001-08-01

Abstract Quinolinic acid (QUIN), a well known excitotoxin that produces pharmacological model of Huntington's disease in rats and primates, has been shown to evoke degenerative events nerve tissue via NMDA receptor (NMDAr) overactivation oxidative stress. In this study, the antioxidant selenium (as sodium selenite) was tested against different markers QUIN‐induced neurotoxicity under both vitro vivo conditions. experiments, concentration‐dependent effect evaluated on regional peroxidative...

10.1046/j.1471-4159.2003.01857.x article EN Journal of Neurochemistry 2003-07-01

Objective The presence in the brain of α-synuclein containing Lewy neurites, or bodies, is histological hallmark Parkinson's disease (PD). discovery aggregates nerve endings heart, digestive tract, and skin has lent support to concept PD as a systemic disease. Our goals were, first, demonstrate inclusions and, second, detect quantitative differences between patients with atypical parkinsonism (AP). Methods Skin biopsies were taken from 67 20 controls. underwent immunohistochemistry (IHC)...

10.1002/acn3.78 article EN cc-by-nc-nd Annals of Clinical and Translational Neurology 2014-07-01

Worldwide, every year there is an increase in the number of people exposed to inorganic arsenic (iAs) via drinking water. Human populations present impaired cognitive function as a result prenatal and childhood iAs exposure, while studies animal models demonstrate neurobehavioral deficits accompanied by neurotransmitter, protein, enzyme alterations. Similar impairments have been observed close association with Alzheimer's disease (AD). In order determine whether promotes pathophysiological...

10.1021/acschemneuro.8b00278 article EN ACS Chemical Neuroscience 2018-08-24

Background: Alpha‐synuclein (ASyn), a marker of Parkinson’s disease (PD) and other neurodegenerative processes, plays pivotal roles in neuronal nuclei synapses. ASyn its phosphorylated form at Serine 129 (p‐ASyn) are involved DNA protection repair, processes altered aging, neurodegeneration, cancer. Objective: To analyze the localization p‐ASyn skin biopsies PD patients melanoma. Methods: Biopsies from 26 patients, 20 melanoma 31 control subjects were probed analyzed with antibody by...

10.1155/nri/1119424 article EN cc-by Neurology Research International 2025-01-01

Abstract Arsenic poisoning due to contaminated water and soil, mining waste, glass manufacture, select agrochemicals, as well sea food, affects millions of people world wide. Recently, an involvement arsenic in Alzheimer's disease (AD) has been hypothesized (Gong O'Bryant, 2010). The present study stresses the hypothesis whether sodium arsenite, its main metabolite, dimethylarsinic acid (DMA), may affect expression processing amyloid precursor protein (APP), using cholinergic cell line...

10.1016/j.ijdevneu.2011.03.004 article EN International Journal of Developmental Neuroscience 2011-03-24

This study characterizes the expression of tau (p-tau) and α-synuclein (α-syn) by immunohistochemistry in skin three different populations: healthy control (HC), Parkinson disease (PD), progressive supranuclear paralysis (PSP) subjects, with purpose finding a biomarker that could differentiate between subjects PD PSP.We evaluated presence p-tau α-syn pilot distinct groups patients: 17 patients PD, 10 PSP. Four millimeters punch biopsies were obtained from occipital area analyzed using...

10.1002/acn3.285 article EN cc-by-nc-nd Annals of Clinical and Translational Neurology 2016-02-01

Chronic arsenic exposure during development is associated with alterations of chemical transmission and demyelination, which result in cognitive deficits peripheral neuropathies. At the cellular level, toxicity involves increased generation reactive species that induce severe such as DNA fragmentation, apoptosis, lipid peroxidation. It has been proposed arsenic-associated neurodegeneration could evolve to Alzheimer disease later life.1,2 In this study, effects chronic inorganic (3 ppm by...

10.1021/acs.chemrestox.7b00215 article EN Chemical Research in Toxicology 2017-11-20

Abstract Background The misfolding and prion‐like propagation of the protein α‐synuclein (α‐syn) is leading molecular signature in Parkinson's disease ( PD ). There a significant coincidence melanoma that may suggest shared pathophysiology. This study compared presence α‐syn neural crest‐derived tissues, such as nevi, melanoma, skin tags, biopsies from patients with healthy controls. Methods Biopsies participants were obtained tertiary referral center for dermatology neurology Mexico private...

10.1002/mdc3.12494 article EN Movement Disorders Clinical Practice 2017-03-31

Since the tau protein is closely involved in physiopathology of Alzheimer´s disease (AD), studying its behavior cellular models might lead to new insights on understanding this devastating at molecular levels. In present study, primary cultures human fibroblasts were established and used determine expression localization distinct phosphorylation states both untransfected gene-transfected cells subjected oxidative stress. Higher immunopositivity phospho-tau was observed cell nuclei response...

10.3389/fnins.2017.00495 article EN cc-by Frontiers in Neuroscience 2017-09-07

Background. Recent reports point to a nuclear origin of Alzheimer’s disease (AD). Aged postmitotic neurons try repair their damaged DNA by entering the cell cycle. This aberrant cycle re-entry involves chromatin modifications where Tau and lamin are involved. The purpose this work was elucidate participation in pathological transformation at early AD. Methodology. study performed hippocampal paraffin embedded sections adult, senile, AD brains I-VI Braak stages. We analyzed phospho-Tau,...

10.3390/ijms21051841 article EN International Journal of Molecular Sciences 2020-03-07

Several single components of mining waste (arsenic, manganese, lead, cadmium) to which humans are exposed at the area Villa de la Paz, Mexico, known provoke alterations striatal dopaminergic parameters. In this study we used an animal model examine neurochemical changes resulting from exposure a metal mixture. We microdialysis compare in vivo dopamine release adult rats subchronically by oral route with those control group and sodium arsenite (25 mg/kg/day). found that arsenic manganese do...

10.1289/ehp.106-1533203 article EN public-domain Environmental Health Perspectives 1998-08-01
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