Publicacións nas que colabora con JOSE LUIS LABANDEIRA GARCIA (34)

2024

  1. Non-HLA angiotensin-type-1 receptor autoantibodies mediate the long-term loss of grafted neurons in Parkinson’s disease models

    Stem Cell Research and Therapy, Vol. 15, Núm. 1

2023

  1. Boolean analysis shows a high proportion of dopamine D2 receptors interacting with adenosine A2A receptors in striatal medium spiny neurons of mouse and non-human primate models of Parkinson's disease

    Neurobiology of Disease, Vol. 188

  2. Interactions between Angiotensin Type-1 Antagonists, Statins, and ROCK Inhibitors in a Rat Model of L-DOPA-Induced Dyskinesia

    Antioxidants, Vol. 12, Núm. 7

  3. The cannabinoid CB1 receptor interacts with the angiotensin AT2 receptor. Overexpression of AT2-CB1 receptor heteromers in the striatum of 6-hydroxydopamine hemilesioned rats

    Experimental Neurology, Vol. 362

2022

  1. Angiotensin Type-1 Receptor Inhibition Reduces NLRP3 Inflammasome Upregulation Induced by Aging and Neurodegeneration in the Substantia Nigra of Male Rodents and Primary Mesencephalic Cultures

    Antioxidants, Vol. 11, Núm. 2

2021

  1. Nadph-oxidase, rho-kinase and autophagy mediate the (Pro)renin-induced pro-inflammatory microglial response and enhancement of dopaminergic neuron death

    Antioxidants, Vol. 10, Núm. 9

  2. Novel Interactions Involving the Mas Receptor Show Potential of the Renin–Angiotensin system in the Regulation of Microglia Activation: Altered Expression in Parkinsonism and Dyskinesia

    Neurotherapeutics, Vol. 18, Núm. 2, pp. 998-1016

2020

  1. Angiotensin AT1and AT2receptor heteromer expression in the hemilesioned rat model of Parkinson's disease that increases with levodopa-induced dyskinesia

    Journal of Neuroinflammation, Vol. 17, Núm. 1

  2. Interactions Between the Serotonergic and Other Neurotransmitter Systems in the Basal Ganglia: Role in Parkinson’s Disease and Adverse Effects of L-DOPA

    Frontiers in Neuroanatomy, Vol. 14

  3. Rho kinase inhibitor fasudil reduces l-DOPA-induced dyskinesia in a rat model of Parkinson's disease

    British Journal of Pharmacology, Vol. 177, Núm. 24, pp. 5622-5641

2018

  1. Physical exercise improves aging-related changes in angiotensin, IGF-1, SIRT1, SIRT3, and VEGF in the substantia Nigra

    Journals of Gerontology - Series A Biological Sciences and Medical Sciences, Vol. 73, Núm. 12, pp. 1594-1601

2016

  1. Hints on the Lateralization of Dopamine Binding to D 1 Receptors in Rat Striatum

    Molecular Neurobiology, Vol. 53, Núm. 8, pp. 5436-5445

  2. Aging-related Increase in Rho Kinase Activity in the Nigral Region is Counteracted by Physical Exercise

    Journals of Gerontology - Series A Biological Sciences and Medical Sciences, Vol. 71, Núm. 10, pp. 1254-1257

  3. Effects of rho kinase inhibitors on grafts of dopaminergic cell precursors in a rat model of Parkinson’s disease

    Stem Cells Translational Medicine, Vol. 5, Núm. 6, pp. 804-815

2015

  1. Stronger Dopamine D1 Receptor-Mediated Neurotransmission in Dyskinesia

    Molecular Neurobiology, Vol. 52, Núm. 3, pp. 1408-1420

2014

  1. Angiotensin type 1 receptor blockage reduces l-dopa-induced dyskinesia in the 6-OHDA model of Parkinson's disease. Involvement of vascular endothelial growth factor and interleukin-1β

    Experimental Neurology, Vol. 261, pp. 720-732

2010

  1. Location of prorenin receptors in primate substantia nigra: Effects on dopaminergic cell death

    Journal of Neuropathology and Experimental Neurology, Vol. 69, Núm. 11, pp. 1130-1142

  2. Nigral and striatal regulation of angiotensin receptor expression by dopamine and angiotensin in rodents: Implications for progression of Parkinson's disease

    European Journal of Neuroscience, Vol. 32, Núm. 10, pp. 1695-1706

2009

  1. Brain oxidative stress and selective behaviour of aluminium in specific areas of rat brain: Potential effects in a 6-OHDA-induced model of Parkinson's disease

    Journal of Neurochemistry, Vol. 109, Núm. 3, pp. 879-888

2008

  1. Brain angiotensin enhances dopaminergic cell death via microglial activation and NADPH-derived ROS

    Neurobiology of Disease, Vol. 31, Núm. 1, pp. 58-73