Publikationen, an denen er mitarbeitet JANNETTE RODRIGUEZ PALLARES (28)

2017

  1. Brain renin-angiotensin system and microglial polarization: Implications for aging and neurodegeneration

    Frontiers in Aging Neuroscience, Vol. 9, Núm. MAY

2015

  1. Interaction between NADPH-oxidase and Rho-kinase in angiotensin II-induced microglial activation

    GLIA, Vol. 63, Núm. 3, pp. 466-482

2013

  1. Brain angiotensin regulates iron homeostasis in dopaminergic neurons and microglial cells

    Experimental Neurology, Vol. 250, pp. 384-396

2012

  1. Brain angiotensin and dopaminergic degeneration: Relevance to Parkinson’s disease

    American Journal of Neurodegenerative Diseases, Vol. 1, Núm. 3, pp. 226-244

  2. Mitochondrial ATP-sensitive potassium channels enhance angiotensin-induced oxidative damage and dopaminergic neuron degeneration. Relevance for aging-associated susceptibility to Parkinson's disease

    Age, Vol. 34, Núm. 4, pp. 863-880

2011

  1. Aging, angiotensin system and dopaminergic degeneration in the substantia nigra

    Aging and Disease, Vol. 2, Núm. 3, pp. 257-274

2010

  1. Effect of inhibitors of NADPH oxidase complex and mitochondrial ATP-sensitive potassium channels on generation of dopaminergic neurons from neurospheres of mesencephalic precursors

    Developmental Dynamics, Vol. 239, Núm. 12, pp. 3247-3259

  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. Aging and sedentarism decrease vascularization and VEGF levels in the rat substantia nigra. Implications for Parkinson's disease

    Journal of Cerebral Blood Flow and Metabolism, Vol. 29, Núm. 2, pp. 230-234

  2. The inflammatory response in the MPTP model of Parkinson's disease is mediated by brain angiotensin: Relevance to progression of the disease

    Journal of Neurochemistry, Vol. 109, Núm. 2, pp. 656-669

  3. The mitochondrial ATP-sensitive potassium channel blocker 5-hydroxydecanoate inhibits toxicity of 6-hydroxydopamine on dopaminergic neurons

    Neurotoxicity Research, Vol. 15, Núm. 1, pp. 82-95

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

  2. Different effects of anti-sonic hedgehog antibodies and the hedgehog pathway inhibitor cyclopamine on generation of dopaminergic neurons from neurospheres of mesencephalic precursors

    Developmental Dynamics, Vol. 237, Núm. 4, pp. 909-917

2007

  1. Effects of GABA and GABA receptor inhibition on differentiation of mesencephalic precursors into dopaminergic neurons in vitro

    Developmental Neurobiology, Vol. 67, Núm. 12, pp. 1549-1559

  2. Mechanism of 6-hydroxydopamine neurotoxicity: The role of NADPH oxidase and microglial activation in 6-hydroxydopamine-induced degeneration of dopaminergic neurons

    Journal of Neurochemistry, Vol. 103, Núm. 1, pp. 145-156

  3. Serotonin decreases generation of dopaminergic neurons from mesencephalic precursors via serotonin type 7 and type 4 receptors

    Developmental Neurobiology, Vol. 67, Núm. 1, pp. 10-22

2005

  1. Angiotensin II and interleukin-1 interact to increase generation of dopaminergic neurons from neurospheres of mesencephalic precursors

    Developmental Brain Research, Vol. 158, Núm. 1-2, pp. 120-122

  2. Expanded mesencephalic precursors develop into grafts of densely packed dopaminergic neurons that reinnervate the surrounding striatum and induce functional responses in the striatal neurons

    Synapse, Vol. 58, Núm. 1, pp. 13-22

2004

  1. Angiotensin II increases differentiation of dopaminergic neurons from mesencephalic precursors via angiotensin type 2 receptors

    European Journal of Neuroscience, Vol. 20, Núm. 6, pp. 1489-1498

2003

  1. Elimination of serotonergic cells induces a marked increase in generation of dopaminergic neurons from mesencephalic precursors

    European Journal of Neuroscience, Vol. 18, Núm. 8, pp. 2166-2174