Selected Publications

Academic Article

Year Title Altmetric
2021 Preventing Parkinson’s Disease: An Environmental AgendaJournal of Parkinson's Disease.  1-24. 2021
2021 VGLUT2 is a determinant of dopamine neuron resilience in a rotenone model of dopamine neurodegeneration 2021
2021 The industrial solvent trichloroethylene induces LRRK2 kinase activity and dopaminergic neurodegeneration in a rat model of Parkinson's diseaseNeurobiology of Disease.  153. 2021
2021 Vesicular glutamate transporter modulates sex differences in dopamine neuron vulnerability to age-related neurodegenerationAging Cell.  20. 2021
2020 Protection from α-Synuclein induced dopaminergic neurodegeneration by overexpression of the mitochondrial import receptor TOM20npj Parkinson's Disease.  6. 2020
2020 Trichloroethylene, a ubiquitous environmental contaminant in the risk for Parkinson's disease 2020
2020 LRRK2 inhibition prevents endolysosomal deficits seen in human Parkinson's diseaseNeurobiology of Disease.  134. 2020
2019 Sex Differences in Rotenone Sensitivity Reflect the Male-to-Female Ratio in Human Parkinson's Disease IncidenceToxicological Sciences.  170:133-143. 2019
2019 Response to Rotenone and Parkinson's Disease; Reduced Sensitivity in FemalesToxicological Sciences.  170:563. 2019
2019 Long-term RNAi knockdown of α-synuclein in the adult rat substantia nigra without neurodegenerationNeurobiology of Disease.  125:146-153. 2019
2019 Correction to: Neuroprotective efficacy and pharmacokinetic behavior of novel anti-inflammatory para-phenyl substituted diindolylmethanes in a mouse model of Parkinson’s disease(J Pharmacol Exp Ther. (2013) 345: 1 (125-38) DOI: 10.1124/jpet.112.201558)Journal of Pharmacology and Experimental Therapeutics.  369:66. 2019
2018 LRRK2 activation in idiopathic Parkinson's diseaseScience Translational Medicine.  10. 2018
2018 Astrocyte-specific DJ-1 overexpression protects against rotenone-induced neurotoxicity in a rat model of Parkinson's diseaseNeurobiology of Disease.  115:101-114. 2018
2018 Alpha-synuclein: Pathology, mitochondrial dysfunction and neuroinflammation in Parkinson's diseaseNeurobiology of Disease.  109:249-257. 2018
2015 The Nurr1 activator 1,1-bis(3′-indolyl)-1-(p-chlorophenyl) methane blocks inflammatory gene expression in BV-2 microglial cells by inhibiting nuclear factor κBMolecular Pharmacology.  87:1021-1034. 2015
2015 Novel para-phenyl substituted diindolylmethanes protect against MPTP neurotoxicity and suppress glial activation in a mouse model of Parkinson's diseaseToxicological Sciences.  143:360-373. 2015
2014 Dopaminergic neurotoxicants cause biphasic inhibition of purinergic calcium signaling in astrocytesPLoS ONE.  9. 2014
2013 Neuroprotective efficacy and pharmacokinetic behavior of novel anti-inflammatory para-phenyl substituted diindolylmethanes in a mouse model of Parkinson's diseaseJournal of Pharmacology and Experimental Therapeutics.  345:125-138. 2013
2011 Low-dose 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine causes inflammatory activation of astrocytes in nuclear factor-κB reporter mice prior to loss of dopaminergic neuronsJournal of Neuroscience Research.  89:406-417. 2011


Year Title Altmetric
2021 The environmental pollutant trichloroethylene disrupts key neural pathways during brain development.  207-217. 2021
2017 Etiology and Pathogenesis of Parkinson’s Disease 2017
2016 Toxin-mediated complex I inhibition and parkinson’s disease.  115-137. 2016

Research Overview

  • My lab is interested in uncovering the mechanisms that drive neurologic disease from environmental exposures. We are currently investigating chlorinated solvents, such as the degreasing compound trichloroethylene (TCE), and their role in dopaminergic neurodegeneration in Parkinson’s disease. Similarly, we are interested in understanding how developmental exposure to chlorinated solvents may induce neurologic and psychiatric disease in adulthood. We take a system wide approach to address these mechanisms – including gut-brain axis, the influence of the microbiome, and gene-regulatory elements (e.g., epigenetics) in exposures that increase risk for neurodegeneration.

    In addition to solvents, we undertake projects assessing how pesticides, metals, and other neurotoxic contaminants induce oxidative stress, impair mitophagy/autophagy, and influence neuroinflammation. Our overall goal is to mitigate toxicity with therapeutic interventions or environmental remediation efforts.
  • Education And Training

  • University of Pittsburgh Neurology, Postdoctoral Fellowship
  • Doctor of Philosophy in Toxicology, Colorado State University 2014
  • Bachelor of Science or Mathematics in Biology / Biological Sciences, Colorado State University 2008
  • Full Name

  • Briana De Miranda