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Towards improved screening of toxins for Parkinson’s risk
Hirsch, E., Graybiel, A. M. & Agid, Y. A. Melanized dopaminergic neurons are differentially susceptible to degeneration in Parkinson’s disease. Nature 334, 345–348 (1988).
Savica, R., Rocca, W. A. & Ahlskog, J. E. When does Parkinson disease start? Arch. Neurol. 67, 798–801 (2010).
Wu, Y., Le, W. & Jankovic, J. Preclinical Biomarkers of Parkinson Disease. Arch. Neurol. 68, 22–30 (2011).
Dauvilliers, Y. et al. REM sleep behaviour disorder. Nat. Rev. Dis. Prim. 4, 1–16 (2018).
Parkinson, J. An essay on the shaking palsy. 1817. Clin. Neurosci. 14, 223–236 (2002).
Morris, A. D. James Parkinson His Life and Times. James Park. His Life Times https://doi.org/10.1007/978-1-4615-9824-4 (1989).
Global, regional, and national burden of Parkinson’s disease, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet. Neurol. 17, 939–953 (2018).
Dorsey, E. R. & Bloem, B. R. The Parkinson Pandemic—A Call to Action. JAMA Neurol. 75, 9–10 (2018).
Ascherio, A. & Schwarzschild, M. A. The epidemiology of Parkinson’s disease: risk factors and prevention. Lancet Neurol. 15, 1257–1272 (2016).
OECD Guidelines for the Testing of Chemicals, Section 4: Health Effects | OECD Guidelines for the Testing of Chemicals | OECD iLibrary. https://www.oecd-ilibrary.org/environment/oecd-guidelines-for-the-testing-of-chemicals-section-4-health-effects_20745788.
Meerman, J. J. et al. ScienceDirect Toxicology Neurodegeneration in a regulatory context: The need for speed. Curr. Opin. Toxicol. 33, 100383 (2023).
Neurotoxicants, E. et al. Workshop on the EFSA NAMs Project on. 1–8 (2022).
Jacobs, M. N. et al. Chemical carcinogen safety testing: OECD expert group international consensus on the development of an integrated approach for the testing and assessment of chemical non-genotoxic carcinogens. Arch. Toxicol. 94, 2899–2923 (2020).
Heusinkveld, H. et al. Towards a mechanism-based approach for the prediction of nongenotoxic carcinogenic potential of agrochemicals. Crit. Rev. Toxicol. 50, 725–739 (2020).
Goldman, S. M. Environmental toxins and Parkinson’s disease. Annu. Rev. Pharmacol. Toxicol. 54, 141–164 (2014).
Gatto, N. M., Cockburn, M., Bronstein, J., Manthripragada, A. D. & Ritz, B. Well-water consumption and Parkinson’s disease in rural California. Environ. Health Perspect. 117, 1912–1918 (2009).
Hristina, V. D. et al. Environmental factors and Parkinson’s disease: A case-control study in Belgrade, Serbia. Int J. Neurosci. 120, 361–367 (2010).
van der Mark, M. et al. Is pesticide use related to Parkinson disease? Some clues to heterogeneity in study results. Environ. Health Perspect. 120, 340–347 (2012).
Hancock, D. B. et al. Pesticide exposure and risk of Parkinson’s disease: A family-based case-control study. BMC Neurol. 8, 6 (2008).
Pouchieu, C. et al. Pesticide use in agriculture and Parkinson’s disease in the AGRICAN cohort study. Int. J. Epidemiol. 47, 299–310 (2018).
Yuan, Y. et al. High pesticide exposure events and dream-enacting behaviors among US farmers. Mov. Disord. 37, 962–971 (2022).
Tanner, C. M. et al. Rotenone, paraquat, and Parkinson’s disease. Environ. Health Perspect. 119, 866–872 (2011).
CDC | Facts about Paraquat. https://emergency.cdc.gov/agent/paraquat/basics/facts.asp.
Hugh-Jones, M. E., Peele, R. H. & Wilson, V. L. Parkinson’s Disease in Louisiana, 1999–2012: Based on hospital primary discharge diagnoses, incidence, and risk in relation to local agricultural crops, pesticides, and aquifer recharge. Int. J. Environ. Res. Public Heal. 17, 1584 (2020).
Pezzoli, G. & Cereda, E. Exposure to pesticides or solvents and risk of Parkinson disease. Neurology 80, 2035–2041 (2013).
Dhillon, A. S. et al. Pesticide/environmental exposures and Parkinson’s disease in East Texas. J. Agromed. 13, 37–48 (2008).
Schneider Medeiros, M., Reddy, P. S., Socal, P. M., Schumacher-Schuh, A. F. & Mello Rieder, C. R. Occupational pesticide exposure and the risk of death in patients with Parkinson’s disease: An observational study in southern Brazil. Environ. Heal. A Glob. Access Sci. Source 19, 1–8 (2020).
Li, S. et al. Proximity to residential and workplace pesticides application and the risk of progression of Parkinson’s diseases in Central California. Sci. Total Environ. 864, 160851 (2023).
Firestone, J. A. et al. Occupational factors and risk of Parkinson’s disease: A population-based case-control study. Am. J. Ind. Med. 53, 217–223 (2010).
Weed, D. L. Does paraquat cause Parkinson’s disease? A review of reviews. Neurotoxicology 86, 180–184 (2021).
Kline, E. M. et al. Genetic and environmental factors in Parkinson’s disease converge on immune function and inflammation. Mov. Disord. 36, 25–36 (2021).
Ott, J. Association of genetic loci. Neurology 63, 955–958 (2004).
Goldman, S. M. et al. Genetic modification of the association of paraquat and Parkinson’s disease. Mov. Disord. 27, 1652–1658 (2012).
Ritz, B. R. et al. Dopamine transporter genetic variants and pesticides in Parkinson’s disease. Environ. Health Perspect. 117, 964–969 (2009).
Kelada, S. N. P. et al. 5′ and 3′ region variability in the dopamine transporter gene (SLC6A3), pesticide exposure and Parkinson’s disease risk: a hypothesis-generating study. Hum. Mol. Genet 15, 3055–3062 (2006).
Tanner, C. M. et al. Occupation and risk of Parkinsonism: A multicenter case-control study. Arch. Neurol. 66, 1106–1113 (2009).
Fleming, L., Mann, J. B., Bean, J., Briggle, T. & Sanchez‐Ramos, J. R. Parkinson’s disease and brain levels of organochlorine pesticides. Ann. Neurol. 36, 100–103 (1994).
Corrigan, F. M., Lochgilphead, C. L., Shore, R. F., Daniel, S. E. & Mann, D. Organochlorine insecticides in substantia nigra in parkinson’s disease. J. Toxicol. Environ. Heal. – Part A 59, 229–234 (2000).
Allen, R. H. et al. Breast cancer and pesticides in Hawaii: The need for further study. Environ. Health Perspect. 105, 679–683 (1997).
Smith, R. J. Hawaiian milk contamination creates alarm. Science 217, 137–140 (1982).
Baker, D. B., Loo, S. & Barker, J. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Hawaii Med. J. 50, 108-12–118 (1991).
Ross, G. W. et al. Association of brain heptachlor epoxide and other organochlorine compounds with lewy pathology. Mov. Disord. 34, 228–235 (2019).
Jayaraj, R., Megha, P. & Sreedev, P. Organochlorine pesticides, their toxic effects on living organisms and their fate in the environment. Interdiscip. Toxicol. 9, 90 (2016).
Egeghy, P. P. et al. The exposure data landscape for manufactured chemicals. Sci. Total Environ. 414, 159–166 (2012).
EU Pesticides Database (v.2.2) Search Active substances, safeners and synergists. https://ec.europa.eu/food/plant/pesticides/eu-pesticides-database/active-substances/index.cfm?event=search.as&s=3&a_from=&a_to=&e_from=&e_to=&additionalfilter__class_p1=&additionalfilter__class_p2=&string_tox_1=&string_tox_1=&string_tox_2=&string_tox_2=&string_tox_3=&string_tox_3=&string_tox_4=&string_tox_4=.
Barbeau, A., Roy, M., Bernier, G., Campanella, G. & Paris, S. Ecogenetics of Parkinson’s disease: Prevalence and environmental aspects in rural areas. Can. J. Neurol. Sci. / J. Can. des. Sci. Neurol. 14, 36–41 (1987).
Liu, C. et al. A scientometric analysis and visualization of research on Parkinson’s disease associated with pesticide exposure. Front. Public Heal. 8, 91 (2020).
Crofton, K. M. et al. Interlaboratory comparison of motor activity experiments: implications for neurotoxicological assessments. Neurotoxicol. Teratol. 13, 599–609 (1991).
Meyer, O. A., Tilson, H. A., Byrd, W. C. & Riley, M. T. A method for the routine assessment of fore- and hindlimb grip strength of rats and mice. Neurobehav. Toxicol. 1, 233–236 (1979).
Homberg, J. R. et al. The continued need for animals to advance brain research. Neuron 109, 2374–2379 (2021).
Höglinger, G. U. et al. Chronic systemic complex I inhibition induces a hypokinetic multisystem degeneration in rats. J. Neurochem. 84, 491–502 (2003).
Johnson, M. E. & Bobrovskaya, L. An update on the rotenone models of Parkinson’s disease: Their ability to reproduce the features of clinical disease and model gene–environment interactions. Neurotoxicology 46, 101–116 (2015).
Sherer, T. B., Betarbet, R., Kim, J. H. & Greenamyre, J. T. Selective microglial activation in the rat rotenone model of Parkinson’s disease. Neurosci. Lett. 341, 87–90 (2003).
Emmrich, J. V., Hornik, T. C., Neher, J. J. & Brown, G. C. Rotenone induces neuronal death by microglial phagocytosis of neurons. FEBS J. 280, 5030–5038 (2013).
Gao, H. M., Hong, J. S., Zhang, W. & Liu, B. Distinct role for microglia in rotenone-induced degeneration of dopaminergic neurons. J. Neurosci. 22, 782–790 (2002).
Zhou, P. et al. Histamine-4 receptor antagonist JNJ7777120 inhibits pro-inflammatory microglia and prevents the progression of Parkinson-like pathology and behaviour in a rat model. Brain. Behav. Immun. 76, 61–73 (2019).
Fang, Q. et al. Histamine-4 receptor antagonist ameliorates Parkinson-like pathology in the striatum. Brain. Behav. Immun. 92, 127–138 (2021).
Cannon, J. R. et al. Expression of human E46K-mutated α-synuclein in BAC-transgenic rats replicates early-stage Parkinson’s disease features and enhances vulnerability to mitochondrial impairment. Exp. Neurol. 240, 44–56 (2013).
George, S. et al. α-synuclein transgenic mice reveal compensatory increases in Parkinson’s disease-associated proteins DJ-1 and Parkin and have enhanced α-synuclein and PINK1 levels after rotenone treatment. J. Mol. Neurosci. 42, 243–254 (2010).
McCormack, A. L. et al. Environmental risk factors and parkinson’s disease: selective degeneration of nigral dopaminergic neurons caused by the herbicide paraquat. Neurobiol. Dis. 10, 119–127 (2002).
Purisai, M. G. et al. Microglial activation as a priming event leading to paraquat-induced dopaminergic cell degeneration. Neurobiol. Dis. 25, 392–400 (2007).
Ossowska, K. et al. Degeneration of dopaminergic mesocortical neurons and activation of compensatory processes induced by a long-term paraquat administration in rats: Implications for Parkinson’s disease. Neuroscience 141, 2155–2165 (2006).
Kuter, K., Nowak, P., Gołembiowska, K. & Ossowska, K. Increased reactive oxygen species production in the brain after repeated low-dose pesticide paraquat exposure in rats. A comparison with peripheral tissues. Neurochem. Res. 35, 1121–1130 (2010).
McCormack, A. L. et al. Role of oxidative stress in paraquat-induced dopaminergic cell degeneration. J. Neurochem. 93, 1030–1037 (2005).
Kuter, K. et al. Toxic influence of subchronic paraquat administration on dopaminergic neurons in rats. Brain Res. 1155, 196–207 (2007).
Huang, C., Ma, J., Li, B. & Sun, Y. Wnt1 silencing enhances neurotoxicity induced by paraquat and maneb in SH‑SY5Y cells. Exp. Ther. Med. 18, 3643–3649 (2019).
Ali, S. F., Binienda, Z. K. & Imam, S. Z. Molecular aspects of dopaminergic neurodegeneration: Gene-environment interaction in Parkin dysfunction. Int. J. Environ. Res. Public Heal 8, 4702–4713 (2011).
Song, C., Kanthasamy, A., Jin, H., Anantharam, V. & Kanthasamy, A. G. Paraquat induces epigenetic changes by promoting histone acetylation in cell culture models of dopaminergic degeneration. Neurotoxicology 32, 586–595 (2011).
Chen, N. et al. Paraquat-induced oxidative stress regulates N6-methyladenosine (m6A) modification of circular RNAs. Environ. Pollut. 290, 117816 (2021).
Thiruchelvam, M., Brockel, B. J., Richfield, E. K., Baggs, R. B. & Cory-Slechta, D. A. Potentiated and preferential effects of combined paraquat and maneb on nigrostriatal dopamine systems: Environmental risk factors for Parkinson’s disease? Brain Res. 873, 225–234 (2000).
Cicchetti, F. et al. Systemic exposure to paraquat and maneb models early Parkinson’s disease in young adult rats. Neurobiol. Dis. 20, 360–371 (2005).
Qiu, X. et al. Inhibition of NLRP3 inflammasome by glibenclamide attenuated dopaminergic neurodegeneration and motor deficits in paraquat and maneb-induced mouse Parkinson’s disease model. Toxicol. Lett. 349, 1–11 (2021).
Li, X. et al. Neuroprotective effects of Polygonum multiflorum on nigrostriatal dopaminergic degeneration induced by paraquat and maneb in mice. Pharmacol. Biochem. Behav. 82, 345–352 (2005).
Anselmi, L. et al. Ingestion of subthreshold doses of environmental toxins induces ascending Parkinsonism in the rat. npj Park. Dis. 4, 1–10 (2018).
Martinez, B. A., Caldwell, K. A. & Caldwell, G. A. C. elegans as a model system to accelerate discovery for Parkinson disease. Curr. Opin. Genet Dev. 44, 102–109 (2017).
Doyle, J. M. & Croll, R. P. A critical review of zebrafish models of Parkinson’s disease. Front Pharm. 13, 835827 (2022).
Ved, R. et al. Similar patterns of mitochondrial vulnerability and rescue induced by genetic modification of α-Synuclein, Parkin, and DJ-1 in Caenorhabditis elegans. J. Biol. Chem. 280, 42655–42668 (2005).
Wang, C. et al. Neurobiology of disease drosophila overexpressing Parkin R275W mutant exhibits dopaminergic neuron degeneration and mitochondrial abnormalities. https://doi.org/10.1523/JNEUROSCI.0218-07.2007 (2007).
Saini, N. et al. Extended lifespan of Drosophila parkin mutants through sequestration of redox-active metals and enhancement of anti-oxidative pathways. Neurobiol. Dis. 40, 82–92 (2010).
Flinn, L. et al. Complex I deficiency and dopaminergic neuronal cell loss in parkin-deficient zebrafish (Danio rerio). Brain 132, 1613–1623 (2009).
Meulener, M. et al. Drosophila DJ-1 mutants are selectively sensitive to environmental toxins associated with Parkinson’s disease. Curr. Biol. 15, 1572–1577 (2005).
Bai, Q., Mullett, S. J., Garver, J. A., Hinkle, D. A. & Burton, E. A. Zebrafish DJ-1 is evolutionarily conserved and expressed in dopaminergic neurons. Brain Res. 1113, 33–44 (2006).
Edson, A. J. et al. Dysregulation in the brain protein profile of zebrafish lacking the Parkinson’s disease-related protein DJ-1. Mol. Neurobiol. 56, 8306–8322 (2019).
Saha, S. et al. LRRK2 modulates vulnerability to mitochondrial dysfunction in caenorhabditis elegans. J. Neurosci. 29, 9210–9218 (2009).
Wolozin, B., Saha, S., Guillily, M., Ferree, A. & Riley, M. Investigating convergent actions of genes linked to familial Parkinson’s disease. Neurodegener. Dis. 5, 182–185 (2008).
Wang, D. et al. Dispensable role of Drosophila ortholog of LRRK2 kinase activity in survival of dopaminergic neurons. Mol. Neurodegener. 3, 1–7 (2008).
Ng, C.-H. et al. Parkin protects against LRRK2 G2019S mutant-induced dopaminergic neurodegeneration in drosophila. J. Neurosci. 29, 11257–11262 (2009).
Venderova, K. et al. Leucine-rich repeat kinase 2 interacts with Parkin, DJ-1 and PINK-1 in a Drosophila melanogaster model of Parkinson’s disease. Hum. Mol. Genet. 18, 4390–4404 (2009).
Sheng, D. et al. Deletion of the WD40 domain of LRRK2 in Zebrafish causes Parkinsonism-like loss of neurons and locomotive defect. PLoS Genet 6, e1000914 (2010).
Prabhudesai, S. et al. LRRK2 knockdown in zebrafish causes developmental defects, neuronal loss, and synuclein aggregation. J. Neurosci. Res. 94, 717–735 (2016).
Ortega-Arellano, H. F., Jimenez-Del-Rio, M. & Velez-Pardo, C. Melatonin increases life span, restores the locomotor activity, and reduces lipid peroxidation (LPO) in transgenic knockdown parkin drosophila melanogaster exposed to paraquat or paraquat/Iron. Neurotox. Res. 39, 1551–1563 (2021).
Vegh, C. et al. Combined ubisol-q10 and ashwagandha root extract target multiple biochemical mechanisms and reduces neurodegeneration in a paraquat-induced rat model of parkinson’s disease. Antioxidants 10, 563 (2021).
Schmidt, E., Seifert, M. & Baumeister, R. Caenorhabditis elegans as a model system for Parkinson’s Disease. Neurodegener. Disord. 4, 199–217 (2007).
van Ham, T. J. et al. C. elegans model identifies genetics modifiers of a-synuclein inclusion formation during aging. PLoS Genet 3, e1999927 (2008).
Harrington, A. J., Hamamichi, S., Caldwell, G. A. & Caldwell, K. A. C. elegans as a model organism to investigate molecular pathways involved with Parkinson’s Disease. Dev. Dyn. 239, 1282–1295 (2010).
Wolozin, B., Gabel, C., Feree, A., Guillily, M. & Ebata, A. Watching worms whither: Modeling neurdegeneration in C. elegans. Prog. Mol. Biol. Transl. Sci. 100, 499–514 (2011).
Gaeta, A. L., Caldwell, K. A. & Caldwell, G. A. Found in translation: The utility of C. elegans alpha-synuclein models of Parkinson’s disease. Brain Sci. 9, 73 (2019).
Chege, P. M. & McColl, G. Caenorhabditis elegans: a model to investigate oxidative stress and metal dyshomeostasis in Parkinson’s disease. Front. Aging Neurosci. 6, 89 (2014).
Lasko, M. et al. Dopaminergic neuronal loss and motor deficits in Caenorhabditis leegans overexpressing human alpha-synuclein. J. Neronchem. 86, 165–172 (2003).
Kuwahara, T. et al. Familial Parkinson mutant alpha-synuclein causes dopamine neuron dysfunction in transgenic Caenorhabditis elegans. J. Biol. Chem. 281, 334–340 (2006).
Hughes, S. et al. Using a caenorhabditis elegans Parkinson’s disease model to assess disease progression and therapy efficiency. Pharmaceuticals 15, 512 (2022).
Cooper, J. F. et al. Delaying aging is neuroprotective in Parkinson’s disease: A genetic analysis in C. Elegans models. Parkinsons. Dis. 1, 15022 (2015).
Hamamichi, S. et al. Hypothesis-based RNAi screening identifies neuroprotective genes in a Parkinson’s disease model. Proc. Natl. Acad. Sci. USA 105, 728–733 (2008).
Su, L. J. et al. Compounds from an unbiased chemical screen reverse both ER-to-Golgi trafficking defects and mitochondrial dysfunction in Parkinson’s disease models. Dis. Model Mech. 3, 194–208 (2010).
Sawin, E. R., Ranganathan, R. & Horvitz, H. R. C. elegans locomotory rate is modulated by the environment through a dopaminergic pathway and by experience through a serotonergic pathway. Neuron 26, 619–631 (2000).
Alavez, S. & Lithgow, G. J. Pharmacological maintenance of protein homeostasis could postpone age-related disease. Aging Cell 11, 187–191 (2012).
Jadiya, P. & Nazir, A. Environmental toxicants as extrinsic epigenetic factors for parkinsonism: studies employing transgenic C. elegans model. CNS Neurol. Disord. Drug Targets 11, 976–983 (2012).
McVey, K. A. et al. Caenorhabditis elegans: An emerging model system for pesticideneurotoxicity. J. Environ. Anal. Toxicol. S4, 1 (2012).
Meyer, D. & Williams, P. L. Toxicity testing of neurotoxic pesticides in Caenorhabditis elegans. J. Toxicol. Environ. Heal. B Crit. Rev. 17, 284–306 (2014).
Zhou, S., Wang, Z. & Klaunig, J. E. Caenorhabditis elegans neuron degeneration and mitochondrial suppression caused by selected environmental chemicals. Int J. Biochem Mol. Biol. 4, 191–200 (2013).
González-Hunt, C. P. et al. Exposure to mitochondrial genotoxins and dopaminergic neurodegeneration in Caenorhabditis elegans. PLoS One 9, e114459 (2014).
Bora, S. et al. Paraquat exposure over generation affects lifespan and reproduction through mitochondrial disruption in C. elegans. Toxicology 447, 152632 (2021).
Braungart, E., Gerlach, M., Riederer, P., Baumeister, R. & Hoener, M. C. Caenorhabditis elegans MPP+ model of Parkinson’s disease for high-throughput drug screenings. Neurodegener. Dis. 1, 175–183 (2004).
Mocko, J. B., Kern, A., Moosmann, B., Behl, C. & Hajieva, P. Phenothiazines interfere with dopaminergic neurodegeneration in Caenorhabditis elegans models of Parkinson’s disease. Neurobiol. Dis. 40, 120–129 (2010).
Ali, S. J. & Rajini, P. S. Elicitation of dopaminergic features of Parkinson’s disease in C. elegans by monocrotophos, an organophosphorous insecticide. CNS Neurol. Disord. Drug Targets 11, 993–1000 (2012).
Harrison Brody, A., Chou, E., Gray, J. M., Pokyrwka, N. J. & Raley-Susman, K. M. Mancozeb-induced behavioral deficits precede structural neural degeneration. Neurotoxicology 34, 74–81 (2013).
Maulik, M., Mitra, S., Bult-Ito, A., Taylor, B. E. & Vayndorf, E. M. Behavioral Phenotyping and Pathological Indicators of Parkinson’s Disease in C. elegans Models. Front Genet 8, 77 (2017).
Nagoshi, E. Drosophila Models of Sporadic Parkinson’s disease. Int. J. Mol. Sci. 19, 3343 (2018).
Feany, M. B. & Bender, W. W. A Drosophila model of Parkinson’s disease. Nature 404, 394–398 (2000).
Bolus, H., Crocker, K., Boekhoff-Falk, G. & SChtarbonova, S. Modeling neurodegenerative disorders in drosophila melanogaster. Int. J. Mol. Sci. 21, 3055 (2020).
Kim, T., Song, B. & Lee, I.-S. Drosophila Glia: Models for human neurodevelopmental and neurodegenerative disorders. Int. J. Mol. Sci. 21, 4859 (2020).
Maitra, U. & Ciesla, L. Using Drosophila as a platform for drug discovery from natural products in Parkinson’s disease. Medchemcomm 10, 867–879 (2019).
Limmer, S., Weiler, A., Volkenhoff, A., Babatz, F. & Klambt, C. The Drosophila blood-brain barrier: development and function of a glial endothelium. Front. Neurosci. 8, 365 (2014).
Coulom, H. & Birman, S. Chronic exposure to rotenone models sporadic Parkinson’s disease in drosophila melanogaster. J. Neurosci. 24, 10993–10998 (2004).
Ayajuddin, M. et al. Adult health and transition stage-specific rotenone-mediated Drosophila model of Parkinson’s disease: Impact on late-onset neurodegenerative disease models. Front Mol. Neurosci. 15, 896183 (2022).
Bonilla-Ramirez, L., Jimenez-Del-Rio, M. & Velez-Pardo, C. Low doses of paraquat and polyphenols prolong life span and locomotor activity in knock-down parkin Drosophila melanogaster exposed to oxidative stress stimuli: Implication in autosomal recessive juvenile Parkinsonism. Gene 512, 355–363 (2013).
Ortega-Arellano, H. F., Jimenez-Del-Rio, M. & Velez-Pardo, C. Minocycline protects, rescues and prevents knockdown transgenic parkin Drosophila against paraquat/iron toxicity: Implications for autosomic recessive juvenile parkinsonism. Neurotoxicology 60, 42–53 (2017).
Reiszadeh Jahromi, S., Ramesh, S. R., Finkelstein, D. I. & Haddadi, M. α -Synuclein E46K Mutation and Involvement of Oxidative Stress in a Drosophila Model of Parkinson’s Disease. Parkinsons. Dis. 2021, 6621507 (2021).
Neves, P. F. R. et al. Age-related tolerance to paraquat-induced parkinsonism in Drosophila melanogaster. Toxicol. Lett. 361, 43–53 (2022).
Panula, P. et al. The comparative neuroanatomy and neurochemistry of zebrafish CNS systems of relevance to human neuropsychiatric diseases. Neurobiol. Disord. 40, 46–57 (2010).
Strähle, U. et al. Zebrafish embryos as an alternative to animal experiments-a commentary on the definition of the onset of protected life stages in animal welfare regulations. Reprod. Toxicol. 33, 128–132 (2012).
Kalueff, A. V., Echevarria, D. J. & Stewart, A. M. Gaining translational momentum: more zebrafish models for neuroscience research. Prog. Neuro-Psychopharmacol. Biol. Psychiatry 55, 1–6 (2014).
Panula, P., Sundvik, M. & Karlstedt, K. Developmental roles of brain histamine. Trends Neurosci. 37, 159–168 (2014).
Maximino, C. et al. Non-mammalian models in behavioral neuroscience: Consequences for biological psychiatry. Front. Behav. Neurosci. 9, 233 (2015).
Razali, K. et al. The promise of the zebrafish model for Parkinson’s disease: Today’s science and tomorrow’s treatment. Front. Genet. 12, 655550 (2021).
Noble, S., Godoy, R., Affaticati, P. & Ekker, M. Transgenic zebrafish expressing mcherry in the mitochondria of dopaminergic neurons. Zebrafish 12, 349–356 (2015).
Hughes, G. L. et al. Machine learning discriminates a movement disorder in a zebrafish model of Parkinson’s disease. DMM Dis. Model. Mech. 13, dmm045815 (2020).
Matsui, H. & Takahashi, R. Parkinson’s disease pathogenesis from the viewpoint of small fish models. J. Neural Transm. 125, 25–33 (2018).
Kalyn, M., Hua, K., Mohd Noor, S., Wong, C. E. D. & Ekker, M. Comprehensive analysis of neurotoxin-induced ablation of dopaminergic neurons in zebrafish larvae. Biomedicines 8, 1 (2019).
Wang, Y. et al. Parkinson’s disease-like motor and non-motor symptoms in rotenone-treated zebrafish. Neurotoxicology 58, 103–109 (2017).
Nellore, J. & P, N. Paraquat exposure induces behavioral deficits in larval zebrafish during the window of dopamine neurogenesis. Toxicol. Rep. 2, 950–956 (2015).
Wang, X. H., Souders, C. L. 2nd, Zhao, Y. H. & Martyniuk, C. J. Paraquat affects mitochondrial bioenergetics, dopamine system expression, and locomotor activity in zebrafish (Danio rerio). Chemosphere 191, 106–117 (2018).
Bortolotto, J. W. et al. Long-term exposure to paraquat alters behavioral parameters and dopamine levels in adult zebrafish (Danio rerio). Zebrafish 11, 142–153 (2014).
Nunes, M. E. et al. Chronic treatment with paraquat induces brain injury, changes in antioxidant defenses system, and modulates behavioral functions in zebrafish. Mol. Neurobiol. 54, 3925–3934 (2017).
Terron, A. et al. An adverse outcome pathway for parkinsonian motor deficits associated with mitochondrial complex I inhibition. Arch. Toxicol. 92, 41–82 (2018).
Fujita, K. A. et al. Integrating pathways of parkinson’s disease in a molecular interaction map. Mol. Neurobiol. 49, 88–102 (2014).
Harkati, D., Belaidi, S., Kerassa, A. & Gherraf, N. Molecular structure, substituent effect and physical-chemistry property relationship of indole derivatives. Quantum Matter 5, 36–44 (2015).
Butler, K. T., Davies, D. W., Cartwright, H., Isayev, O. & Walsh, A. Machine learning for molecular and materials science. Nat 2018 5597715 559, 547–555 (2018).
Trisciuzzi, D. et al. Molecular docking for predictive toxicology. Methods Mol. Biol. 1800, 181–197 (2018).
Sachana, M. Adverse outcome pathways and their role in revealing biomarkers. Biomarkers Toxicol. 163–170. https://doi.org/10.1016/B978-0-12-814655-2.00009-8 (2019).
Paul, K. C. et al. A pesticide and iPSC dopaminergic neuron screen identifies and classifies Parkinson-relevant pesticides. Nat. Commun. 14, 2803 (2023).
Mohamed, N. V. et al. Microfabricated disk technology: Rapid scale up in midbrain organoid generation. Methods 203, 465–477 (2022).
Pamies, D. et al. Human IPSC 3D brain model as a tool to study chemical-induced dopaminergic neuronal toxicity. Neurobiol. Dis. 169, 105719 (2022).
Jo, J. et al. Midbrain-like Organoids from Human Pluripotent Stem Cells Contain Functional Dopaminergic and Neuromelanin-Producing Neurons. Cell Stem Cell 19, 248–257 (2016).
Attene-Ramos, M. S. et al. The Tox21 robotic platform for the assessment of environmental chemicals – from vision to reality. Drug Discov. Today 18, 716–723 (2013).
Burden, N. et al. Advancing the 3Rs in regulatory ecotoxicology: A pragmatic cross-sector approach. Integr. Environ. Assess. Manag. 9999, 1–5 (2015).
DeMicco, A., Cooper, K. R., Richardson, J. R. & White, L. A. Developmental neurotoxicity of pyrethroid insecticides in zebrafish embryos. Toxicol. Sci. 113, 177–186 (2010).
Gonçalves, Í. et al. Toxicity testing of pesticides in zebrafish-a systematic review on chemicals and associated toxicological endpoints. Environ. Sci. Pollut. Res Int 27, 10185–10204 (2020).
Zhang, S., Li, F., Zhou, T., Wang, G. & Li, Z. Caenorhabditis elegans as a useful model for studying aging mutations. Front. Endocrinol. (Lausanne) 11, 1–9 (2020).
Boyd, W. A. et al. Developmental effects of the ToxCastTM phase I and phase II chemicals in caenorhabditis elegans and corresponding responses in Zebrafish, Rats, and Rabbits. Environ. Health Perspect. 124, 586–593 (2016).
Cooper, J. F. & Van Raamsdonk, J. M. Modeling Parkinson’s disease in C. elegans. J. Parkinsons. Dis. 8, 17–32 (2018).
Kuwahara, T. et al. A systematic RNAi screen reveals involvement of endocytic pathway in neuronal dysfunction in α-synuclein transgenic C. elegans. Hum. Mol. Genet. 17, 2997–3009 (2008).
Ruszkiewicz, J. A. et al. C. elegans as a model in developmental neurotoxicology. Toxicol. Appl. Pharmacol. 354, 126–135 (2018).
Fernández‐Hernández, I., Scheenaard, E., Pollarolo, G. & Gonzalez, C. The translational relevance of Drosophila in drug discovery. EMBO Rep. 17, 471–472 (2016).
Legradi, J., el Abdellaoui, N., van Pomeren, M. & Legler, J. Comparability of behavioural assays suing zebrafish larvae to assess neurotoxicity. Environ. Sci. Pollut. Res. Int. 22, 16277–16289 (2015).
Svendsen, C., Siang, P., Lister, L. J., Rice, A. & Spurgeon, D. J. Similarity, independence, or interaction for binary mixture effects of nerve toxicants for the nematode Caenorhabditis elegans. Environ. Toxicol. Chem. 29, 1182–1191 (2010).
Wittkowski, P. et al. Caenorhabditis elegans as a promising alternative model for environmental chemical mixture effect assessment-a comparative study. Environ. Sci. Technol. 53, 12725–12733 (2019).
Huang, P., Liu, S. S., Xu, Y. Q., Wang, Y. & Wang, Z. J. Combined lethal toxicities of pesticides with similar structures to Caenorhabditis elegans are not necessarily concentration additives. Environ. Pollut. 286, 117207 (2021).
Homberg, J. R., Wöhr, M. & Alenina, N. Comeback of the Rat in biomedical research. ACS Chem. Neurosci. 8, 900–903 (2017).
Zucca, F. A. et al. Interactions of iron, dopamine and neuromelanin pathways in brain aging and Parkinson’s disease. Prog. Neurobiol. 155, 96–119 (2017).
Zucca, F. A. et al. Neuromelanins in brain aging and Parkinson’s disease: synthesis, structure, neuroinflammatory, and neurodegenerative role. IUBMB Life 75, 55–65 (2023).
Test No. 424: Neurotoxicity Study in Rodents. https://doi.org/10.1787/9789264071025-EN (1997).
Kyriakou, E. I., Nguyen, H. P., Homberg, J. R. & Van der Harst, J. E. Home-cage anxiety levels in a transgenic rat model for Spinocerebellar ataxia type 17 measured by an approach-avoidance task: The light spot test. J. Neurosci. Methods 300, 48–58 (2018).
Grieco, F. et al. Measuring behavior in the home cage: Study design, applications, challenges, and perspectives. Front. Behav. Neurosci. 15, 219 (2021).
Fleming, S. M. Mechanisms of Gene-Environment Interactions in Parkinson’s Disease. Curr. Environ. Heal Rep. 4, 192–199 (2017).
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