Granulocyte macrophage-colony stimulating factor protects against substantia nigra dopaminergic cell loss in an environmental toxin model of Parkinson's disease

Mangano, Emily; Peters, Sarah; Litteljohn, Darcy; So, Remmick; Bethune, Cheri; Bobyn, Jessica; Clarke, Melanie; Hayley, Shawn

doi:10.1016/j.nbd.2011.02.011

Cited by 64 publications

(80 citation statements)

References 85 publications

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“…9,10 GM-CSF, however, has since been demonstrated to also have a function in the central nervous system because GM-CSF can cross the blood-brain barrier 11,12 and both GM-CSF and its receptor are expressed by various brain cells. 13,14 GM-CSF has also been reported to have neuroprotective effects in animal models of Alzheimer disease, 15 Parkinson disease, 16 stroke, 14,17 spinal cord injury, [18][19][20] and stab wound-induced brain injury, 21 all of which bear pathological similarities to TBI. Furthermore, a post-mortem study of human brain tissue taken from acute TBI victims reported elevated levels of inflammatory cytokines including GM-CSF, 22 and the modulation of GM-CSF in animal studies has been shown to alter other inflammatory cytokines involved in TBI, including tumor necrosis factor-alpha and interleukin-1 beta.…”

Section: Introductionmentioning

confidence: 99%

Granulocyte-Macrophage Colony-Stimulating Factor Is Neuroprotective in Experimental Traumatic Brain Injury

Shultz

Tan

Wright

et al. 2014

Journal of Neurotrauma

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Traumatic brain injury (TBI) is an international health concern with a complex pathogenesis resulting in major long-term neurological, neurocognitive, and neuropsychiatric outcomes. Although neuroinflammation has been identified as an important pathophysiological process resulting from TBI, the function of specific inflammatory mediators in the aftermath of TBI remains poorly understood. Granulocyte-macrophage colony-stimulating factor (GM-CSF) is an inflammatory cytokine that has been reported to have neuroprotective effects in various animal models of neurodegenerative disease that share pathological similarities with TBI. The importance of GM-CSF in TBI has yet to be studied, however. We examined the role of GM-CSF in TBI by comparing the effects of a lateral fluid percussion (LFP) injury or sham injury in GM-CSF gene deficient (GM-CSF -/-) versus wild-type (WT) mice. After a 3-month recovery interval, mice were assessed using neuroimaging and behavioral outcomes. All mice given a LFP injury displayed significant brain atrophy and behavioral impairments compared with those given sham-injuries; however, this was significantly worse in the GM-CSF -/-mice compared with the WT mice. GM-CSF -/-mice given LFP injury also had reduced astrogliosis compared with their WT counterparts. These novel findings indicate that the inflammatory mediator, GM-CSF, may have significant protective properties in the chronic sequelae of experimental TBI and suggest that further research investigating GM-CSF and its potential benefits in the injured brain is warranted.

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Section: Introductionmentioning

confidence: 99%

Granulocyte-Macrophage Colony-Stimulating Factor Is Neuroprotective in Experimental Traumatic Brain Injury

Shultz

Tan

Wright

et al. 2014

Journal of Neurotrauma

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“…Protection against paraquat-induced DA neurodegeneration can also be achieved by providing trophic support (intranigral or peripheral injection of GDNF or GM-CSF, respectively), which is reduced upon paraquat treatment (Mangano et al, 2011).…”

Section: Paraquatmentioning

confidence: 99%

“…dose, timing of treatment, species or strain, age of animal, iron accumulation, strain specific gene ontology) can explain contradictory effects observed following treatment with the chemical stressor paraquat in mice. Fei et al, 2008;Cristovao et al, 2009;Fernagut et al, 2009;Mangano et al, 2009Mangano et al, , 2011Watson, 2013;. In order to integrate data on paraquat toxicity from widely different experimental models, ranging from cell cultures to repeat dose animal studies, the concentrations close to the target site were compared by classical approaches of in vitro in vivo extrapolation (IVIVE) based on the available publications.…”

Section: Weight Of Evidence For the Ker Biological Plausibilitymentioning

confidence: 99%

Investigation into experimental toxicological properties of plant protection products having a potential link to Parkinson's disease and childhood leukaemia†

Ockleford¹,

Adriaanse²,

Berny³

et al. 2017

EFS2

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In 2013, EFSA published a literature review on epidemiological studies linking exposure to pesticides and human health outcome. As a follow up, the EFSA Panel on Plant Protection Products and their residues (PPR Panel) was requested to investigate the plausible involvement of pesticide exposure as a risk factor for Parkinson's disease (PD) and childhood leukaemia (CHL). A systematic literature review on PD and CHL and mode of actions for pesticides was published by EFSA in 2016 and used as background documentation. The Panel used the Adverse Outcome Pathway (AOP) conceptual framework to define the biological plausibility in relation to epidemiological studies by means of identification of specific symptoms of the diseases as AO. The AOP combines multiple information and provides knowledge of biological pathways, highlights species differences and similarities, identifies research needs and supports regulatory decisions. In this context, the AOP approach could help in organising the available experimental knowledge to assess biological plausibility by describing the link between a molecular initiating event (MIE) and the AO through a series of biologically plausible and essential key events (KEs). As the AOP is chemically agnostic, tool chemical compounds were selected to empirically support the response and temporal concordance of the key event relationships (KERs). Three qualitative and one putative AOP were developed by the Panel using the results obtained. The Panel supports the use of the AOP framework to scientifically and transparently explore the biological plausibility of the association between pesticide exposure and human health outcomes, identify data gaps, define a tailored testing strategy and suggests an AOP's informed Integrated Approach for Testing and Assessment (IATA).

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“…Given the involvement of oxidative stress and dopaminergic cell loss in paraquat toxicity, various phytochemicals and other compounds have been studied to abrogate neurotoxic response. [41][42][43][44][45] Maneb (manganese ethylene-bis-dithiocarbamate), is a contact fungicide that synergistically interacts with paraquat to markedly reduce locomotor function and increased striatal terminals and nigral neuronal damage. 46 Such synergistic interactions have been considered for the role in PD etiology and are of interest since they reflect actual human exposures.…”

Section: -4mentioning

confidence: 99%

Toxin-Induced Parkinson’s Disease Models

Krishna¹

2017

Neuro – Open Journal

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Granulocyte macrophage-colony stimulating factor protects against substantia nigra dopaminergic cell loss in an environmental toxin model of Parkinson's disease

Cited by 64 publications

References 85 publications

Granulocyte-Macrophage Colony-Stimulating Factor Is Neuroprotective in Experimental Traumatic Brain Injury

Granulocyte-Macrophage Colony-Stimulating Factor Is Neuroprotective in Experimental Traumatic Brain Injury

Investigation into experimental toxicological properties of plant protection products having a potential link to Parkinson's disease and childhood leukaemia†

Toxin-Induced Parkinson’s Disease Models

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