Peter Teismann

University of Aberdeen

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Heather L. Martin

University of Leeds

Serge Przedborski

Columbia University

Sarah Mustafa

University of Victoria

Kinnari Sathe

University of Aberdeen

Miquel Vila

Institució Catalana de Recerca i Estudis Avançats

Boris Ferger

Boehringer Ingelheim (Germany)

Ross B. Mounsey

University of Aberdeen

Jörg B. Schulz

Jülich Aachen Research Alliance

Olaf Rieß

University of Tübingen

Kim Tieu

Florida International University

Cooperative Institutions

University of Tübingen

University of Aberdeen

University of Göttingen

Heidelberg University

Columbia University

Universitätsmedizin Göttingen

Universitätsklinikum Tübingen

Hertie Institute for Clinical Brain Research

Philipps University of Marburg

German Center for Neurodegenerative Diseases

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The salicylate hydroxylation assay to measure hydroxyl free radicals induced by local application of glutamate in vivo or induced by the Fenton reaction in vitro

Brain Research Protocols (2000)

Peter Teismann Boris Ferger

Hydroxyl radical

Hydroxylation

Microdialysis

Scavenger

10.1016/s1385-299x(00)00014-3

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Citations (45)

Ablation of major histocompatibility complex II provides neuroprotection in the MPTP mouse model of Parkinson’s Disease

Heather L. Martin Kinnari Sathe Sarah Mustafa John V. Forrester Peter Teismann

MPTP

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NADPH oxidase mediates oxidative stress in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of Parkinson's disease

Proceedings of the National Academy of Sciences (2003)

Du‐Chu Wu Peter Teismann Kim Tieu Miquel Vila Vernice Jackson‐Lewis

Parkinson's disease (PD) is a neurodegenerative disorder of uncertain pathogenesis characterized by a loss of substantia nigra pars compacta (SNpc) dopaminergic (DA) neurons, and can be modeled by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Both inflammatory processes and oxidative stress may contribute to MPTP- and PD-related neurodegeneration. However, whether inflammation may cause oxidative damage in MPTP and PD is unknown. Here we show that NADPH-oxidase, the main reactive oxygen species (ROS)-producing enzyme during inflammation, is up-regulated in SNpc of human PD and MPTP mice. These changes coincide with the local production of ROS, microglial activation, and DA neuronal loss seen after MPTP injections. Mutant mice defective in NADPH-oxidase exhibit less SNpc DA neuronal loss and protein oxidation than their WT littermates after MPTP injections. We show that extracellular ROS are a main determinant in inflammation-mediated DA neurotoxicity in the MPTP model of PD. This study supports a critical role for NADPH-oxidase in the pathogenesis of PD and suggests that targeting this enzyme or enhancing extracellular antioxidants may provide novel therapies for PD.

MPTP

Pars compacta

Neurotoxin

Neurotoxicity

Pathogenesis

10.1073/pnas.0937239100

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Citations (616)

Increased expression of the pro-inflammatory enzyme cyclooxygenase-2 in amyotrophic lateral sclerosis

Annals of Neurology (2001)

Gabrielle Almer Christelle Gu�gan Peter Teismann Ali Naini Gorazd Rosoklija

Mutations in the copper/zinc superoxide dismutase (mSOD1) gene are associated with a familial form of amyotrophic lateral sclerosis (ALS), and their expression in transgenic mice produces an ALS-like syndrome. Recent observations suggest a role for inflammatory-related events in the progression and propagation of the neurodegenerative process in ALS. Consistent with this view, the present study demonstrates that, during the course of the disease, the expression of cyclooxygenase type 2 (Cox-2), a key enzyme in the synthesis of prostanoids, which are potent mediators of inflammation, is dramatically increased. In both early symptomatic and end-stage transgenic mSOD1 mice, neurons and, to a lesser extent, glial cells in the anterior horn of the spinal cord exhibit robust Cox-2 immunoreactivity. Cox-2 mRNA and protein levels and catalytic activity are also significantly increased in the spinal cord of the transgenic mSOD1 mice. The time course of the spinal cord Cox-2 upregulation parallels that of motor neuronal loss in transgenic mSOD1 mice. We also show that Cox-2 activity is dramatically increased in postmortem spinal cord samples from sporadic ALS patients. We speculate that Cox-2 upregulation, through its pivotal role in inflammation, is instrumental in the ALS neurodegenerative process and that Cox-2 inhibition may be a valuable therapeutic avenue for the treatment of ALS.

10.1002/1531-8249(20010201)49:2<176::aid-ana37>3.0.co;2-x

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Citations (272)

Mitochondrial dysfunction triggered by loss of HtrA2 results in the activation of a brain-specific transcriptional stress response

Cell Death and Differentiation (2008)

Nicoleta Moisoi Kristina Klupsch Valentina Fedele Philip East Sushant Sharma

XBP1

Integrated stress response

10.1038/cdd.2008.166

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Citations (166)

Characterisation of a conditional mouse-model of Parkinson's disease

Aktuelle Neurologie (2006)

Silke Nuber Elisabeth Petrasch‐Parwez Tobias Schmidt Hans‐Werner Habbes Marlen Löbbecke‐Schumacher

alpha-Synuclein has been implicated in the pathophysiology of many neurodegenerative disorders, including Parkinson's disease (PD). In order to elucidate the role of this protein in the pathogenesis of PD, transgenic mice were created by using the tet-regulatable system driving the expression of human wildtype and mutated [A30P] alpha-synuclein in CNS neurons. Our studies demonstrate that the expression pattern depends on both the neuron-specific promoter and the integration site of the transgene constructs. Mice expressing high levels of human wildtype alpha-synuclein developed neuropathology and progressive motor impairment which could be stopped after blockade of expression in symptomatic mice. Mice expressing the mutated [A30P] alpha-synuclein restricted to the olfactory bulb showed significantly lower levels of dopamine and metabolites in this brain region. Thus our conditional mouse-model may help to define the role of human alpha-synuclein in synucleinopathies and might be used to demonstrate at which stage neuropathological symptoms of these diseases are reversible.

Synucleinopathies

Neuropathology

Pathogenesis

10.1055/s-2006-953108

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The effect of neuronal conditional knock-out of peroxisome proliferator-activated receptors in the MPTP mouse model of Parkinson’s disease

Neuroscience (2015)

Ross B. Mounsey Heather L. Martin Michael C. Nelson Ronald M. Evans Peter Teismann

Activation of peroxisome proliferator-activated receptors (PPARs), namely PPARγ and PPARδ, has been shown to provide neuroprotection in a number of neurodegenerative disorders, such as Alzheimer's and Parkinson's disease (PD). The observed neuroprotective effects in experimental models of PD have been linked to anti-oxidant and anti-inflammatory actions. This study aimed to analyze the full influence of these receptors in neuroprotection by generating a nerve cell-specific conditional knock-out of these receptors and subjecting these genetically modified mice to the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxin to model dopaminergic degeneration. Mice null for both receptors show the lowest levels of tyrosine hydroxylase (TH)-positive cell bodies following MPTP administration. Presence of one or both these receptors show a trend toward protection against this degeneration, as higher dopaminergic cell immunoreactivity and striatal monoamine levels are evident. These data supplement recent studies that have elected to use agonists of the receptors to regulate immune responses. The results place further importance on the activation of PPARs and the neuroprotective roles these have in inflammatory processes linked to neurodegenerative processes.

MPTP

Neurotoxin

10.1016/j.neuroscience.2015.05.048

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MHCII and the innate immune system: what is their role in Parkinson's disease?

Social Neuroscience (2011)

Peter Teismann Heather Martin Kinnari Sathe Sarah Mustafa John V. Forrester

CCL18

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