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SRC ProMyelo

München, DE

ProMyelo GmbH is a highly specialized preclinical research organization offering services that focus on the development of new neural therapies, especially in the field of Multiple Sclerosis research. ProMyelo’s various preclinical MS model Systems (cuprizone, EAE, LPC etc.) and applications (immunohistochemistry, ultrastructural analyses, gene expression studies, cell culture approaches, etc.) provide high-quality standard and customizable solutions for basic science, preclinical and clinical research. We provide these specialized research services to pharmaceutical & biotechnology companies, non-profit organizations and academic researchers.

Selected Publications

  • Kipp M, Remyelination strategies in multiple sclerosis: a critical reflection. Expert Rev Neurother. 2016;16(1):1-3.
  • Zendedel A, Beyer C, Kipp M, Cuprizone-induced demyelination as a tool to study remyelination and axonal protection. *J... Show more »

ProMyelo GmbH is a highly specialized preclinical research organization offering services that focus on the development of new neural therapies, especially in the field of Multiple Sclerosis research. ProMyelo’s various preclinical MS model Systems (cuprizone, EAE, LPC etc.) and applications (immunohistochemistry, ultrastructural analyses, gene expression studies, cell culture approaches, etc.) provide high-quality standard and customizable solutions for basic science, preclinical and clinical research. We provide these specialized research services to pharmaceutical & biotechnology companies, non-profit organizations and academic researchers.

Selected Publications

  • Kipp M, Remyelination strategies in multiple sclerosis: a critical reflection. Expert Rev Neurother. 2016;16(1):1-3.
  • Zendedel A, Beyer C, Kipp M, Cuprizone-induced demyelination as a tool to study remyelination and axonal protection. J Mol Neurosci. 2013 Oct;51(2):567-72.
  • van der Star BJ, Vogel DY, Kipp M, Puentes F, Baker D, Amor S. In vitro and in vivo models of multiple sclerosis. CNS Neurol Disord Drug Targets. 2012 Aug;11(5):570-88.
  • Clarner T, Janssen K, Nellessen L, Stangel M, Skripuletz T, Krauspe B, Hess FM, Denecke B, Beutner C, Linnartz-Gerlach B, Neumann H, Vallières L, Amor S, Ohl K, Tenbrock K, Beyer C, Kipp M. CXCL10 triggers early microglial activation in the cuprizone model. J Immunol. 2015 Apr 1;194(7):3400-13.
  • Janssen K, Rickert M, Clarner T, Beyer C, Kipp M, Absence of CCL2 and CCL3 Ameliorates Central Nervous System Grey Matter But Not White Matter Demyelination in the Presence of an Intact Blood-Brain Barrier. Mol Neurobiol. 2016 Apr;53(3):1551-64.
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Experimental Autoimmune Encephalomyelitis (EAE) Animal Models
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EAE is the model most commonly used to study efficacy of potential drugs for treatment of multiple sclerosis (MS).

Because of its many similarities to MS, EAE is used to study pathogenesis of autoimmunity, CNS inflammation, demyelination, cell trafficking and tolerance induction. EAE is characterized by paralysis (in some... Show more »

EAE is the model most commonly used to study efficacy of potential drugs for treatment of multiple sclerosis (MS).

Because of its many similarities to MS, EAE is used to study pathogenesis of autoimmunity, CNS inflammation, demyelination, cell trafficking and tolerance induction. EAE is characterized by paralysis (in some models the paralysis is remitting-relapsing), CNS inflammation and demyelination. EAE is mediated by myelin-specific CD4+ T cells, but CD8+ cells and B cells may also play a role in some models of EAE.

In principal, EAE can be induced in two ways:

By immunizing animals with myelin-derived proteins or peptides (active EAE) or by injecting animals with CD4+ T cells specific for myelin-derived peptides (adoptive or passive EAE).

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Neuroprotection Animal Models
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Protecting demyelinated axons is critical to maintain neural integrity as transection/loss of axons is the major cause of neurological decline in MS patients. The extent of axonal damage can be studied in various animal models.

Axonal transection or loss is a notable pathology in MS as a consequence of demyelination of... Show more »

Protecting demyelinated axons is critical to maintain neural integrity as transection/loss of axons is the major cause of neurological decline in MS patients. The extent of axonal damage can be studied in various animal models.

Axonal transection or loss is a notable pathology in MS as a consequence of demyelination of axons in the brain. Protecting demyelinated axons is critical to maintain neural integrity as transection/loss of axons is the major cause of neurological decline in MS patients. ProMyelo’s mouse models can evaluate neuroprotection potential

of pharmaceutical compounds and biologics by analyzing the swollen and transected axons that are reminiscent of neuronal damage. In addition, ProMyelo’s electron microscopy capabilities allow comprehensive analysis of the neuroprotective effect by studying neuronal ultrastructural changes.

Experimental End Points

  • Quantification of axonal damage (identified by axonal ovoids)
  • Evaluation of survival/health of axons by immunohistochemistry
  • Electron micoscopy evaluation of ultrastructural changes in axons
  • Evaluation of mitochondrial integrity and changes
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Demyelination Animal Models
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Characteristic for Multiple Sclerosis lesions is the loss of myelinating oligodendrocytes and demyelination. ProMyelo’s modified cuprizone model shows consistent levels of axonal demyelination providing an excellent platform for qualitative and quantitative readouts of demyelination.

Cuprizone intoxication is one of several... Show more »

Characteristic for Multiple Sclerosis lesions is the loss of myelinating oligodendrocytes and demyelination. ProMyelo’s modified cuprizone model shows consistent levels of axonal demyelination providing an excellent platform for qualitative and quantitative readouts of demyelination.

Cuprizone intoxication is one of several animal models used to study demyelination. Early treatment protocols exposed mice to cuprizone for 6 weeks to induce demyelination; however, more recent reports have varied exposure times from 4 to 5 weeks. We found that an abbreviated insult of only 3 weeks of exposure to cuprizone induces oligodedrocyte apoptosis with significant and reproducible demyelination 2 weeks later (5-week time point).

Once mature oligodendrocytes are perturbed after a 3-week treatment, the progression to demyelination occurs without requiring further exposure. This short, “hit and run” model triggers a cascade of events leading to demyelination 2-3 weeks later and is an excellent model to study the development of new therapeutic strategies for treatment of multiple sclerosis.

Experimental End Points

  • Quantification of myelination in diverse brain regions
  • Quantification of apoptotic oligodendrocytes
  • Quantification of oligodendrocyte stress
  • Additional histological quantification (OPCs, astrocytes, microglia, etc)
  • Quantification of myelin protein expression levels
  • Electron microscopy evaluation of distinct myelin and axonal parameters
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Myelination Animal Models
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Myelin repair (i.e. remyelination) restores the functional integrity of axons and is neuroprotective. Our remyelination models capture several important attributes of Multiple sclerosis and has been successfully used to test remyelination therapeutics.

The most commonly used models used to study remyelination biology and... Show more »

Myelin repair (i.e. remyelination) restores the functional integrity of axons and is neuroprotective. Our remyelination models capture several important attributes of Multiple sclerosis and has been successfully used to test remyelination therapeutics.

The most commonly used models used to study remyelination biology and pathology is the focal Lysophosphatidylcholine-induced Remyelination model and the Cuprizone Remyelination model.

Cuprizone Model of Remyelination

Cuprizone ingestion in mice induces a highly reproducible demyelination of distinct brain regions, among them the corpus callosum which represents the most frequently investigated white matter tract in this animal model. After 5–6 weeks of cuprizone treatment, the Corpus callosum is almost completely demyelinated, a process called ‘‘acute demyelination’’. Acute demyelination is followed by spontaneous remyelination during subsequent weeks when mice are fed normal chow.

In contrast, remyelination is highly restricted when cuprizone administration is prolonged (13 weeks or longer), a process called ‘‘chronic demyelination’’. To study the effectiveness of pharmaceutical substances on myelin repair, acute or chronic demyelination will be induced in mice and animals treated during the recovery period. Test compound can be delivered either per os, intravenously, intraperitonealy, intraventricularily by stereotaxis, or by subcutaneous depot-injections.

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Preclinical Histology
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ProMyelo offers a complete range of standard and customized neurohistology services. Our specialized histology and immunohistochemistry capabilities combined with our custom analysis techniques provide increased throughput and decreased variability for high quality tissue evaluation. We offer neurohistology either as a complete... Show more »

ProMyelo offers a complete range of standard and customized neurohistology services. Our specialized histology and immunohistochemistry capabilities combined with our custom analysis techniques provide increased throughput and decreased variability for high quality tissue evaluation. We offer neurohistology either as a complete service or specific expertise to complement your in-house capabilities, including:

  • Tissue Processing
  • Immunohistochemistry
  • Histochemical-Staining
  • Imaging
  • Analysis
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High Content Screening
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High content screening (HCS) to evaluate Oligodendrocyte precursor cell (OPC) differentiation.

Endogenous remyelination of axons occurs in the central nervous system (CNS) of Multiple Sclerosis (MS) patients, however, this regenerative process is sometimes inefficient and decreases as the disease progresses. Remyelination not... Show more »

High content screening (HCS) to evaluate Oligodendrocyte precursor cell (OPC) differentiation.

Endogenous remyelination of axons occurs in the central nervous system (CNS) of Multiple Sclerosis (MS) patients, however, this regenerative process is sometimes inefficient and decreases as the disease progresses. Remyelination not only restores proper axonal conduction, but also protects axons from degeneration. Improving remyelination efficiency therefore directly exerts neuroprotection and halts disease progression. For remyelination to occur, oligodendrocyte progenitor cells (OPC) must survive and proliferate, differentiate into mature oligodendrocytes and then produce new myelin sheaths.

ProMyelo offers cell-based assays to identify and evaluate compounds that stimulate OPC proliferation and differentiation. Differentiation of OPC is analyzed using state of the art methods such as quantification of morphological characteristics, immunocytochemistry, western blotting, and analyses of gene expression levels. Proliferation of OPC is addressed using standard proliferations assays or the advanced xCelligence system (Roche Applied Science).

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Animal Models and Studies
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Animal Models of Disease
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CNS/Neurology Animal Models
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Biology
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Cell-Based Assays
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Cell-Based Screening Methods
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Cells and Tissues
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