Friday, 13 October 2017

Introducing MouseDoctor3

Hello, and thank you for reading my first post as MouseDoctor3.  Here's a brief introduction so you know my background...


Name: Dr Jodie Stephenson

Role: postdoctoral research assistant

Bosses: MouseDoctor and Dr Love

Location: primarily the Blizard Institute, QMUL, but also Imperial College London and VU University of Amsterdam (i.e. I get to travel around a lot).

Project (briefly): testing potential drugs for MS in a mouse model.

Project (in more detail): translocator protein (TSPO) has been under investigation for many years in MS and it may be involved in unwanted activation of certain cell types in MS. My project will try to further understand the role and function of TSPO in MS. I will also be testing the efficacy of TSPO ligands (drugs) as a treatment in the experimental autoimmune encephalomyelitis (EAE) mouse model. The EAE mouse model is currently the most common model used in MS and will hopefully give us an indication of whether the drugs will work in patients. Another post to explain TSPO will be written soon.

Previous experience: I did my PhD at the University of Sheffield working in amyotrophic lateral sclerosis (ALS). During the project I was investigating a new mouse model of ALS, looking in to the motor function, behaviour and pathology of the mice. Prior to this, I worked with the ALS clinical team and did a Masters in Translational Neuroscience. 

Aims on the blog: to bring you updates on my project and help increase understanding of the translation between the EAE mouse model and MS patients. 

Follow me on twitter @neuroruncake

12 comments:

  1. Wonderful news. Nice to have a new persona to relate to more.

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  2. Welcome to the blog, and congratulations on the new job!

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  3. Welcome!
    Hope you really enjoy your new job and I'd like to wish you every success with your research.

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  4. Welcome, too.

    But I am interested in one thing. This review comes to this conclusion: "he dominance of CD4+-T cells in most EAE models used for therapeutic studies contrasts with the CD8+-shift observed in multiple sclerosis lesions. There is a clear need for more CD8+-based models, in analogy to human multiple sclerosis pathology. Finally, owing to the complexities of human diseases, it is obvious that there is no single EAE model, but rather a combination of different approaches that will finally help us to develop new and more effective therapeutic approaches." (https://academic.oup.com/brain/article/129/8/1953/330800/Understanding-pathogenesis-and-therapy-of-multiple)

    As we have - on this blog - entered a major debate about B cell mediated disease, too, is the EAE model fit for purpose?

    Is EAE the MS equivalent, if you will, of Henrietta Lacks?

    Will be ever find a cure for MS if we keep on returning to an animal model that has not given us a cure yet?

    This isn't meant to be a horrible introduction to Dr Stephenson, just a question from someone who would love to know her view on whether - in the end - those mice might be barking up the wrong tree (to mix my animal metaphors)?

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    1. Thanks for your Q. I hope to follow up on this with a blog about how useful the EAE model is/isn't so this should answer your Qs. Watch this space :)

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  5. Welcome Dr. Stephenson. As a new post doc what do you feel is or are the pressing questions regarding neurodegeneration, not only in MS but in other conditions as well? I realize this is a general question.

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    1. Thanks for your Q. As I'm sure you understand, there are an infinite amount of Qs to be answered when it comes to neurodegeneration. There are many potential causes, some confirmed; others not, most of which we don't yet know how to target. Therefore, the most pressing (and general) Qs to be answered are, which mechanisms are involved in neurodegeneration in which diseases? And how can we target these for treatment/prevention? I hope this answers your Q, if not, perhaps you could be more specific?

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  6. Thanks everyone. Iaino, I hope to follow up on this with a blog about how useful the EAE model is/isn't so this should answer your Qs. Watch this space :)

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