Showing posts with label Research plan. Show all posts
Showing posts with label Research plan. Show all posts

Saturday, 20 June 2020

Updated PhD Research Project Plan

In the earlier time line was it looked at doing all the experiments one after the other, then all the statistical analysis would follow and finally the thesis chapters would be written. The problem with this process is you will not know if some of the experimental runs have failed until much later down the track when you are doing the statistical analysis.

The changes made to the project plan now group each experiment as a self contained unit, doing the experimental run then the analysis for that run to find out how the results turned out. If the run was a success the analysis can be used to write up the chapter and journal paper for the thesis. In this way the thesis is progress as the experiments are done and hopefully each experiment results in both a published paper and completed thesis chapter.

The benefit of this is that I do not have to strain my memory at the end to think back to when I did the experiments to create the thesis chapters. As they are done as I progress the data, ideas and conclusions should be fresh and accurate.


Detailed PhD Research Plan (click to enlarge)


A summary version of the above detailed version will be used for the confirmation text.


Summary PhD Research Plan (click to enlarge)




Friday, 21 June 2019

Searching PROSPERO for similar research

In the PRISMA-2015 document, there is mention of registering our research idea and the type of systematic review we are going to undertake on PROSPERO. 


I thought I would go onto PROSPERO & see if anybody is already in our space and found that only one group (Mirian 2018 – attached) are currently close to out idea. Their objective is very similar to ours:

“Review question: What are the neuroinflammatory cellular mechanisms associated with the neurodegenerative process in Parkinson's Disease?
Main outcome(s): To observe cellular alterations, specifically, in microglia, mast cells and astrocytes through post mortem tissue of individuals with Parkinson's Disease. To compare the results with cellular characteristics of post mortem tissue of individuals without Parkinson's Disease.”

Whilst we may have a similar review question, and look to investigate similar variables i.e. microglia & astrocytes as part of the immune system response to neuroinflammation, I think there is still a big difference between the two studies. Their study will be based on post mortem tissue samples, which I feel is a reactive and slow study, whilst ours is a pro-active study which plans to use current whole blood & plasma samples from existing PD patients to compare normal controls against PD patients to establish some of the following:

  1. Does neuroinflammation as a result of an immune response lead to neurodegeneration and trigger PD, OR does the presence of cellular/protein changes such as Lewy bodies present in neurodegenerative cases such as PD, cause an increased immune response leading to a heightened level of neuroinflammation ?
  2. Correlation between controls & PD for protein mutations i.e. LRRK2 linked to the onset of PD using proteomic and statistical analysis
  3. Corroboration of mutation and identification of aberrant genetic mutation and malfunction using genomic & statistical analysis
  4. Levels of oxidative respiration dysfunction, mutation and/or failure in mitochondria implicated in PD and their associated areas in the brain
  5. In each of the analyses above how are neuroinflammation response markers such as microglia, astrocytes and macrophages manifested and are 5their differences between a normal control and PD group?

Another key difference in their study, is that their patient is already dead so cannot be helped, ours are still alive and for those just entering the study as part of assisting us to set up a temporal database, any finding we make, may be able to be exploited to infer an early high correlation bio-marker that could assist in making early changes to their medication and clinical treatment, resulting in slowing the onset of further neurodegeneration, neuroinflammation and subsequent onset of PD symptoms.

Finally, If we can register our research gap to protect our idea and subsequent IP, it might be good to approach this team down the track to see if each of our results are pointing in the same direction i.e. are their post mortem results showing the terminal results we anticipate from our temporal proteomics and mitochondrial analysis from bloods?

Registering on PROSPEROPROSPERO Home page: