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:
- 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 ?
- Correlation between
controls & PD for protein mutations i.e. LRRK2 linked to the onset of
PD using proteomic and statistical analysis
- Corroboration of
mutation and identification of aberrant genetic mutation and malfunction
using genomic & statistical analysis
- Levels of oxidative
respiration dysfunction, mutation and/or failure in mitochondria
implicated in PD and their associated areas in the brain
- 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?
