Hi park_bear,
I thought I remember you mentioning a better animal model for PD awhile back? If that is correct could you post it again? Thank you!
I always felt like the best PD animal model would be the animals that got PD like symptoms after getting a Fecal Microbiota Transplantation from people with PD. Well at least that makes sense to me. It doesn't seem like you can get much closer than that to the real thing.
Art
First, by way of comparison, the really poor animal model is whether a substance protects an animal from a toxin, such as MPTP, that induces nerve damage that results in a parkinsonism. All kinds of things could be effective for this purpose that would not touch actual Parkinson's.
A good animal model starts with an animal that exhibits neurodegeneration, including Parkinson's symptoms, as a result of a human type defective alpha synuclein. It turns out this mouse model has been around since 2002:
cell.com/fulltext/S0896-627...
"[I]n dominantly inherited α-syn substitutions, A53T was found in at least 12 families with familial PD"
"[W]we generated transgenic mice expressing wild-type[=healthy] and A53T[mutant] human α-synuclein in CNS neurons. Mice expressing mutant, but not wild-type, α-synuclein developed a severe and complex motor impairment leading to paralysis and death. These animals developed age-dependent intracytoplasmic neuronal α-synuclein inclusions paralleling disease onset, and the α-synuclein inclusions recapitulated features of human counterparts. Moreover, immunoelectron microscopy revealed that the α-synuclein inclusions contained 10–16 nm wide fibrils similar to human pathological inclusions. These mice demonstrate that A53T α-synuclein leads to the formation of toxic filamentous α-synuclein neuronal inclusions that cause neurodegeneration "
"These findings represent compelling evidence for the detrimental role of α-syn inclusion formation, a position that is still controversial." [Emphasis added to this little bonus]
Then, substances are tested to see whether they improve that animal's condition. This model was used to test the effectiveness of cinnamon:
link.springer.com/article/1...
"The present investigation underlines the importance of a naturally used spice and flavoring agent viz. cinnamon in reducing α-syn deposits in transgenic mice expressing mutant A53T human α-syn. Upon oral administration, cinnamon markedly reduced the level of insoluble α-syn in nigra, hippocampus and brain stem of A53T mice... Glial activation plays an important role in the pathogenesis of various neurodegenerative disorders including PD... and we found suppression of microglial and astroglial activation in the nigra of A53T mice upon cinnamon treatment. Moreover, neuroprotective proteins like DJ-1 and Parkin are known to reduce the formation of Lewy bodies in the CNS. Accordingly, we observed upregulation and/or normalization of DJ-1 and Parkin in the nigra of A53T mice by treatment with cinnamon..."
Apparently a somewhat different model was used in testing the effect of Farnesol on mice:
stm.sciencemag.org/content/...
"Farnesol prevented dopaminergic neuronal loss and behavioral deficits via farnesylation of PARIS in PARIS transgenic mice"
which may also be a good animal model.
Good reading:
Animal Models of Parkinson’s Disease
ncbi.nlm.nih.gov/books/NBK5...
Some pretty interesting conversations going on here regularly. I wish I understood them. 😂. I guess I get the gist of what’s being said. Your link was a help here. 🤔🤔🤔
Gwendoline
Usually I just glaze over as I read through these papers. Blah Blah Blah... but then, after seeing the same paper 10 times, I start catching more detail.
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