There is a LOT to read in this article. And it is very detailed and I did not understand most of it. But if you browse through it, things will pop out. Tidbits. Clues.
Parkinson’s Disease: Can Targeting Inflammation Be an Effective Neuroprotective Strategy? frontiersin.org/articles/10...
"The reason why dopamine neurons die in Parkinson’s disease remains largely unknown. Emerging evidence points to a role for brain inflammation in neurodegeneration. Essential questions are whether brain inflammation happens sufficiently early so that interfering with this process can be expected to slow down neuronal death and whether the contribution from inflammation is large enough so that anti-inflammatory agents can be expected to work. Here I discuss data from human PD studies indicating that brain inflammation is an early event in PD. I also discuss the role of T-lymphocytes and peripheral inflammation for neurodegeneration. I critically discuss the failure of clinical trials targeting inflammation in PD."
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Thank you, very informative. My HWP is idiopatic, I think he has had gut issues for a while and the gut/brain connection is injured contributing to his PD. Hah who I am to say as the MS said we don't know why he has it. Trying to reduce over all inflamation in his body through supplements, exercise and gentle reminders to meditate.
It is not clear if NSAIDs will help. According to the article:
"It should also be mentioned that non-steroid anti-inflammatory drugs (NSAIDs) have been extensively examined for neuroprotective effects. Experimental PD models have shown somewhat confliction results. Acetyl salisylate and ibuprofen have been reported to be neuroprotective in MPTP mouse models of PD (Aubin et al., 1998; Swiątkiewicz et al., 2013). However, using the same model, recently ibuprofen given alone was not protective (only when given along with a metalloprotease inhibitor) (Costa et al., 2020). Likewise, results from epidemiological studies are somewhat conflicting. Two meta-analyses concluded that ibuprofen could slightly lower the risk of PD (Samii et al., 2009; Gagne and Power, 2010). However, later this has not been verified in meta-analyses including a larger number of studies (Ren et al., 2018; Poly et al., 2019). There are no randomized clinical trials investigating the effect of NSAIDs. Likewise, rosacea patients who have used tetracyclines appear to have a reduced risk of PD (Egeberg et al., 2016). As mentioned above, tetracyclines may work to reduce inflammation, but in clinical trials using minocycline there was no effect on PD progression (NINDS Net-PD Investigators, 2008; Parashos et al., 2014)."
I have suspected early brain inflammation, in my particular case of being diagnosed with PD, and would like to see more studies done on this subject. I have suspected a strong connection between neurodegenerative inflammation, and the dying of dopamine neurons, for many years, so this report is of interest to my wondering if researchers could come up with a solution to reduce, or stop inflammation. Thanks for sharing!
Thank you for finding and posting this! Realizing there’re a lot of scientific assumptions made re: where it’s all going/how the many isolated studies if considered together paint a plausible picture, the logic points to what we’ve been suspecting as we investigate causal relationships between PD and other diseases, in particular blood cancers, i.e, chronic lymphocytic leukemia (CLL).
As my husband experiences near remission of CLL due in part to the introduction of a biological treatment designed to inhibit B-cell proliferation and now has the added the onset of PD to deal with, we believe it makes sense that there are causal relationships at play. (“Ibrutinib treatment increased the in vivo persistence of activated T cells, decreased the Treg/CD4+ T cell ratio, and diminished the immune-suppressive properties of CLL cells through BTK-dependent and -independent mechanisms.” pubmed.ncbi.nlm.nih.gov/287...
The studies sited in this paper … re: T-cell lymphocytes and cytokine reactions with regard to brain inflammatory, neurodegenerative and autoimmune responses…the blood/brain and gut/Vagus nerve and A-syn processes …compiled in one place, illustrating potential relationship, commonality, reactive responses, is exciting to read.
What if PD is fundamentally an autoimmune response and not a disease as currently approached by standard practice after all???? From the article, “These interactions may generate autoreactive T-lymphocytes, recognizing disease-altered self-proteins as foreign antigens, suggesting that Parkinson’s disease could be an autoimmune disease (Sulzer et al., 2017)”
We have been investigating, meeting with specialists, reading many studies, trials and treatments on both sides of my husband’s two diagnosis, trying to ascertain a best approach while factoring in that any treatment he chooses for one could have a positive or negative impact on the other.
As we had already come to suspect this path of collaborative thinking in our effort to go beyond treating PD symptoms and choose proactive treatments to attack the blockages, inflammation, neurodegeneration and cellular insufficiencies, this article is sending me down the rabbit hole. Hope! There’s so much here to dig in on! Bookmarked!
"the logic points to what we’ve been suspecting as we investigate causal relationships between PD and other diseases, in particular blood cancers, i.e, chronic lymphocytic leukemia (CLL)"
"What if PD is fundamentally an autoimmune response and not a disease as currently approached by standard practice after all???"
What if all neurodegenerative diseases, not just PD - are in fact autoimmune conditions and that are in effect a form of cancer? This would make them treatable with IVIG, plasmapheresis and other low toxicity modalities.
You're in a very good position to test this hypothesis. Please keep us posted.
SE
“What if PD is fundamentally an autoimmune response and not a disease as currently approached by standard practice after all???”Agreed!!
This has been postulated for ALZ as well and by prominent neurologists.
And, like autism, I think PD is really “Parkinson’s spectrum disorder”. It’s a disorder that causes (at present) irreversible neuronal loss but I believe there are means of stopping or at least decreasing the root causes of the disorder that leads to the death and dysfunction of neurons that in turn leads to the hallmark symptoms.
I was elated to learn that many of the “dead neurons” are not dead. They are in a zombie like state. Astrocytes play a major roll in this
In another words, delaying the disease occurrence.In my opinion PD isn’t developed overnight but within years. PD is an aging disease. All of us even the most healthy ones might experience PD .
Some experience in their fifties some at age 90 depending what we have done with our body and mind. If we were under too much stress and eating bad foods , drinking alcohol, smoking cigarettes, exposed to herbicides,…. then our chance is bigger to get PD in younger ages plus genetics tendencies in how strong our body is in response to physical and emotional stressors.
Yes! “Disorder” which implies it can be Re-ordered….reversed! Please point me to the “zombie state” neuron info. I believe it without even reading it but would like to read source info.
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