“Increased oxidative stress and chronic inflammation may cause neurodegeneration in Parkinson’s Disease by altering the levels of microRNAs and their target proteins. Antioxidants may provide neuroprotection by changing the levels of microRNAs and their target proteins”
I think conventional medicine sometimes overthinks chronic diseases like Parkinson’s Disease (PD). I understand that pharmaceutical companies only research and market drugs that they can patent. That makes business sense. But if patients understand the profit motive controlling conventional medicine then it is in their best interest to think beyond what their medical doctors tell them.
The study linked and excerpted below is a good example of what I am talking about. The medical jargon in the study is difficult to fully understand but I think those of us at risk for cognitive decline or PD have good reason to think that nutritional supplementation can slow or even prevent PD.
I am not talking about curing PD once this disease has had a chance to damage one’s brain. I’m talking about slowing the neurodegenerative decline in early PD.
I have lived with a form of cognitive impairment caused by aggressive chemotherapy since the late nineties. I work at maintaining my brain health the same way that I work at healing my heart, and my nerves. Evidence-based nutrition, supplementation, frequent, moderate exercise and more. Omega 3 fatty acids and curcumin have both been shown to reduce inflammation as well as enhance brain and heart health. I take those formulas that have been evaluated and approved by third-party evaluation services.
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David Emerson
- Cancer Survivor
- Cancer Coach
- Director PeopleBeatingCancer
“Background: Parkinson’s disease (PD) is a slow progressive neurodegenerative disease associated with abnormal function of extrapyramidal system. Although several biochemical and genetic defects are identified, increased oxidative stress and chronic inflammation are one of the earliest events that initiate and promote PD. Oxidative stress also participates in impaired nonmotor symptoms. The levels of microRNAs that are evolutionarily conserved single-stranded noncoding RNAs of approximately 22 nucleotide in length may have a role in PD.
Method: Published studies on changes in the levels of microRNAs in PD were critically reviewed, and the role of Reactive Oxygen Species (ROS), pro-inflammatory cytokines, and antioxidants in regulating the levels of microRNAs was evaluated.
Results: MicroRNAs levels were altered in PD. Downregulated microRNAs cause neurodegeneration by decreasing the levels of Nrf2 (nuclear transcriptional factor-2), mTOR (mammalian target of rapamycin), and DJ-1 and Parkin genes; and by increasing the levels of alpha-synuclein, RelA, Bim and Calpain-1, and A2AR (adenosine A2A receptor). Upregulated microRNAs cause degeneration of nerve cells by decreasing the levels of IGF-1 (Insulin Growth Factor-1), GRP78 (glucose regulated protein 78), DJ-1, and Hsc-70 (Heat- Shock Protein-70) that enhanced alpha-synuclein levels. ROS and pro-inflammatory cytokines cause neurodegeneration by altering the levels of microRNAs. Antioxidants that protect neurons by reducing oxidative stress and chronic inflammation altered the levels of microRNAs.
Conclusion: Increased oxidative stress and chronic inflammation may cause neurodegeneration in PD by altering the levels of microRNAs and their target proteins. Antioxidants may provide neuroprotection by changing the levels of microRNAs and their target proteins.
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