Sustained-release nutrients and other therapies target underlying cause of Parkinson’s disease, review shows
- Parkinson’s disease is caused by oxidative/nitrosative stress in the midbrain
- Dopaminergic neurons in the substantia nigra are damaged
- A DNA transcription factor for dopamine activity is also impaired
- Sustained-release nutrients and other relatively non-toxic therapies may help combat or reduce this damage
This review by Professor Knox Van Dyke, Ph.D., West Virginia University Medical School, outlines numerous therapies, including sustained-release dietary supplements, that have the potential to target the underlying cause of Parkinson’s disease (PD).
Dr. Van Dyke notes that PD is a result of damage from oxidative and nitrosative stress in microglia in the substantia nigra area of in the midbrain. While causes may vary – viruses, brain trauma, exposure to certain chemicals – the result is the same. Nearby dopaminergic neurons are damaged, and the activity of nuclear receptor-related 1 protein (NURR-1) is impaired.
NURR-1 is a DNA transcription factor encoded by the NR4A2 gene, and it is responsible for the production, storage, and transport or reuptake of dopamine.
If NURR-1 becomes defective or if there is a loss of dopamine production, explains Dr. Van Dyke, this is the basis for PD. The damage to the dopaminergic neurons occurs because microglia in the area generate a toxic peroxide called peroxynitrite (PN) which reacts with carbon dioxide to produce peroxynitrite carbonate (PC), which is even more chemically reactive.
Dr. Van Dyke describes a variety of potential oral therapies, including several sustained-release nutrients, that may help protect the neurons. For example:
- Sustained-release antioxidants (e.g., vitamin C). To help protect dopaminergic neurons from oxidative and nitrosative stress.
- Sustained-release inosine. To help increase blood levels of purines that produce urate, which destroys PN and help control damage caused by PN or PC.
- Sustained-release L-arginine. To help produce extra and continuous amounts of nitric oxide to inhibit excessive PN production.
- Sustained-release acetaminophen. To help inhibit excessive PN production.
- To help inhibit excessive PN production.
- Glutathione or glutathione precursors. To help replenish glutathione levels.
- Sustained-release L-tyrosine. To help maintain dopamine continuously without damaging protective mechanisms for NURR-1.
- NURR-1 agonists (e.g., chloroquine, amodiaquine and derivatives). To help stimulate dopamine production.
- L-amino acids (e.g., l-tyrosine, L-tryptophan, 5 hydroxytryptophan). To help replace depleted levels.
- Sustained-release L-Dopa with or without L-tyrosine. Using L-tyrosine as a precursor for dopamine production may help reduce potential side effects.
Dr. Van Dyke further notes that these therapies are relatively non-toxic, making them useful for the prevention of or early and continuous treatment of PD.
More details, including specific dosing suggestions, are provided in the full review, which is available online at the AsclepiusOpen website.