Sustained-release nutrients and other therapies may help support neurological health, review shows
Highlights
- Variety of nutritional therapies described
- Multifactorial actions to support neuron health
Summary
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.
