A new study has been published in the journal Antioxidants and Redox Signaling by Dr. Bobby Thomas who is a neuroscientist with the Medical College of Georgia at Georgia Health Sciences University. His study shows that NRF2 activation in an animal model boosts the cell’s production of its own antioxidant enzymes and manages inflammation at the same time. This helps the cells recover from the damaging effects of high oxidative stress associated with Parkinson’s disease.

More specifically, Thomas and his fellow researchers proved that they were able to block the death of dopamine-producing brain cells that occurs in Parkinson’s by activating Nrf2, a natural antioxidant and inflammation fighter.

Parkinson’s Disease Symptoms Include:

• Tremors
• Slowed movement (bradykinesia).
• Rigid muscles/Muscle stiffness
• Loss of automatic movements including blinking, smiling or swinging your arms when you walk.
•  Speech changes

This is not the first study to have been completed on NRF-2 and Parkinson’s. Pubmed has the following additional studies.

• The Nrf2-ARE Pathway: A Valuable Therapeutic Target for the Treatment of Neurodegenerative Diseases.
• 15-Deoxy-Δ12,14-prostaglandin J₂ modulates manganese-induced activation of the NF-κB, Nrf2, and PI3K pathways in astrocytes.
• Molecular mechanism underlying the cerebral effect of Gly-Pro-Glu tripeptide bound to L: -dopa in a Parkinson‘s animal model.
• Genetic activation of Nrf2 signaling is sufficient to ameliorate neurodegenerative phenotypes in a Drosophila model of Parkinson‘s disease.
• Maneb and paraquat-mediated neurotoxicity: involvement of peroxiredoxin/thioredoxin system.
• Regulation of dopaminergic neuronal death by endogenous dopamine and proteasome activity].
• Controlled enzymatic production of astrocytic hydrogen peroxide protects neurons from oxidative stress via an Nrf2-independent pathway.
• Different susceptibility to the Parkinson‘s toxin MPTP in mice lacking the redox master regulator Nrf2 or its target gene heme oxygenase-1.
• Decaffeinated coffee and nicotine-free tobacco provide neuroprotection in Drosophila models of Parkinson‘s disease through an NRF2-dependent mechanism.
• Association of Nrf2-encoding NFE2L2 haplotypes with Parkinson‘s disease.
• Therapeutic approaches to mitochondrial dysfunction in Parkinson‘s disease.
• Genome-wide microarray analysis of the differential neuroprotective effects of antioxidants in neuroblastoma cells overexpressing the familial Parkinson‘s disease alpha-synuclein A53T mutation.
• Nrf2-mediated neuroprotection in the MPTP mouse model of Parkinson‘s disease: Critical role for the astrocyte.
• Transcribe to survive: transcriptional control of antioxidant defense programs for neuroprotection in Parkinson‘s disease.
• Bromocriptine activates NQO1 via Nrf2-PI3K/Akt signaling: novel cytoprotective mechanism against oxidative damage.
• Expression of Nrf2 in neurodegenerative diseases.
• Proteasome inhibition induces glutathione synthesis and protects cells from oxidative stress: relevance to Parkinson disease.The Nrf2-ARE Signalling pathway: promising drug target to combat oxidative stress in neurodegenerative disorders.

Information provided on this site is for educational purposes only. Do your own research, and consult with a medical professional about your findings.