Parkinson's Disease

People who have Parkinson's report that their symptoms have decreased after taking an Nrf2 activator.  Following the testimonials are current research articles that report new information about the cause of Parkinson's Disease and how Nrf2 activators can be effective in treating it at the cellular level where it starts.


Kalei Migniola:  "I suffer from Parkinsons Disease. It's been 20 days since I started taking Protandim. I'm feeling great, and I've seen major improvement in the movement of my left arm. My Parkinsons symptoms are improving, and I'm feeling better. My arm movement is now really fluid. I haven't had any big improvements in the tremors yet, but I think that's already a little better. Overall I'm feeling better, although I'm still having the tremors. I've been able to start exercising, trying to do twice a day for 15 minutes. I've been sleeping better, feeling better, having more energy, and I'm really excited about this, especially about how my arm movement has improved so greatly, because it's helpful for life."   youtube.com

Joe:  On this video you will Joe.  He is a 66 year-old vet who was exposed to agent orange and has Parkinson's Disease.  He is on Mirapex and Cinemet, but they have not seemed to relieve his symptoms.  He is unable to repeat sentences well, frequently stuttering as he attempts to speak.  He shuffles down the hallway, at the end using rapid short steps to turn around to go the other way, and sometimes needing to hold the wall for balance.  30 minutes after a glutathione injection the video resumes, and he is walking fairly normally and can use longer strides.  When he turns at the end of the hallway it is done with only a few steps.  He can speak now without stuttering, saying "I feel a lot better; My legs are so much better; I can't believe I'm walking; This is wonderful; I feel like a regular guy, I'm serious."   Watch the video.


Paula Pursley:   I am 58, Chuck is 78.  We’ve been married 24 years.  He is the love of my life.  What I didn’t know way back before we met, was that I was in love with him even before I knew he existed.  Do you know what I mean?  That’s the kind of relationship we have.  About 5 years ago Chuck was diagnosed with Parkinson’s  Disease – a progressive neurological disorder, no cure.  When you hear Parkinson’s you may think of Michael J. Fox, or the former Pope, who lived with Parkinson’s for many, many years.  Chuck has a very relaxed attitude about his PD, he figures something would eventually get him, and it could be worse.   For those of you not familiar with PD, some of the symptoms are:  tremors in the hand and legs; slow walk, eventually becoming a shuffle; hunched posture; balance and coordination issues; impaired large and small muscle dexterity; speech problems; drooling; facial ‘mask’ – people with PD begin to lose their expression, have a quiet dullness about them, or as I refer to it, their lights go out.   

Okay, so that’s what we have been dealing with for the last 5 years.  Chuck has been taking Shaklee supplements for 7 years and is on prescription meds for the PD.  I’ve done a lot of research, talked with others, and have him on a pretty solid Shaklee program – which we are constantly tweaking as we learn more.

At convention this year, when Vivix, our new anti-aging tonic, was announced, Dr. Jamie McManus, Director of Health Sciences at Shaklee, said people with diabetes, heart disease and neurological diseases would have the most results.  Well, you can imagine the cheer that went up in OUR section!  My dear friends all did a zizzt stare at me.  Talk about a heart flutter!

I brought Vivix home from convention and Chuck began taking it mid August and has been faithful with it every day!  He promised me he would do that for 6 months before making any decision on whether to continue it or not.  Keep in mind, my darling husband is my very best skeptic!   

Now if you would ask him how he feels today, he’d say he doesn’t feel any different.  I did invite him to come along tonight so you could meet him, but he really isn’t fond of meetings like this – plus he’s at a party with a bunch of his buddies!

My report to you is that little things are happening.  And it’s often the little things in life that mean the most!  He’s back to:  1. laughing, 2. participating in conversations at family gatherings, 3. whistling around the house, 4. doing his cute little two step when he’s being funny, 5. standing straighter when he hugs me, 6. he’s just more engaged in life –  7. and the best of all – his lights are back on!

Is Vivix making a difference in Chuck’s health and in our hope for him?  You bet it is!  And is he going to keep taking it after his promised 6 months?  He better!  (http://jswank.myhomebizniz.com/)

RESEARCH ARTICLE (from pubmed.gov):

On November 2, 2017, Dr. Chao and others in the Department of Neurosurgery at The First Affiliated Hospital of Nanjing Medical University in Nanjing, China, reported that Parkinson’s disease and some other neurodegenerative disorders is caused by oxidative stress on mitochondria, causing abnormal mitochondrial function within cells and cell death, causing reduction of dopamine and lowered survival. People with Parkinson’s have reduced glutathione levels. Prevention of mitochondrial degeneration in the first place is a rational approach for the prevention and treatment of Parkinson’s Disease (i.e. increase glutathine levels to reduce oxidative stress to reduce cell damage).  (see pubmed.gov, 29104115).


RESEARCH ARTICLE (from pubmed.gov): 

PLoS One. 2015 May 29;10(5):e0127549. doi: 10.1371/journal.pone.0127549. eCollection 2015.
A DJ-1 Based Peptide Attenuates Dopaminergic Degeneration in Mice Models of Parkinson's Disease via Enhancing Nrf2.
Abstract

Drugs currently used for treating Parkinson's disease patients provide symptomatic relief without altering the neurodegenerative process. Our aim was to examine the possibility of using DJ-1 (PARK7), as a novel therapeutic target for Parkinson's disease. We designed a short peptide, named ND-13. This peptide consists of a 13 amino acids segment of the DJ-1-protein attached to 7 amino acids derived from TAT, a cell penetrating protein. We examined the effects of ND-13 using in vitro and in vivo experimental models of Parkinson's disease. We demonstrated that ND-13 protects cultured cells against oxidative and neurotoxic insults, reduced reactive oxygen species accumulation, activated the protective erythroid-2 related factor 2 (Nrf2) system and increased cell survival. ND-13 robustly attenuated dopaminergic system dysfunction and in improved the behavioral outcome in the 6-hydroxydopamine mouse model of Parkinson's disease, both in wild type and in DJ-1 knockout mice. Moreover, ND-13 restored dopamine content in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model. These findings validate DJ-1 as a promising therapeutic target in Parkinson's disease and identify a novel peptide with clinical potential, which may be significant for a broader range of neurological diseases, possibly with an important impact for the neurosciences.

PMID: 26024237 [PubMed - in process] PMCID: PMC4449207

RESEARCH ARTICLE (from pubmed.gov):

Autophagy. 2015 Jun 5:0. [Epub ahead of print]
Parkinsonian toxin-induced oxidative stress inhibits basal autophagy in astrocytes via NQO2/Quinone Oxidoreductase 2: implications for neuroprotection.
Abstract

Oxidative stress (OS) stimulates autophagy in different cellular systems, but it remains controversial if this rule can be generalized. We have analyzed the effect of chronic OS induced by the parkinsonian toxin paraquat (PQ) on autophagy in astrocytoma cells and primary astrocytes, which represent the first cellular target of neurotoxins in the brain. PQ decreased the basal levels of LC3-II and LC3-positive vesicles, and its colocalization with lysosomal markers, both in the absence and presence of chloroquine. This was paralleled by increased number and size of SQSTM1/p62 aggregates. Downregulation of autophagy was also observed in cells chronically exposed to hydrogen peroxide or nonlethal concentrations of PQ, and it was associated with a reduced astrocyte capability to protect dopaminergic cells from OS in co-cultures. Surprisingly, PQ treatment led to inhibition of MTOR, activation of MAPK8/JNK1 and MAPK1/ERK2-MAPK3/ERK1 and upregulation of BECN1/Beclin 1 expression, all signals typically correlating with induction of autophagy. Reduction of OS by NMDPEF, a specific NQO2 inhibitor, but not by N-acetylcysteine, abrogated the inhibitory effect of PQ and restored autophagic flux. Activation of NQO2 by PQ or menadione and genetic manipulation of its expression confirmed the role of this enzyme in the inhibitory action of PQ on autophagy. PQ did not induce NFE2L2/NRF2, but when it was co-administered with NMDPEF NFE2L2 activity was enhanced in a SQSTM1-independent fashion. Thus, a prolonged OS in astrocytes inhibits LC3 lipidation and impairs autophagosome formation and autophagic flux, in spite of concomitant activation of several pro-autophagic signals. These findings outline an unanticipated neuroprotective role of astrocyte autophagy and identify in NQO2 a novel pharmacological target for its positive modulation.



RESEARCH ARTICLE (from pubmed.gov):

Mitochondrion. 2015 Feb 8. pii: S1567-7249(15)00022-7. doi: 10.1016/j.mito.2015.02.001. [Epub ahead of print]

Mitochondrial iron homeostasis and its dysfunctions in neurodegenerative disorders.

Abstract

Synthesis of the iron-containing prosthetic groups-heme and iron-sulfur clusters-occurs in mitochondria. The mitochondrion is also an important producer of reactive oxygen species (ROS), which are derived from electrons leaking from the electron transport chain. The coexistence of both ROS and iron in the secluded space of the mitochondrion makes this organelle particularly prone to oxidative damage. Here, we review the elements that configure mitochondrial iron homeostasis and discuss the principles of iron-mediated ROS generation in mitochondria. We also review the evidence for mitochondrial dysfunction and iron accumulation in Alzheimer's disease, Huntington Disease, Friedreich's ataxia, and in particular Parkinson's disease. We postulate that a positive feedback loop of mitochondrial dysfunction, iron accumulation, and ROS production accounts for the process of cell death in various neurodegenerative diseases in which these features are present.

Copyright © 2015. Published by Elsevier B.V.

PMID:  25667951  [PubMed - as supplied by publisher]

[INTERPRETATION:  The energy-producing part of the cell also produces oxidants (ROS), and in certain situations the oxidants result in cell death and diseases such as Parkinson’s.]