The Huntingtons and JNK3 connection was discovered in research from the University of Illinois at Chicago College of Medicine. Before you get too excited about this report, you need to know that this is only a piece of the puzzle. Other pieces include MADD, DENN, Bcl-2 and glutathione to name a few.
The research was able to show that mutated Huntington's gene activates the JNK3 enzyme. This discovery helps to answer the question of why are those born with the disease symptom free at age three or four and at 30 0r 40 they start to develop the debilitating disease.
The study found there is a neuro-degenrative process that takes place as a result of the JNK3 activation. Once the nerve cell drops below its minimal threshold of activity, it will die.
Add this information to ...another piece of the puzzle.
A splicing variant of a death domain protein that is regulated by a mitogen-activated kinase is a substrate for c-Jun N-terminal kinase in the human central nervous system.
It is a bit geekey look at Huntingtons and JNK3 but here it is as the abstract.
The mitogen-activated kinase activating death domain protein (MADD) that is deferentially expressed in neoplastic vs. normal cells (DENN) was identified as a substrate for c-Jun N-terminal kinase 3 (JNK3), the first demonstration of such an activity for this stress-activated kinase that is predominantly expressed in the brain. A splice isoform was identified that is a variant of MADD. A protein identical to MADD has been reported to be expressed deferentially in neoplastic vs. normal cells and is termed "DENN."
These findings place DENN/MADD and JNK in important hypoxia insult-induced intracellular signaling pathways. Our conclusions are important for future studies for understanding these stress-activated mechanisms.
Regulation of Neuronal Cell Death and Neurodegeneration by Members of the Bcl-2 Family: Therapeutic Implications.
The Bcl-2 family of proteins contains both anti and pro-apoptotic members that have been shown to regulate neuronal cell death during development and in many models of acute and chronic neurodegeneration.
The article indicated there are three distinct classes which are based on structure and function:
pro-apoptotic multi-domain sub-group
pro-apoptotic BH3 domain-only sub-group
Alterations in expression (production) of Bcl-2 family members occur in several neurodegenerative diseases including Alzheimer’s, Huntington’s and Parkinson’s diseases and Amyotrophic Lateral Sclerosis.
Did you note the connection with the other diseases?
One more piece of the Huntingtons and JNK3 puzzle...
This was a study to look at the effects of Bcl-2 on reduced glutathione (GSH) metabolism.
The study indicates that the Bcl 2 alters glutathione distribution. It basically sequesters it to the nucleus. One conclusion was that Bcl-2 (among other things) sequesters GSH into the nucleus, nuclear alterations characteristic of cellular death (apoptosis). It was further speculated that this mechanism contributes to the suppression of cell death in cells with elevated Bcl-2 levels.
When the Bcl-2 expression was suppressed, glutathione was uniformly distributed.
One more piece of the puzzle...is this perhaps the sky we are looking at (as in heaven sent)?
Therapeutic potential of N-acetylcysteine in age-related mitochondrial neurodegenerative diseases.
It is from Medical Hypotheses, Volume 56, Issue 4, Pages 472-477
The abstract indicated there is evidence to suggest a key role for mitochondrial damage in neurodegenerative diseases.
Diseases and conditions such as brain aging, Parkinson’s disease, Alzheimer’s disease, Huntington’s disease and Friedreich’s ataxia are associated with these alterations.
When the mitochondria is impaired, there can be a resulting increase the generation of reactive oxygen species. This results in oxidative damage and eventually programmed cell death.
The paper looks at how N-acetylcysteine works at the cellular level, and the possible usefulness of this antioxidant for the treatment of age-associated neurodegenerative diseases.
Note it indicated it was being looked at as a treatment.
First, NAC acts as a precursor for glutathione synthesis and stimulates glutathione regeneration.
Second, N-acetylcysteine directly reacts by reducing thiol group and reactive oxygen species (the oxidants: think of them as cellular rust).
Third, N-acetylcysteine can prevent programmed cell death in cultured neuronal cells.
Fourth, N-acetylcysteine also increases mitochondrial complex I and IV specific activities both in vitro and in vivo in synaptic mitochondrial preparations from aged mice.
The abstract concluded, "In view of the above, and because of the ease of its administration and lack of toxicity in humans, the potential usefulness of N-acetylcysteine in the treatment of age-associated mitochondrial neurodegenerative diseases deserves investigation."
There is indeed a glutathione connection. The studies that look at NAC or other sources of boosting glutathione do not necessarily have the best source of NAC. There are currently supplements that produce 30 to 200 percent increases in glutathione.
Each has its place. The point is, the studies did not look at the current super charges glutathione boosting products on the market. Could the outcomes be even better?
Become an educated consumer regarding Huntingtons and JNK3.
There is more pieces of the puzzle than Huntingtons and JNK3.
Good health to you.
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