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Innovative Study on Brain Cell Death May Lead to New Alzheimer’s Treatment

Posted by on Monday, August 28th, 2017

research for Alzheimer's treatment

An innovative study has targeted a new way that brain cells die from Alzheimer’s Disease (AD).  This is the first EVER evidence of a new biological pathway linked to AD severity & loss of brain tissue-all hallmark symptoms of AD.  The pathway is called necroptosis, and it causes nerve loss.   This new research is thought to lead to innovative methods of Alzheimer’s treatment in the future. 

The study was published by Arizona State University-Banner Health neuroscientist Salvatore Oddo and his colleagues from Phoenix’s Translational Genomics Research Institute (TGen) — as well as the University of California, Irvine, and Mount Sinai in New York.

“We anticipate that our findings will spur a new area of Alzheimer’s disease research focused on further detailing the role of necroptosis and developing new therapeutic strategies aimed at blocking it,” said Oddo, the lead author of this study, and scientist at the ASU-Banner Neurodegenerative Disease Research Center at the Biodesign Institute and associate professor in the School of Life Sciences.  The findings of the study were published in Natural Neuroscience.

The term necroptosis is considered a form of necrosis, or inflammatory cell death.  It is usually associated with the death of a cell due to cellular damage, as compared to orderly, programmed cell death that occurs via a pathway called apoptosis.  This disorderly type of cell death results in the cell bursting from the inside out; it is triggered by a triad of proteins.  Necroptosis has been associated with multiple sclerosis and Lou Gehrig’ disease.  This is the first time scientific evidence has linked necroptosis with Alzheimer’s disease.

“There is no doubt that the brains of people with Alzheimer’s disease have fewer neurons,” said Oddo. “The brain is much smaller and weighs less; it shrinks because neurons are dying. That has been known for 100 years, but until now, the mechanism wasn’t understood.”

Inflammation has long been associated with AD.  In necroptosis, there are 3 proteins involved, RIPK1, RIPK3 and MLKL.  In the study, a key event was discovered in the process of necroptosis,  when RIPK1 and RIPK3 from a structure called a necrosome.  The formation of this necrosome is what is thought to start the process of cell death from necroptosis, by activating MLKL, which in turn adversely affects the powerhouse of the cell (called the mitochondria)–eventually leading to cell death.  So, the MLKL is thought to execute necroptosis which eventually results in brain cell death.

“In this study, we show for the first time that necroptosis is activated in Alzheimer’s disease, providing a plausible mechanism underlying neuronal loss in this disorder,” said Liang, who contributed to the study’s gene expression analyses.

The Study

The research team used donated samples from the Body Donation Program at the Banner Sun Health Research Institute and Mount Sinai VA Medical Center Brain Bank.  Scientists then utilized the samples to measure RIPK1, RIPK3 and MLKL in a particular area of the brain that has been found to be adversely affected by AD-called the temporal gyrus.  During necroptosis, the RIPK1, RIPK3 and MLKL markers were increased in the brains of those with AD.  When examining postmortem (after death) brain tissue levels of protein, elevated MLKL and RIPK1 levels were discovered in those with AD, compared with normal postmortem brains.   In addition, the necroptosis activation was linked to the abnormal tau protein, considered a hallmark symptom of AD.  Interestingly, the necroptosis was NOT associated with the other abnormal protein found in the brains of those with AD, called amyloid plaque.

Conclusion

This study provides an opportunity for new hope for future research.  Scientists hope to discover  innovative new Alzheimer’s treatment modalities, that will effectively target nerve cell loss in the brain. “One may not agree as to which molecules trigger Alzheimer’s disease, ” said Oddo, “but everybody agrees that the end result is the neuronal loss. If you can prevent that you may have a beneficial effect.”

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