Mitochondrial Dysfunction in E4 carriers

Insights and discussion from the cutting edge with reference to journal articles and other research papers.
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Re: Mitochondrial Dysfunction in E4 carriers

Post by mike »

Mitochondria are cell's main energy suppliers. People who get AD tend to have neuron loss decades prior to symptoms. It would make sense that anyone who has mitochondrial issues could accelerate that trend.
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Re: Mitochondrial Dysfunction in E4 carriers

Post by Nikki2019 »

TheBrain wrote:Hi Nikki,

No one in my family wants to talk about Alzheimer’s prevention, not even my two cousins who recently lost their mother to Alzheimer’s and who also lost their father to the same disease. I don’t get it, but I stay off my soapbox.
Hi TheBrain,
I can relate!!! How many times have I stopped myself from asking my uncles their ApoE status. Their brother, my father is a 4/4 and in a memory home, now late stage AD. It would be helpful to know and then try to prevent, since they both are likely to have at least one 4 allele. So many just want to bury the head in the sand or cover the ears and close eyes " Bla, Bla. I can't hear you... scary monster go away!"
A pat on the back to all of us on this site to grab life by its horns.
As E4 s, we are inherent fighters and don't give up so easily.
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Re: Mitochondrial Dysfunction in E4 carriers

Post by lawson415 »

Tincup wrote: Tue Feb 03, 2015 7:56 pm Alysson,
Does your ex feel like the neutrotransmitter balancing program was effective and worth doing?
Mixing Hinz’ ideas of balancing neurotransmitters with amino acid precursors with the nutragenomics popularized by Amy Yasko could work very well.

Several years ago, I was hired by a Hinz associate to measure how brainwaves change with neurotransmitter amino acid precursor supplementation. I added myself to the treatment group in order to increase the number of participants. I found taking the dopamine precursor tyrosine made a huge improvement in cognition, energy, and mood. This was in 2004. Since then, I've continued using tyrosine. A decade after starting tyrosine, I reanalyzed my 23andMe data and discovered I have an overactive MAOA SNP. Monoaminoxidase A (MAOA) breaks down dopamine and too much of it can lower dopamine levels enough to cause depression. (They used to believe it was MAOb that degraded dopamine but newer research is showing this is not so.) This SNP explains why I did so well with tyrosine. On the other hand, my partner who has the underactive SNP became so anxious she developed agoraphobia when she took a dopamine agonist because she could not break down the increased dopamine.

The nutragenomics also helped my partner and her sister in a different way. They both had a SNP that kept them from converting cyanocobalamin (B12) to the active form, methylcobalamin. My sweetheart said she felt like she had nervous system again when we started her on the methylcobalamin.

I do not know if Dr. Bredesen is using SNPs to guide his interventions but I do know doing so has helped my family and me quite a bit.
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