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In this issue:

1. Share Success: Letters From Readers
2. Research News: TREM2 Protein May Slow Down Progression of Alzheimer’s
3. Useful Links
4. What Are Others Saying About EZorb and Marvlix?

Letter I: From Sandra, Orlando FL
Received at Testimonial Submit Form Tuesday, August 29, 2023 at 13:06:31 PDT
(Unedited)

Hi, my name is Sandra. About 7 months ago I purchased 6 Bottles of the Ezorb powder. My 2019 bone density test said that I had mild osteopenia in my hips, and my spine density was normal.

After taking e-zorb for about 6 months, I went for my bone density in 8-2023. To my surprise, the bone density in my hips showed No osteopenia, and were in the normal range!

The bone density in my spine, however, had gone up from normal from what my 2019 bone density test showed. The comment on the 2023 bone density regarding my spine was: The spinal density is elevated probably due to associated facet disease and sclerosis.

I am not sure if I should continue taking the E-Zorb if it will continue to raise the bone density in my spine far above normal ranges.

Please advise.

I have referred at least 5 of my friends to your product!

Regards,

Sandra
Orlando, FL

Letter II: From Audrey P.
Received at Share Success Friday, July 28, 2023 at 10:07 AM PDT
(Unedited)

Well I just have to let you know just how great Ezorb really is. I have been amazed just how great I feel since taking Ezorb.

I started suffering from a heel spur on my right heel about 5 months ago. It got so bad that I couldn't put my foot on the floor. I was getting desperate, so I looked on the net to see if I could find something that would heal the pain.

Lucky enough I saw Ezorb and read some of the testimonials how people that had tried it were feeling. So I thought can't hurt to give it a try and it has been the best decision that I have ever made.

I am on my 4th bottle and I feel fantastic. I can actually walk bare foot now the pain is gone and I have reduced the amount of pills I take from 8 pills a day to 4 and I still feel fantastic.

Thank you Ezorb for giving me my life back! I can't say enough about Ezorb it is fantastic. Thank you Ezorb.

Sent from my Galaxy

Our newsletter reaches over 230,000 subscribers worldwide. Success stories you shared in the past have made a great impact on many people's life.

Please email your story to sharesuccess@ezorbonline.com or simply post it to Testimonial Submit Form. Your personal information will never be revealed to the public.

Researchers have identified an association between faster rates of increase of TREM2 levels in soluble cerebrospinal fluid (CSF) and slower progression of several markers of disease evolution in participants of the Dominantly Inherited Alzheimer Network (DIAN), which they say points to a likely protective effect of TREM2 during the early pathogenesis of Alzheimer’s disease.

“These findings support ongoing efforts to develop TREM2-boosting therapies as disease-modifying treatments for Alzheimer’s disease and suggest an early window for therapeutic intervention”, say Estrella Morenas-Rodríguez (Hospital Universitario 12 de Octubre, Madrid, Spain) and co-authors in The Lancet Neurology.

They explain that TREM2 is a protein associated with microglial function and inflammation, and rare mutated versions are associated with an increased risk of Alzheimer’s disease.

The researchers used a novel immunoassay to assess cleaved soluble TREM2 levels in CSF samples collected annually or every 2 years from 239 DIAN participants enrolled between 2009 and 2019. One hundred of the participants were presymptomatic carriers of pathogenic variants in the PSEN1, PSEN2 or APP genes, 48 were symptomatic carriers and the remaining 91 were noncarriers.

The team found that a faster annual rate of increase of soluble TREM2 levels was associated with a significantly reduced rate of decrease of amyloid-B (AB)42 in CSF samples from presymptomatic carriers and a significantly reduced rate of increase of Pittsburgh compound B-positron emission tomography (PiB-PET) uptake in symptomatic carriers.

Further investigation showed that among presymptomatic carriers, there were contrasting associations between CSF AB42 levels and PiB-PET uptake depending on whether the rates of increase of soluble TREM2 were above or below the median, say Morenas-Rodríguez and colleagues.

They additionally identified a correlation between greater annual rates of increase of phosphorylated-tau in CSF and increased PiB-PET uptake in presymptomatic carriers with annual rates of increase of soluble TREM2 that were below the median. But there was no such correlation among those with rates above the median.

Finally, assessment of neuroimaging and cognitive outcomes in presymptomatic carriers showed a significant correlation between greater rates of soluble TREM2 increase and slower cortical shrinkage in the precuneus as well as with slower progression of cognitive decline.

Taken together, these results suggest “a potential protective role of TREM2 function on amyloid-dependent tau pathology, in line with results in mouse models”, say the researchers.

The authors of a related commentary agree that “these new data support the hypothesis that TREM2 might have a protective function in the early pathogenesis of Alzheimer’s disease and support a rationale for the development of TREM2-targeted therapeutics.”

But they point out that despite the longitudinal study design, “the associations identified are, at their core, correlational and causation cannot be inferred from this study alone.”

Denis Smirnov and Douglas Galasko, both from UC San Diego in La Jolla, California, USA, also note that the “study did not identify the mechanisms that might underlie variable soluble TREM2 responses in CSF that could provide guidance towards personalised therapeutic approaches.”

And they conclude: “Continued laboratory studies with direct manipulation of TREM2 activity will be essential, although the limitations of animal models might mean that human trials will be the ultimate test of the authors’ hypotheses, and the present study provides a roadmap towards that goal.”

Original research was published in Lancet Neurol 2022; 21: 329–341.

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