NEW blood test to predict AD

[RBK]

Another reason outside of my HSV-1 to get lysine. I've been tracking my dietary intake and on new ratios I'm always well above the suggested 1500mg in Dr. P's suggested protocol, so I'm not supplementing... Yet.

[Silverlining]

Hey Jules...I listened to the Federof podcast and I think he said "genes", rather than one singular gene. This part of the podcast is at 8:50mm in a 10 minute broadcast. It is very intriguing.

[Julie G]

A ha, another clue I perused his published papers for more, but got nowhere. Unfortunately, he's rather prolific... I'm signed up for google alerts on further papers. Stay tuned for updates.

[Julie G]

I queried Dr. Federoff yesterday about trying to glean dietary information from his recent paper. He very promptly responded and advised that he could NOT provide nutrition advice based on that research. He noted that they collected no dietary information; but agreed it would be an interesting are to explore. He very kindly commended US for our important work

I'm intrigued by this Georgetown group and have google alerts set for several of the authors.

[Julie G]

Well, well well...we weren't the only ones who wondered if we could work the equation backwards by supplementing the deficient lipid metabolites. I would LOVE to see full text on this one.

A Nutritional Approach to Ameliorate Altered Phospholipid Metabolism in Alzheimer's Disease
http://www.ncbi.nlm.nih.gov/pubmed/24898653

Abstract
Recently, a biomarker panel of 10 plasma lipids, including 8 phosphatidylcholine species, was identified that could predict phenoconversion from cognitive normal aged adults to amnestic mild cognitive impairment or Alzheimer's disease (AD) within 2-3 years with >90% accuracy. The reduced levels of these plasma phospholipids could reflect altered phospholipid metabolism in the brain and periphery. We show that a 24-week nutritional intervention in drug-naïve patients with very mild to mild AD significantly increased 5 of the 7 measured biomarker phosphatidylcholine species. By providing nutrients which normally rate-limit phospholipid synthesis, this nutritional intervention could be useful in asymptomatic subjects with a plasma lipid biomarker profile prognostic of AD.

[Julie G]

Ever wonder what happened to Federoff's new test for Alzheimer's? I just read in Forbes that he's taken it to the marketplace I still contend that the most benefit from the new test may be found in identifying modifiable biomarkers early enough to PREVENT Alzheimer's from occurring...but will patents now prevent us from identifying them?
http://www.forbes.com/sites/nicolefishe ... o-take-it/

I've got full-text of the original paper. PM me with your email if you'd like a copy.

[circular]

I have to get off my computer and didn't read the whole article, but did I miss news that you can now get LTC or life insurance without consideration of what's in your medical file, or was this quote flat wrong? If wrong that statement needs correcting:

"Additionally, because a preexisting condition no longer means that you can be precluded from long-term care and life insurance, financial planning is now possible for individuals, families, employers and societies.”

I'd think if there was a recent change in this policy Forbes would have reported on it and provided a link in the text to the coverage.

[Julie G]

Plasma 24-metabolite Panel Predicts Transition to Clinical Stages of Alzheimer’s Disease
http://journal.frontiersin.org/article/ ... 00237/full

Here’s full-text of a brand new paper from Howard Federoff et al. They’ve expanded upon their initial paper that found a deficiency of 10 lipid metabolites from a simple blood test that were found to predict conversion to Alzheimer’s with 85-90% accuracy. They’ve expanded the list of metabolites to 24 and have increased the accuracy of the test to 95-100%. HOWEVER, they seemed to have somewhat reined in their earlier exuberance about using this as a commercially available assay to predict Alzheimer’s and now suggest the test may be best used to internally predict which subjects will develop AD and therefore be good candidates for interventional trials. Hmmm ... I still contend that we may be able to somehow use the information to tweak our prevention protocols as evidenced by the Souvenaid paper referenced earlier in this thread and cited in this paper.

If you want to track down the specific metabolites, Figure 3 (below) would be most helpful. Keep in mind that orange represents the non-converter group and light blue represents the group that converted to Alzheimer’s. All the converter results are reduced in comparison to non-converter levels, except for three acylcarnitine species (bottom of figure), C16:2, C12:1, and C10:1, which are elevated.

fneur-06-00237-g003.jpg

It’s interesting to note that all of the 13 PCs in the new blood panel feature PUFAs. These are found to be deficient in the peripheral blood years before a patient converts to full-blown Alzheimer’s. I found this interesting from the Discussion section of the paper:

The mechanistic link between reduction of brain lipid in association with LOAD, and in peripheral blood, has yet to be fully elucidated. Interestingly, the PCs in our 24-metabolite panel all feature polyunsaturated fatty acids (PUFAs) (Table 3), as has been reported by others (25, 27). While the brain has the capacity to generate all the lipid species it requires for normal function, along with most saturated and monounsaturated FAs (28, 29), specific substrates required to maintain brain lipid homeostasis, especially sources of energy and certain PUFAs, are delivered to the brain via the bloodstream. In normal brain metabolic processing, phospholipid components are efficiently recycled and have relatively long central half-lives (28). Essential PUFAs such as docosahaxaenoic acid (DHA; 22:6 n-3) and arachidonic acid (AA; 20:4 n-6) provide structural functionality as phospholipid components in bilayer membranes.

[TheBrain]

I've got to work on my MAO-A methylation defect that apparently renders all of my neurotransmitters (serotonin included) randomly high/low- can't be good. I think G and Spunky have the same issue...anybody worked on that one yet?

Julie, have you learned anything about how to work on your MAO-A methylation defect? I have the same defect. My functional medicine practitioner has said one of her skills is helping patients with methylation defects, though we haven't gotten to that yet. If/when I learn anything relevant, I'll pass it along.

[Julie G]

Alysson, your question deserves it's own topic. I've moved it to a new thread entitled "Hacking the MAO-A methylation defect" viewtopic.php?f=14&t=1777