It doesn’t seem to be in the 23 and Me data. Some people in this APOE4 forum are saying you need a whole genome done, or some new version of 23 & me. I’m not sure how accurate this is.
“Two mutations (rs116558455 and rs140926439) in the FN1 gene (Fibronectin-1) were found in healthy elderly ε4 homozygous carriers in EFIGA/WHICAP and NIA AD-FBS cohorts with MAF=1.85% and 3.33%, respectively…”
See this thread: New Study. FN1 modifiers and APOE4 - ApoE4.Info
Found My Fitness by Rhonda Patrick offers a program where members can download the raw data from 23andme for free. Promertheus is a good option for $12.
Rhonda is very interested in Alzheimer’s disease because of her family history and her having one APOE-4 allele (she often talks about it during her presentations). There is a lot of mentioning of research, even recommendations on supplements pertaining to different SNPs besides APOE-4 in her program.
VERY INTERESTING!
Here is the link, scroll down and press “try it” for ApoE Report.
23andme reports include APOE status. See PDF below.
I have an archived report that explicitly says ‘e3/e4’, but I don’t see e3 called out now, just tells you whether you have e4 or not.
Leonard Glassner Late-Onset Alzheimer’s Disease Report - 23andMe.pdf (221.2 KB)
And then there’s post-partum depression and worse, not to mention severe sleep deprivation.
Source: https://twitter.com/Drlipid/status/1745458968603037884
More Alzheimer’s discussion in this thread: Optimal Blood Pressure we Should Target? Systolic Under 110 or 100? - #342 by Neo
Overlapping authors with this also exciting study:
Establish biorepository of blood-based biomarkers for neurodegenerative diseases (ND); assess feasibility of biomarker collection/processing in subjects at risk for dementia; incorporate concurrent phenotypic clinical data; and explore utility of blood-based biomarkers as outcome measures for n-of-1 trials.
ND have an extended preclinical period. Early identification and intervention prior to dementia may offer the best opportunity to prevent or delay cognitive decline. Research suggests that blood-based biomarkers may be a reliable predictor of disease progression. The opportunity to use blood-based biomarkers to identify risk, monitor progression, and potentially guide individualized care represents a significant opportunity.
Subjects with family history of ND with no or minimal cognitive and/or neurological complaints were recruited. Demographics, medical history, cognitive assessments and blood-based biomarkers for ND (via venipuncture and/or at-home finger prick card testing) were collected at baseline and longitudinally. Blood-based biomarkers included: Amyloid beta 42/40 ratio, pTau181, pTau231, pTau217, Neurofilament light and glial fibrillary acidic protein. Subjects may also opt-in to share relevant data from preventive clinical care.
53 subjects (66% male, mean age 57.2, range 22–93, 62% ApoE4+) were enrolled. 75% of eligible subjects returned for follow-up assessments. A majority of subjects provided clinical data with biomarkers measured before and after risk reduction interventions prescribed by their physicians. Individualized clinical management consisted of various pharmacological therapies to address modifiable risk factors (e.g., tirzepatide, rosuvastatin, escitalopram), anti-amyloid therapies (e.g., aducanumab, lecanemab), other agents (e.g., rapamycin) and multi-modal lifestyle interventions (e.g., exercise, diet).
In subjects at risk for dementia, it was feasible to collect/process blood-biomarkers. Several subjects had measurable changes in biomarkers of ND pathology and/or improvements or stabilization of cognition. Further research using blood-based biomarkers to evaluate the effectiveness of individualized ND preventive care in real-world clinical settings is needed.
https://www.neurology.org/doi/abs/10.1212/WNL.0000000000204525
yesterday, old chip. I 23andme’d a decade ago, no update.
And if there are still doubters, look at the options offered comparision on the website. It states ‘late onset alzheimers risk’ (aka apoe status) as one of the ‘health predisposition reports’ provided.
The test got many of its predictions right, but it isn’t infallible. For example, according to them, I have no variants for macula, and yet I have the eye disease. We’ll see if the peptide visoluten can help. As for AD, they told me that I don’t have one of the variants, but there are other variants not tested for. I still have a 5-10 percent chance of getting AD. So I will improve my odds today by doing some sprinting drills.
P.S. I just payed 80 bucks to get tested with the latest chip.
What is this based on?
who’s estimate/statistics? based on what life expectancy?
Male, no e4
Good question but I haven’t studied it. I think the science is pretty accurate. Maybe 80 percent?
Then again, high fat and high protein diets kill mice first.
Hence my comment— has to be Mediterranean keto. Not all fats and proteins are equal, neither are all carbs of course. But all things equal ketosis is very beneficial for dementia prone brains as glucose metabolism is impaired there.
Thanks @Tim and @anon16510610
If you are aiming for older age, say mid 90s or past 100, the probability appears to sky rocket though - for everyone including even for people who have one e2 even. The only one that is still ok is the uncommon double e2.
So a correct take away may not be
I still have a 5-10 percent chance of getting AD.
But rather, without changing things, the risks is very, very large if we succeed in becoming old - and hence AD prevention should be a top, top, top priority whenever goal is to live long):
