Plasmalogen Test Kit (Full Report)


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Plasmalogen Testing and Alkyl-Acylglycerol Supplementation: A Breakthrough in Neurological Disorders
By Chris D. Meletis, N.D

Neurodegenerative diseases such as Alzheimer’s disease (AD) and related dementias, Parkinson’s, Multiple Sclerosis, and autism are reaching epidemic proportions.   An estimated 25% of individuals older than 65 years have some form of dementia1  Furthermore, the cumulative incidence of dementia in people living to 95 years is more than 80%.2 3 Multiple sclerosis, another neurological disorder, affects 400,000 people in the United States and 2.1 million people globally.4 It places a large burden on the national healthcare system and on the patient and the patient’s family.
A common feature of all neurodegenerative diseases is the depletion of critical membrane lipids called plasmalogens.  Plasmalogen depletion is believed to occur due to either reduced biosynthesis associated with aging (Alzheimer’s/Parkinson’s) or due to excess degradation due to oxidative stress/inflammation (multiple sclerosis/autism).  Previously, there was no reliable way to measure an individual’s plasmalogen status or to take meaningful clinical steps to restore plasmalogens to healthy levels. Fortunately, plasmalogen levels decrease years  before development of dementia, so measurements of plasmalogen status can be used to guide prevention and treatment in these types of patients. Based on test results, plasmalogen levels can be replenished through supplementation with a very specific type of phospholipid.
Utilizing this type of testing and subsequent supplementation is cutting edge, novel, and scientifically validated in the peer-review literature. It will help set your therapeutic offerings apart from slow adapters. In this article, I’ll explain the role of plasmalogens in Alzheimer’s, dementia, MS, and autism as well as the clinical usefulness of testing for this biochemical indicator, and the importance of supplementation with the most effective type of phospholipid to restore plasmalogen levels.

Plasmalogens: Their Role in Protecting Against AD and Dementia
  Plasmalogens are a naturally occurring substance in our bodies. They are glycerophospholipids that play a critical role in the function of the brain, heart, lungs, kidneys, and eyes.5,6 The primary species of plasmalogens that occur in the human body are plasmalogen ethanolamines (PlsEtn).7 In fact, greater than 50% of the ethanolamine phospholipids in the brain are PlsEtn.7
Aging is not a friend to phospholipid concentrations. Plasmalogen levels in the brain increase up to approximately 30 to 40 years of age.8 Levels then undergo a significant drop by the time an individual is about 70 years old.8 This corresponds to the time of life when Alzheimer’s disease incidence rises exponentially.9 Brain PlsEtn levels are lower in AD patients compared with age-matched controls,10-12 and low brain levels are associated with low serum concentrations.11 Research indicates that plasmalogen levels decline before the development of Alzheimer’s disease and dementia. For example, a study published in the Journal of Lipid Research found that circulating PlsEtn levels were dramatically decreased in serum from more than 400 clinically demented patients with dementia of the Alzheimer’s type at all stages of the disease.13 Additionally, the extent of the decline was associated with dementia severity. This study also determined that serum PlsEtn concentrations declined years before clinical symptoms developed. Other studies have shown that serum and brain plasmalogen deficiencies are closely linked to the progression of age-related neurodegenerative diseases such as AD and Parkinson’s Disease.5 13,14
Low plasmalogen levels are also associated with worse cognition in patients with AD. Wood and colleagues found that in 40 AD patients with lower plasmalogen levels (<or= 75% of that of age-matched controls at baseline) Alzheimer Disease Assessment Scale-Cognitive (ADAS-Cog) scores increased significantly.15 In participants with normal serum plasmalogen concentrations at baseline (> 75%) there were no declines in cognitive scores.

Plasmalogens and Beta Amyloid
  The link between plasmalogen deficits and the development of β-amyloid (Aβ) plaques provides further evidence that low plasmalogens contribute to AD and dementia. Aβ deposition is a hallmark of AD. Plasmalogens act upstream of Aβ formation to stop the deposition of these damaging plaques.7 There is an association between lower serum PlsEtn and the buildup of Aβ plaques in the central nervous system (CNS).13The timing of the decrease in serum PlsEtn coincides with the deposition of Aβ in humans.13 Other evidence indicates that declining plasmalogen levels are implicated in the accumulation of Aβ plaques, which may play a role in AD pathology.16
Studies using human AD postmortem brains suggest optimal plasmalogen concentrations lead to a decrease in the activity of γ-secretase, an enzyme that catalyzes the production of Aβ.16 It becomes a viscous circle, where Aβ reduces plasmalogen levels, which in turn directly elevate γ-secretase activity, resulting in even greater buildup of Aβ plaques.16

APOE and Plasmalogens
  Apolipoprotein E (APOE) is the most abundant lipoprotein in the brain.17 There are three common genetic variants (ɛ2, ɛ3, ɛ4) resulting in 6 possible combinations.  Typically, ɛ2ɛ3 is associated with lower risk (3%), ɛ3ɛ3 with average/low risk (18%) and ɛ3ɛ4 and ɛ4ɛ4 with higher risk of AD (up to 70%).  The majority of the population is ɛ3ɛ3. The APOE epsilon 4 allele is the primary genetic risk factor for AD.18 Low PlsEtn levels may determine the effects of APOE on AD and dementia. Dr. Goodenowe, a pioneer in the plasmalogen research field, and his colleagues conducted a study in 1,205 elderly individuals to investigate the relationship between APOE genotype and serum PlsEtn on cognition and dementia.19 The scientists found that the ability of APOE to adversely affect cognition and the prevalence of dementia was dependent upon the plasmalogen status of the subjects. When concentrations of the PlsEtn Biosynthesis Value (PBV, a combination of three important PlsEtn species) were higher, the probability of dementia was close to zero, regardless of the APOE genotype. Even in elderly subjects who had an increased risk of dementia, a higher PBV index correlated with a close to zero probability of dementia, regardless of age. These results provide evidence that PlsEtn levels can protect against dementia despite the existence of significant risk factors. The study authors wrote that the prevalence of dementia “could be reduced to at least that of the ɛ2ɛ3 genotype. This would result in an overall reduction in AD cases by 75% or more.”
The connection between APOE and PlsEtn involves cholesterol homeostasis. Cholesterol dysregulation is linked to cognitive impairment and AD. For example, in human post-mortem brain samples, higher concentrations of free cholesterol correlated with decreased cognition.20 The fact that both APOE and PlsEtn play a role in cholesterol homeostasis may explain the mechanism by which PlsEtn can reduce the APOE-mediated AD risk.

Multiple Sclerosis, Autism, and Plasmalogens
  The relationship between multiple sclerosis, autism, and plasmalogens is less straightforward. Multiple sclerosis (MS) and autism are caused by an underlying, pre-existing mitochondrial insufficiency in neuronal support cells, the glia. Due to overall changes in diet and lifestyle, mitochondrial insufficiency is increasing in our society. This increase is one of the primary reasons why the incidence of MS and autism have increased. As an inflammatory response to mitochondrial insufficiency, the body responds by activating microglia.21 These microglia target damaged cells by exporting glutamate, which in high levels is a mitochondrial toxin. Weak or damaged cells die, while healthy surrounding cells survive. However in MS and autism, the surrounding “healthy” cells are characterized by weak mitochondria and are not optimally healthy.22,23 This leads to the spread of inflammation, which in turn damages the healthy cells and further exacerbates an inflammatory response.
In events leading up to MS and autism, mitochondrial insufficiency results in the fatty acids that are supposed to be metabolized by the mitochondria being metabolized by the peroxisome, a tiny organelle located in the cytoplasm of most cells that is involved in the synthesis of plasmalogens. This results in higher levels of plasmalogens, very long chain fatty acids, elevated cholesterol, and higher triglycerides.24
However, the damaged glial cells at the MS lesion in the brain need to be repaired. To accomplish this, the local requirement for plasmalogens is much greater compared with the small increase caused by the mitochondrial insufficiency.25 Plasmalogens are needed so that the surrounding glial cells can replenish the white matter in the healthy cells at the rate that the inflammation damages it. This leads to a significantly faster glial cell recovery rate, which in turn results in a healthy inflammatory response and the inhibition of white matter loss caused by inflammation. Once a practitioner determines the rate of inflammation and mitochondrial stress through testing of plasmalogens and other biochemical indicators, supplementation can be used to deliver and keep in reserve excess glial plasmalogen building material.
In multiple sclerosis, the immune system targets myelin, the protective coating of nerve fibers. Human research indicates myelin contains certain species of ethanolamine plasmalogens.26 Furthermore, supplementing with a specific plasmalogen precursor completely prevented demyelination in animal models of multiple sclerosis.27 Autism is also associated with impaired peroxisome function and plasmalogen deficits in plasma and red blood cells.28-30

A New Test for Detecting Plasmalogens and Other Biochemical Indicators
  In clinical practice, my motto has always been “test, don’t guess.” The same is true with plasmalogens and other biochemical risk factors for conditions like Alzheimer’s, MS, and autism. A new blood test ( can detect plasmalogen deficiencies as well as measurements of other important biomarkers. For example, in addition to plasmalogens, the blood scan report identifies levels of anti-inflammatory gastrointestinal tract acids (GTAs). Evidence in the medical literature supports a role of GTA deficiencies in the progression of MS.25 GTAs may also predict the risk of colorectal cancer.31 Approximately 90% of all CRC cases occur in persons with GTA levels below the 10th percentile.31

The Most Effective Way To Replenish Plasmalogen Levels
  After testing, the next step is to restore plasmalogen levels or to deliver and keep in reserve excess glial plasmalogen building material. Plasmalogen replenishment in both preclinical and clinical studies blocked the development and/or reduced the progression of neurodegenerative disorders, atherosclerosis, insulin resistance, and hepatosteatosis.6 The challenge is that dietary plasmalogens are degraded by stomach acids, resulting in minimal bioavailability from food sources. Therefore, the most effective way to restore plasmalogen levels is through supplementation with 1-O-alkyl-2-acyl glycerols with DHA at the 2-acyl position. 1-O-alkyl-2-acyl glycerols are orally bioavailable. A 10 mg/kg dose leads to a 2-fold increase and a 50 mg/kg dose to an almost 4-fold increase in blood DHA-plasmalogen concentrations. This type of plasmalogen supplement suppressed the ability of cholesterol to increase Aβ1-42 and also dose dependently decreased levels of Aβ1-42 by increasing the activity of the α-secretase pathway, which is protective against amyloid plaque formation.27 Conversely, stearic, oleic, and linoleic, three other plasmalogen precursors that exhibited other side chains, had no effect.
Extensive peer-reviewed publications have found 1-O-alkyl-2-acyl glycerol oils are a highly effective natural means of resolving plasmalogen deficiencies and elevating plasmalogens to protective levels. 1-O-alkyl-2-acyl glycerol oils work with the body’s natural biochemical pathways in the liver and gut, which significantly elevates blood plasmalogen levels.32 In the gut, they release a plasmalogen precursor. This plasmalogen precursor retains its DHA sn-2 fatty acid, which allows it to be absorbed into the circulation, where it is converted to the target plasmalogen.32In a mouse model of Parkinson’s disease, 1-O-alkyl-2-acyl glycerols blocked neurodegeneration and may have played a role in remyelination.27,33 Decreased myelination is implicated in AD and MS pathology. Furthermore, plasmalogens serve as myelin markers, which decline in AD.34
In aging and disease, peroxisomes lose their ability to produce optimal levels of plasmalogens and DHA. Supplementation with 1-O-alkyl-2-acyl glycerols bypass peroxisomal biosynthetic pathways,27,35,36 thereby restoring or enhancing DHA and plasmalogen levels.27 This is important because data indicate DHA-PlsEtn levels drop according to the severity of dementia,34 and subjects with low, moderate, and severe dementia have progressively lower concentrations of DHA-PlsEtn.27 As phospholipid-linked DHA, 1-O-alkyl-2-acyl glycerols oils contain an abundant amount of plasmalogens and have profound effects on cognition.37 Conversely, triglyceride-linked DHA has only a miniscule effect.37
Alkylglycerols have an established safety profile and have been administered to humans at large doses for long periods. For example, Das and colleagues gave alkylglycerols to genetically compromised infants for up to 4 years with no adverse reactions.38 Recently, 1-O-alkyl-2-acyl glycerol oils with either DHA (ProdromeNeuro) or oleic acid (ProdromeGlia) at the 2-acyl position have become commercially available. 1-O-alkyl-2-acyl glycerol oils with oleic acid provide excess glial plasmalogen building material needed for optimal glial cell recovery rate, leading to a healthy inflammatory response and suppression of white matter loss.

  Plasmalogens play a critical role in brain health. However, their levels decline during aging and various diseases such as Alzheimer’s and dementia are characterized by low plasmalogen levels. A great deal of evidence points to the involvement of low levels of plasmalogens in AD and dementia and research has shown that plasmalogen levels decline before the development of these disorders. Imbalanced plasmalogen levels also are involved in MS and autism. A new blood test can now measure plasmalogen levels as well as concentrations of other biochemical measurements of neurological disorders. Based on the results of the test, 1-O-alkyl-2-acyl glycerols oils can be used as a highly effective and scientifically supported means to raise  plasmalogen levels.




  1. Canadian study of health and aging: study methods and prevalence of dementia. Cmaj. 1994;150(6):899-913.
  2. Breitner JC. Dementia–epidemiological considerations, nomenclature, and a tacit consensus definition. J Geriatr Psychiatry Neurol. 2006;19(3):129-136.
  3. Khachaturian AS, Corcoran CD, Mayer LS, Zandi PP, Breitner JC. Apolipoprotein E epsilon4 count affects age at onset of Alzheimer disease, but not lifetime susceptibility: The Cache County Study. Arch Gen Psychiatry. 2004;61(5):518-524.
  4. Dilokthornsakul P, Valuck RJ, Nair KV, Corboy JR, Allen RR, Campbell JD. Multiple sclerosis prevalence in the United States commercially insured population. Neurology. 2016;86(11):1014-1021.
  5. Bennett SA, Valenzuela N, Xu H, Franko B, Fai S, Figeys D. Using neurolipidomics to identify phospholipid mediators of synaptic (dys)function in Alzheimer’s Disease. Front Physiol. 2013;4:168.
  6. Paul S, Lancaster GI, Meikle PJ. Plasmalogens: A potential therapeutic target for neurodegenerative and cardiometabolic disease. Prog Lipid Res. 2019;74:186-195.
  7. Senanayake V, Goodenowe DB. Plasmalogen deficiency and neuropathology in Alzheimer’s disease: Causation or coincidence? Alzheimers Dement (N Y). 2019;5:524-532.
  8. Rouser G, Yamamoto A. Curvilinear regression course of human brain lipid composition changes with age. Lipids. 1968;3(3):284-287.
  9. Hugo J, Ganguli M. Dementia and cognitive impairment: epidemiology, diagnosis, and treatment. Clin Geriatr Med. 2014;30(3):421-442.
  10. Ginsberg L, Rafique S, Xuereb JH, Rapoport SI, Gershfeld NL. Disease and anatomic specificity of ethanolamine plasmalogen deficiency in Alzheimer’s disease brain. Brain Res. 1995;698(1-2):223-226.
  11. Guan Z, Wang Y, Cairns NJ, Lantos PL, Dallner G, Sindelar PJ. Decrease and structural modifications of phosphatidylethanolamine plasmalogen in the brain with Alzheimer disease. J Neuropathol Exp Neurol. 1999;58(7):740-747.
  12. Farooqui AA, Rapoport SI, Horrocks LA. Membrane phospholipid alterations in Alzheimer’s disease: deficiency of ethanolamine plasmalogens. Neurochem Res. 1997;22(4):523-527.
  13. Goodenowe DB, Cook LL, Liu J, et al. Peripheral ethanolamine plasmalogen deficiency: a logical causative factor in Alzheimer’s disease and dementia. J Lipid Res. 2007;48(11):2485-2498.
  14. Brites P, Waterham HR, Wanders RJ. Functions and biosynthesis of plasmalogens in health and disease. Biochim Biophys Acta. 2004;1636(2-3):219-231.
  15. Wood PL, Mankidy R, Ritchie S, et al. Circulating plasmalogen levels and Alzheimer Disease Assessment Scale-Cognitive scores in Alzheimer patients. J Psychiatry Neurosci. 2010;35(1):59-62.
  16. Rothhaar TL, Grösgen S, Haupenthal VJ, et al. Plasmalogens inhibit APP processing by directly affecting γ-secretase activity in Alzheimer’s disease. ScientificWorldJournal. 2012;2012:141240.
  17. Pitas RE, Boyles JK, Lee SH, Hui D, Weisgraber KH. Lipoproteins and their receptors in the central nervous system. Characterization of the lipoproteins in cerebrospinal fluid and identification of apolipoprotein B,E(LDL) receptors in the brain. J Biol Chem. 1987;262(29):14352-14360.
  18. Corder EH, Saunders AM, Strittmatter WJ, et al. Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer’s disease in late onset families. Science. 1993;261(5123):921-923.
  19. Goodenowe DB, Senanayake V. Relation of Serum Plasmalogens and APOE Genotype to Cognition and Dementia in Older Persons in a Cross-Sectional Study. Brain Sci. 2019;9(4).
  20. Cutler RG, Kelly J, Storie K, et al. Involvement of oxidative stress-induced abnormalities in ceramide and cholesterol metabolism in brain aging and Alzheimer’s disease. Proc Natl Acad Sci U S A. 2004;101(7):2070-2075.
  21. Banati RB, Egensperger R, Maassen A, Hager G, Kreutzberg GW, Graeber MB. Mitochondria in activated microglia in vitro. J Neurocytol. 2004;33(5):535-541.
  22. Varhaug KN, Vedeler CA, Tzoulis C, Bindoff LA. [Multiple sclerosis – a mitochondria-mediated disease?]. Tidsskr Nor Laegeforen. 2017;137(4):284-287.
  23. Maes M, Anderson G, Betancort Medina SR, Seo M, Ojala JO. Integrating Autism Spectrum Disorder Pathophysiology: Mitochondria, Vitamin A, CD38, Oxytocin, Serotonin and Melatonergic Alterations in the Placenta and Gut. Curr Pharm Des. 2019;25(41):4405-4420.
  24. Salemi G, Gueli MC, Vitale F, et al. Blood lipids, homocysteine, stress factors, and vitamins in clinically stable multiple sclerosis patients. Lipids Health Dis. 2010;9:19.
  25. Senanayake VK, Jin W, Mochizuki A, Chitou B, Goodenowe DB. Metabolic dysfunctions in multiple sclerosis: implications as to causation, early detection, and treatment, a case control study. BMC Neurol. 2015;15:154.
  26. Boggs JM, Stamp D, Moscarello MA. Comparison of two molecular species of ethanolamine plasmalogen in multiple sclerosis and normal myelin. Neurochem Res. 1982;7(8):953-964.
  27. Wood PL KM, Mankidy R, Smith T, Goodenowe DB. Plasmalogen deficit: a new and testable hypothesis for the etiology of Alzheimer’s disease. . London, UK: InTech2011.
  28. Berger J, Dorninger F, Forss-Petter S, Kunze M. Peroxisomes in brain development and function. Biochim Biophys Acta. 2016;1863(5):934-955.
  29. Wiest MM, German JB, Harvey DJ, Watkins SM, Hertz-Picciotto I. Plasma fatty acid profiles in autism: a case-control study. Prostaglandins Leukot Essent Fatty Acids. 2009;80(4):221-227.
  30. Bell JG, MacKinlay EE, Dick JR, MacDonald DJ, Boyle RM, Glen AC. Essential fatty acids and phospholipase A2 in autistic spectrum disorders. Prostaglandins Leukot Essent Fatty Acids. 2004;71(4):201-204.
  31. Ritchie SA, Tonita J, Alvi R, et al. Low-serum GTA-446 anti-inflammatory fatty acid levels as a new risk factor for colon cancer. Int J Cancer. 2013;132(2):355-362.
  32. Khan MA WP, Goodenowe D, Inventor. Methods for the synthesis of plasmalogens and plasmalogen derivatives and therapeutic uses thereof. US patent US 9,169,280 B2 October 27, 2015.
  33. Miville-Godbout E, Bourque M, Morissette M, et al. Plasmalogen Augmentation Reverses Striatal Dopamine Loss in MPTP Mice. PLoS One. 2016;11(3):e0151020.
  34. Han X, Holtzman DM, McKeel DW, Jr. Plasmalogen deficiency in early Alzheimer’s disease subjects and in animal models: molecular characterization using electrospray ionization mass spectrometry. J Neurochem. 2001;77(4):1168-1180.
  35. Martínez M. Severe deficiency of docosahexaenoic acid in peroxisomal disorders: a defect of delta 4 desaturation? Neurology. 1990;40(8):1292-1298.
  36. Zoeller RA, Raetz CR. Isolation of animal cell mutants deficient in plasmalogen biosynthesis and peroxisome assembly. Proc Natl Acad Sci U S A. 1986;83(14):5170-5174.
  37. Hiratsuka S, Koizumi K, Ooba T, Yokogoshi H. Effects of dietary docosahexaenoic acid connecting phospholipids on the learning ability and fatty acid composition of the brain. J Nutr Sci Vitaminol (Tokyo). 2009;55(4):374-380.
  38. Das AK, Holmes RD, Wilson GN, Hajra AK. Dietary ether lipid incorporation into tissue plasmalogens of humans and rodents. Lipids. 1992;27(6):401-405.


Weight1 lbs
Dimensions2 × 2 × 2 in
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