Supporting Research of Plasmalogen

Anti-inflammatory and anti-amyloidogenic:

supporting research of plasmalogen

Paper published in 1999 found evidences linking decreased plasmalogen levels in brains with occurrences of Alzheimer’s disease. Levels of plasmalogen have been reported to be significantly reduced in the frontal cortex and hippocampus of the brain in affected patients (Guan Z et al., 1999).

supporting research of plasmalogen - decreased DHA

Paper published in 2007 showed that DHA-containing ethanolamine plasmalogen was detected in the serum of patients with Alzheimer’s disease. However, reduced levels of plasmalogen has been reported in the Alzheimer’s patients from Canada, USA. This research also included patients with Alzheimer’s disease from Osaka, Japan. This epoch-making paper proved that plasmalogen levels decreased in the serum of surviving patients with Alzheimer’s disease (Goodenowe DB et al., 2007).

Analysis of disease severity (ADAS-Cog) and serum DHA-plasmalogen levels in 256 participants with Alzheimer’s disease. X = predicted initiation of plasmalogen depletion. Values are expressed as means ± SEM (standard error of the mean). Clinical progression assumes 7.5 ADAS-Cog points per year. CN = cognitively normal with MMSE score ≥ 28. ADAS-Cog scores of low, moderate or severe cognitive impairment are 5 – 19, 20 – 39 and 40 – 70, respectively (Goodenowe DB et al., 2007).

High serum plasmalogen levels are shown to be protective against APOE risk factor for Alzheimer’s disease:

The probability of developing Alzheimer’s disease decreases with higher levels of serum plasmalogen in the body. At any particular serum plasmalogen level, a person who inherits one allele of APOEϵ3 and one allele of APOEϵ4 would have higher odds of developing Alzheimer’s disease as compared to another person with both alleles of APOEϵ3. A person inherited with one allele of APOEϵ2 and one allele of APOEϵ3 would have the lowest chance of developing underlying changes to the brain leading to Alzheimer’s disease.

Based on the chart on the left, it can be concluded that when the serum plasmalogen levels in the body are sufficiently higher, the probability of developing Alzheimer’s disease is close to zero regardless of genotype. On the other hand, impaired plasmalogen biosynthesis is linked to higher probability of Alzheimer’s disease with those having APOEϵ4 at the highest risk. In short, the association between plasmalogen levels and probability of Alzheimer’s disease appears to be altered by APOE allele status.

Measurement of blood plasmalogen levels as a biomarker for Alzheimer’s disease:

The development of a test method by the research team in Japan aims to measure the levels of plasmalogen in the blood, they observed decreased levels of plasmalogens in the erythrocytes of Alzheimer’s disease patients. In this test, relative composition of phospholipid classes was determined from each chromatographic area and the ratios of glycerophospholipids to sphingomyelin (SM) were calculated (Oma S et al., 2012).

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Previous studies found evidences of reduced plasmalogens in the brain of patients with Alzheimer’s disease (Ginsberg L et al., 1995; Guan Z et al., 1999). Epidemiological study also showed that plasmalogen was significantly lower in the serum of Alzheimer’s disease brain (Goodenowe DB et al., 2007). Conventionally, MMSE score is used in assessing the level of cognitive impairment in a patient with dementia of Alzheimer’s type. However, the drawback of this method as a form of assessment include the inspection of a person’s answers, the educational level of the individual and objective discretion of the clinician. To further enhance the sensitivity of the diagnosis, the research team from Japan chaired by Takehiko Fujino, Emeritus Professor of Kyushu University had developed a simple and accurate method of evaluating the risk of dementia by measuring blood plasmalogen levels. In this clinical research, alongside the assessment of cognitive functions using MMSE tests; clinicians also assessed the plasmalogens in red blood cells were measured using high performance liquid chromatography (HPLC) and the ratio of each phospholipid to sphingomyelin (SM) was derived.

Reduction in the ratio of ethanolamine plasmalogen (pl-PE), phosphatidylethanolamine (PE) and phosphatidylserine (PS) to SM was observed. It has been suggested that the reduction in pl-PE is caused by oxidative stress of amyloid β. This suggests viability of using the measurement of plasmalogens in red blood cells as a new biomarker for Alzheimer’s disease, complementing the result of conventional MMSE method in improving the accuracy of test results.

Dietary plasmalogens increase plasmalogen levels in red blood cells:

The effect of dietary plasmalogens (from chicken skin) on the replenishment of tissue plasmalogens in mammals was studied using rat models. Evidences showed that dietary plasmalogens increased the relative composition of plasmalogens of the red blood cell membranes and caused the decrease of plasma cholesterol and phospholipid as compared to control diet. No differences were detected between the levels of triacylglycerol, glucose, liver and renal functions, albumin in the plasma and body weight between the subjects from the plasmalogen diet and control diet. Thus, the consumption of dietary plasmalogens for 9 weeks seemingly causes no negative effect to the health of rats (Mawatari S et al., 2012).

Supporting Research of Plasmalogen - increase ethanolamine

Change in red blood cell phospholipids of rats after being given the dietary plasmalogens for 9 weeks. Abbreviation: PlsEtn = ethanolamine plasmalogen; PE: phosphatidylethanolamine; PlsCho = choline plasmalogen; PC = phosphatidylcholine; PS = phosphatidyl serine; PI = phosphatidyl inositol; SM = sphingomyelin (Mawatari S et al., 2012).

Changes in plasma cholesterol and phospholipids in rats after being given the dietary plasmalogens for 9 weeks. Abbreviation: chol = cholesterol; HDL = high density lipoprotein; LDL = low density lipoprotein; TG = triacylglycerol; P-lipid = phospholipid; Urea N = urea nitrogen; AST = aspartate aminotransferase; ALT = alanine aminotransferase (Mawatari S et al., 2012).