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Plasmalogen Deficiency and Evaluation in Alzheimers, Dementia, Parkinosn’s Disease, Multiple Sclerosis, and Autism

One of the most common features discovered from research of neurodegenerative diseases such as Alzheimers, dementia, multiple sclerosis, and autism is the depletion of critical membrane lipids called plasmalogens. Plasmalogens are naturally occurring lipids incorporated within all cell membranes of our bodies, playing a particularly important role in the brain, heart, lungs, kidneys, and eyes. A significant body of research indicates that brain plasmalogen levels decline decades before the development of Alzheimer’s, dementia, and Parkinson’s. Deficiencies in both serum and brain plasmologens are also correlated with the progression of these age-related neurodegenerative diseases. Further, the observed depletion of plasmalogen in alzheimers, dementia, and Parkinson’s is believed to occur as a result of reduced biosynthesis associated with aging. 

Another root cause of deficient plasmologens arises from excess degradation of neural support cells following oxidative stress and inflammation as seen with multiple sclerosis and autism. A leading theory for development of Multiple Sclerosis (MS) and the onset of Autism link mitochondrial insufficiency within the neuronal support cells known as the glia. Environmental toxins, inflammation, stress, and food additives are some of the leading causes of mitochondrial insufficiency in genetically susceptible individuals. Mitochondrial insufficiency leads to higher levels of neurotoxic glutamate which causes inflammation in the surrounding neural support networks. Inflammation leads to further cellular damage invoking further inflammation. In the presence of excessive inflammation, normal production of plasmalogen is insufficient to maintain optimal health of the neural cells. Autism research has also been associated with plasmalogen deficiencies in both plasma and red blood cells.  

An increase in plasmologens can help rebalance the neural system reducing observed depletion, inflammation, mitochondrial deficiency, and restoring optimal myelin production. Plasmalogen levels can be replenished through oral supplementation with very specific phospholipids known to be highly absorbed and effective in restoring optimal neural inflammation and activity.

Prodrome labs now offer reliable measurements to evaluate an individual’s plasmalogen levels with a simple blood draw to be completed at the offices of EVND. With the observation that plasmalogen levels can be low or depleted with aging or as result of inflammation in the brain of select diseases, we are provided hope that we are both able to measure and provide therapy to restore plasmologens to optimal levels both slowing progression and improving function in Alzheimers, dementia, Parkinson’s disease, multiple sclerosis, and autism.