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Fig. 3 | Lipids in Health and Disease

Fig. 3

From: Plasmalogens and Alzheimer’s disease: a review

Fig. 3

Proposed mechanistic association of ethanolamine plasmalogens deficiency and Alzheimer’s disease. Abbreviations: Aβ, β-amyloid; PlsEtns, ethanolamine plasmalogens; VLCFAs, very long chain fatty acids. PlsEtns have a close association with Alzheimer’s disease (AD). Decreased levels of PlsEtns have been commonly found in AD patients, and are correlated with cognition deficit and severity of disease, although it is not known whether it is the cause or the consequence of the disease. It has been suggested maybe it is both. A few possible mechanisms with regards to the decrease of PlsEtns in AD have been suggested: peroxisome dysfunction, oxidative stress, alterations in membrane lipid rafts and inflammatory responses. Decreased PlsEtns may further enhance oxidative damage and alter membrane properties in AD. This plus increased membrane free cholesterol associated with PlsEtns deficiency could increase the production of Aβ. Aβ and reactive oxygen species could further decrease PlsEtns level. PlsEtns are major lipids facilitating membrane fusion of synaptic vesicles associated with neurotransmitter release, thus loss of PlsEtns could potentially contribute to the synaptic dysfunction and neurotransmitter depletion in Alzheimer’s disease. The association of decreased level of PlsEtns and neuroinflammation may be related to antioxidant properties of plasmalogens that protect cells from oxidative stress. Neuroinflammation has been reported to be associated with Aβ accumulation

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