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Benefits of Plasmalogen

Introducing the four main benefits of plasmalogen.

Inhibition of Neuronal Cell Death by Plasmalogens

Plasmalogens have been found to inhibit neuronal cell death associated with Alzheimer's disease. Research in 1995 reported a decrease in plasmalogens in the brains of Alzheimer's patients (deceased). Subsequent studies by Dr. Takehiko Fujino's team at Kyushu University confirmed a significant decrease in plasmalogens in the blood of living patients as well. Supplementing these depleted plasmalogens could be key to improving dementia.

Plasmalogens derived from scallops have been clinically validated by Dr. Fujino's research team for their effectiveness in preventing and improving dementia.

[Research findings]

Observations of neuronal cell death in the hippocampus of Alzheimer's patients revealed a significant decrease in plasmalogens.

Using hippocampal primary cultures and cultured neurons from mice, we validated the effect of plasmalogens on serum starvation-induced neuronal cell death. The study results showed that administration of plasmalogens activated AKT and ERK1/2, leading to inhibition of Caspase-9 and Caspase-3 activation induced by serum starvation. Furthermore, the study confirmed that AKT and ERK1/2, as phospho-enzymes, activated survival signals for Bcl-2 and Bax in mitochondria.

To elucidate the signaling mechanism of plasmalogens, we investigated their presence in the cell membrane after plasmalogen intake and found that plasmalogens were present in concentrations nearly ten times higher post-intake. Lipid rafts, which contain not only cholesterol and sphingolipids but also G-protein coupled receptors (GPCRs), including TrkB receptors for brain-derived neurotrophic factor (BDNF), harbor numerous signaling molecules. Dr. Fujino's team confirmed that plasmalogen-induced activation of AKT and ERK occurs through orphan GPCRs expressed in cultured neurons.

Improvement of Learning and Memory

Plasmalogens have been confirmed to play a crucial role in enhancing and improving memory function.

[Research Findings]

Disruption of the expression of GNPAT, the synthetic enzyme of plasmalogens, by injecting a minute amount of sh-RNA Lentiviral Vector into both sides of the hippocampus in mice resulted in a reduction of plasmalogen content in the hippocampus. This interference affected hippocampus-dependent spatial cognitive learning in the Morris water maze test. Ultimately, it was demonstrated that plasmalogens promote learning and memory behaviors. These results indicate that plasmalogens activate cAMP CREB downstream of AKT or ERK in neurons, leading to increased expression of BDNF in the nucleus.

Additionally, lipid rafts, known to contain numerous TrkB receptors for BDNF, further suggest that plasmalogens facilitate learning and memory through lipid raft pathways.

Through this research, it has been confirmed that plasmalogens not only enhance learning ability but also hold potential as a novel substance for the treatment and prevention of cognitive disorders such as Alzheimer's disease.

The mechanism by which plasmalogen (Pls) inhibits glial cell activation (neuroinflammation) induced by LPS involves the suppression of endocytosis of LPS and its receptor, Toll-like receptor 4 (TLR4), which recognizes and activates LPS. It also inhibits the activation of NF-κB and Caspase-3. Additionally, it has been found that the expression of glyceronephosphate O-acyltransferase (GNPAT), a crucial enzyme for plasmalogen synthesis, is inhibited in an NF-κB-dependent manner (Figure 5).

Plasmalogen's Anti-Neuroinflammatory Action

The primary functions of plasmalogen are to suppress neuroinflammation and provide antioxidant protection, making it a crucial defense mechanism when cells are under oxidative stress.

[Research Findings]

Neuroinflammation refers to the condition in which inflammation in the brain is heightened due to the activation of glial cells, leading to a rapid increase in the production of cytokines and free radicals. This condition is observed in various neurodegenerative diseases such as Alzheimer's.

When the endotoxin LPS (lipopolysaccharide) is administered peripherally to adult mice, it induces neuroinflammation and accumulation of β-amyloid protein (Aβ) in the brain.

Using this neuroinflammation model, it was discovered that the simultaneous administration of plasmalogen (Pls) inhibits the activation of glial cells, the expression of cytokines such as IL-1β and TNF-α, and the accumulation of Aβ in the brain induced by LPS.

The mechanism by which plasmalogen (Pls) acts in the brain is still under investigation, particularly regarding its ability to cross the blood-brain barrier (BBB).

Recent studies have shown that a protein molecule called Mfsd2a, a member of the Major Facilitator Superfamily (MFS)*, functions as a transporter of glycerophospholipids in the brain's microvasculature. This discovery indicates that plasmalogen functions in the brain via this transport mechanism.

*Mfsd2a is a sodium-dependent lysophosphatidylcholine symporter that facilitates DHA absorption into the brain.

(Figure 5) The important expression of GNPAT as a synthetic enzyme for plasmalogens is inhibited in an NF-κB-dependent manner.

Benefits of Plasmalogen

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