Simultaneous Intake of Chlorella and Ascidian Ethanolamine Plasmalogen Accelerates Activation of BDNF-TrkB-CREB Signaling in Rats.
Hideo TakekoshiMasaki FujishimaTaiki MiyazawaOhki HiguchiTakahiko FujikawaTeruo MiyazawaPublished in: Molecules (Basel, Switzerland) (2024)
Brain-derived neurotrophic factor (BDNF) plays an important role in neurogenesis, synaptic plasticity, and cognition. BDNF is a neurotrophin that binds to tropomyosin receptor kinase B (TrkB), a specific receptor on target cell surfaces; it acts on neuronal formation, development, growth, and repair via transcription factors, such as cAMP response element-binding protein (CREB), and it is involved in learning and memory. BDNF expression is decreased in patients with Alzheimer's disease (AD). Exercise and the intake of several different foods or ingredients can increase BDNF expression, as confirmed with lutein, xanthophylls (polar carotenoids), and ethanolamine plasmalogen (PlsEtn), which are present at high levels in the brain. This study examined the effects of combining lutein and PlsEtn using lutein-rich Chlorella and ascidian extracts containing high levels of PlsEtn bearing docosahexaenoic acid, which is abundant in the human brain, on the activation of the BDNF-TrkB-CREB signaling pathway in the hippocampus of Sprague-Dawley rats. Although activation of the BDNF-TrkB-CREB signaling pathway in the hippocampus was not observed in Chlorella or ascidian PlsEtn monotherapy, activation was observed with combination therapy at an equal dose. The results of this study suggest that the combination of Chlorella and ascidian PlsEtn may have a preventive effect against dementia, including AD.
Keyphrases
- binding protein
- combination therapy
- stress induced
- signaling pathway
- poor prognosis
- cerebral ischemia
- transcription factor
- cognitive impairment
- pi k akt
- epithelial mesenchymal transition
- clinical trial
- stem cells
- randomized controlled trial
- cystic fibrosis
- white matter
- weight gain
- single cell
- physical activity
- high intensity
- long non coding rna
- cell proliferation
- open label
- induced apoptosis
- oxidative stress
- escherichia coli
- cell therapy
- study protocol
- biofilm formation
- tyrosine kinase
- brain injury