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Published on: May 22, 2018
Phosphatidylserine and phosphatidylcholine-containing liposomes inhibit amyloid beta and interferon-gamma-induced
Sadayuki Hashioka1, Youn-Hee Han, Shunsuke Fujii
1Department of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. hashioka@interchange.ubc.ca
Abstract:
There is increasing evidence that microglial activation is one of the major pathogenic factors for Alzheimer's disease (AD) and the inhibition of the inflammatory activation of the microglia thus appears to be neuroprotective and a potentially useful treatment for AD. Phospholipids such as phosphatidylserine (PS) and phosphatidylcholine (PC) have been reported to modulate the immune function of phagocytes. In addition, PS has been reported to be a nootropics that can be used as nonprescription memory or cognitive enhancers. We therefore evaluated the effects of liposomes, which comprise both PS and PC (PS/PC liposomes), on the microglial production of tumor necrosis factor-alpha (TNF-alpha), nitric oxide (NO), and superoxide (*O(2)-) induced by amyloid beta (Abeta) and interferon-gamma (IFN-gamma). Pretreatment of microglia with PS/PC liposomes considerably inhibited the TNF-alpha, NO and *O(2)- production induced by Abeta/IFN-gamma. These results suggest that PS/PC liposomes have both neuroprotective and antioxidative properties through the inhibition of microglial activation, thus supporting the nootropic and antidementia effect of PS.
Insights
Phosphatidylserine and phosphatidylcholine liposomes reduce microglial activation, a key factor in Alzheimer's disease (AD). This inhibition of inflammatory responses suggests neuroprotective and cognitive-enhancing benefits for AD treatment.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Microglial activation is a significant factor in Alzheimer's disease (AD) pathogenesis.
- Inhibiting microglial inflammatory responses offers potential neuroprotection and AD treatment strategies.
- Phospholipids like phosphatidylserine (PS) and phosphatidylcholine (PC) modulate immune cell function.
Purpose of the Study:
- To investigate the effects of PS/PC liposomes on microglial activation.
- To assess the impact of PS/PC liposomes on the production of inflammatory mediators by microglia.
Main Methods:
- Microglial cells were pretreated with PS/PC liposomes.
- Microglial production of tumor necrosis factor-alpha (TNF-alpha), nitric oxide (NO), and superoxide (*O(2)-) was induced by amyloid beta (Abeta) and interferon-gamma (IFN-gamma).
- The levels of TNF-alpha, NO, and *O(2)- were measured post-treatment.
Main Results:
- PS/PC liposomes significantly inhibited Abeta/IFN-gamma-induced TNF-alpha production.
- PS/PC liposomes considerably reduced Abeta/IFN-gamma-induced NO production.
- PS/PC liposomes substantially decreased Abeta/IFN-gamma-induced *O(2)- production.
Conclusions:
- PS/PC liposomes demonstrate neuroprotective and antioxidative properties by inhibiting microglial activation.
- These findings support the nootropic and antidementia effects of phosphatidylserine.
- PS/PC liposomes represent a promising therapeutic approach for Alzheimer's disease.
