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Electronegative very-low-density lipoprotein induces brain inflammation and cognitive dysfunction in mice
Ying-Shao Lin1, Ching-Kuan Liu1,2,3, Hsiang-Chun Lee4,5
1Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University (KMU), 100 Shiquan 1st Rd, Sanmin Dist., Kaohsiung City, 807, Taiwan.
Scientific Reports
|March 17, 2021
Summary
Metabolic syndrome (MetS) patients have higher levels of harmful electronegative very-low-density lipoprotein (VLDL). This type of VLDL causes brain inflammation, neuronal loss, and cognitive dysfunction in mice, suggesting it as a therapeutic target.
Area of Science:
- Neuroscience
- Metabolic Disorders
- Lipid Metabolism
Background:
- Dyslipidemia is linked to cognitive dysfunction progression.
- Metabolic syndrome (MetS) patients exhibit elevated plasma electronegative very-low-density lipoprotein (VLDL) compared to healthy individuals.
- The specific impact of electronegative-VLDL on brain health and cognition is not well understood.
Purpose of the Study:
- To investigate the effects of electronegative-VLDL from MetS patients on cognitive function and brain pathology in a mouse model.
- To determine if electronegative-VLDL contributes to neuroinflammation and neuronal damage.
Main Methods:
- Very-low-density lipoprotein (VLDL) was isolated from healthy volunteers (nVLDL) and MetS patients (metVLDL).
- VLDL was administered intravenously to mice.
- Cognitive function was assessed using the Y maze test.
- Plasma and brain tissues were analyzed for neuronal loss, glial activation, and inflammatory markers (TNF-α, Aβ-42).
Main Results:
- Mice injected with metVLDL showed significant hippocampus CA3 neuronal cell loss and cognitive impairment.
- Mice injected with metVLDL exhibited increased plasma and brain levels of TNF-α and Aβ-42.
- metVLDL administration led to heightened glial cell activation in the medial prefrontal cortex (mPFC) and hippocampus.
- nVLDL administration resulted in only mild glial cell activation.
Conclusions:
- Long-term exposure to metVLDL induces elevated TNF-α, Aβ-42, and glial cell activation in the brain.
- These changes contribute to the progression of cognitive dysfunction.
- Electronegative-VLDL may represent a novel therapeutic target for cognitive dysfunction associated with metabolic disorders.
