Electronegative very-low-density lipoprotein (VLDL) induces cognitive dysfunction and brain inflammation in mice as shown in several studies.
The world’s aging population is increasing rapidly, and the number of individuals with neurodegeneration is increasing as well. Many researchers are seeking to identify the novel pathogenic factors that induce neurodegeneration in people. Prevention is a key objective and a leading public goal.
Alzheimer’s disease (AD) and non-AD dementias are just several examples of neurodegenerative diseases that share similar symptoms, including the relentless progression of cognitive dysfunction, neuronal apoptosis, memory loss, and brain atrophy.
Scientists have previously identified some factors like oxidative stress, neuronal inflammation, and neurotransmitter deficiency. Therapies seek to prevent or delay the onset and progression of neurodegenerative diseases. The form the foundation of current treatment modalities, which primarily lesson symptoms temporarily.
However, much more is needed to actually stop the progression of neurodegeneration in order to improve functionality and quality of life. Therefore, it is critical that studies pinpoint the novel risk factors at play in neurodegeneration.
Two risk factors are dyslipidemia and metabolic syndrome (MetS) as they also play a part in cardiovascular diseases. One epidemiologic study found that AD is significantly more likely to develop in elderly patients with MetS than those without MetS. In addition, one 20 year study of middle aged people with higher blood lipid levels showed more cognitive decline than those with healthy lipid levels. Other studies have found that long-term, high fat diets cause cognitive dysfunction in rodents. Still, the role of blood lipid molecules in the central nervous system and cognitive function needs more investigation.
However, some elderly patients with hyperlipidemia do not experience cognitive dysfunction, which means that more research is necessary to comprehend the relationship between cognitive dysfunction and blood lipids.
Several studies have shown that VLDL is important for developing dyslipidemia. The overproduction of VLDL points directly to dyslipidemia in patients with MetS. Some of them have found that the most electronegative VLDL (V5) can produce endothelial cell apoptosis. The patients with MetS had a significantly higher percentage of V5 and plasma V5 concentration than did the healthy control subjects. In addition, when mice were continually exposed to VLDL obtained from patients with MetS, researchers found it produced cardiomyocyte apoptosis and left atrial enlargement. This result has produced greater insight into cardiovascular disease induced by VLDL.
The scientists who conducted this study suggested that higher levels of electronegative VLDL in patients with MetS contributed to damaged cardiomyocytes that compromised heart function. They believe that the role is determined by electronegativity rather than cardio cytotoxicity.
They conducted another study to determine the relationship between VLDL electronegativity and cognitive dysfunction. Specifically, they wanted to investigate the pathologic effects of electronegative VLDL on cognitive function and the central nervous system. They did this by injecting VLDL preparations with varying levels of electronegativity into mice, and studied the long-term effects on behavior and the brain. They suggested that this long-term exposure to VLDL with high levels of electronegativity produced deterioration of neuronal function.
What this means
The new data show the association between cognitive function and blood lipids.
The researchers found that the long-term injection of metVLDL in mice produced significantly increased cognitive dysfunction versus mice that did not receive the injections. They noted that the injection of human VLDL may have induced a small immunologic reaction in the mouse model. However, the data also showed direct in vivo evidence that VLDL with higher levels of electronegativity exerted different effects on cognitive function. This is the first study to investigate how VLDL electronegativity impacts the central nervous system.
VLDL is the primary carrier of triglycerides in the blood. VLDL is composed of approximately 35% cholesterol, 35% phospholipids, and various apolipoproteins; it facilitates lipoprotein formation and function. Therefore, paying attention to cholesterol levels and eating healthy is an important habit to form.
Final thoughts
The scientists found that higher levels of electronegative VLDL in the blood produced systemic inflammation and neuronal inflammation in the brain, resulting in adverse effects on cognitive function. Science may now be able to develop ways of monitoring levels of electronegative VLDL and help patients manage those levels. The development may be an exciting pathway to new therapeutics for patients with neurodegenerative diseases. In the meantime, focus on healthy practices and eating a diet that helps reduce inflammation.
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