Researchers from Texas A&M University’s College of Agricultural and Biomedical Sciences discovered that cholesterol significantly boosts the toxicity of a peptide linked to the development of Alzheimer’s disease.
The College of Agriculture and Biological Sciences at Texas A&M University researchers found that cholesterol dramatically increases the toxicity of a peptide connected to the progression of Alzheimer’s disease.
Dmitry Kurouski, PhD, and research assistants Kiryl Zhaliazka and Mikhail Matyeyenka’s study, “Lipids uniquely alter the secondary structure and toxicity of amyloid beta 1-42 aggregates,” was made possible by a $1.5 million Maximizing Investigators’ Research Award from the National Institutes of Health. The publication of the Federation of European Biochemical Societies, FEBS Journal, published it.
“The study discovered that some lipids can increase the toxicity of amyloid beta peptides, which are known to have a role in the development of Alzheimer’s disease,” said Kurouski, an assistant professor and the study’s principal investigator from Bryan-College Station. We specifically found that the interaction of amyloid beta with lipids can develop oligomers, which are tiny, hazardous groupings.
The study also demonstrated that these lipids can change the primary shape, or secondary structure, of amyloid beta peptides, which can increase their toxicity even further. The processes underlying the harmful consequences of amyloid beta on the brain are now better understood, according to Kurouski. According to him, the study’s findings demonstrate a clear link between Alzheimer’s disease and the alteration of the lipid content of neuronal membranes, which is in turn influenced by a person’s diet.
The brain shrinks as a result of Alzheimer’s disease, and eventually, brain cells pass away. A steady decline in memory, reasoning, conduct, and social skills that impairs a person’s ability to carry out daily tasks is the most typical cause of dementia. Protein fragments known as amyloid beta that accumulate in the gaps between nerve cells are what give Alzheimer’s disease its characteristic look. These protein fragments are capable of forming amyloid plaques, which are thought to play a role in the development of senility.
Although the exact causes of Alzheimer’s disease are not entirely understood, there is evidence to support Kurouski’s assertion that the accumulation of amyloid beta peptides in the brain contributes to the progression of the illness. It is specifically believed that the formation of amyloid beta plaques can impair neuronal connection and ultimately result in cell death.
According to him, the connection between amyloid beta plaques and Alzheimer’s disease is complicated and may also be influenced by other elements, including inflammation and the buildup of the protein tau. According to Kurouski, lipids in the brain are known to interact with amyloid peptides, particularly amyloid beta. “These interactions may contribute to the pathophysiology of Alzheimer’s disease and the development of amyloid plaques.”
The study discovered that the oligomers generated in the presence of lipids were more harmful than other forms of amyloid beta, even though not all amyloid peptides necessarily interact with lipids in the brain. About the negative consequences of amyloid beta in Alzheimer’s disease, this shows that the interaction may be particularly significant, the researcher added.
What happens to the brain in the Alzheimer’s disease?
The brain shrinks as a result of Alzheimer’s disease, and eventually, brain cells pass away.