Researchers from the Texas A&M College of Agriculture and Life Sciences found that cholesterol significantly increases the toxicity of a peptide associated with the progression of Alzheimer’s disease. The study, “Lipids uniquely alter the secondary structure and toxicity of amyloid beta 1-42 aggregates,” was supported by a $1.5 million Maximizing Investigators Research Award to Dmitry Kurovsky, PhD, and research assistants Kirill Zhaliazka and Mikhail Matyenka. National Institute of Health. It was published in FEBS Journal – Journal of the Federation of European Biochemical Societies.
“The study found that certain lipids may increase the toxicity of amyloid beta peptides, which play a role in the development of Alzheimer’s disease,” said Kurowski, an assistant professor and primary investigator for the study at Bryan-College Station. “Specifically, we found that the interaction between amyloid beta and lipids can lead to the formation of small, toxic clusters called oligomers.”
Additionally, studies have shown that these lipids can alter the native shape, or secondary structure, of amyloid beta peptides, which may further increase their toxicity. “This provides new insight into the mechanisms behind the toxic effects of amyloid beta in the brain,” said Kurowski.
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They said the study results show a strong link between Alzheimer’s disease and changes in the lipid composition of neuronal membranes, which, in turn, can be affected by a person’s diet. Alzheimer’s disease causes the brain to shrink and brain cells eventually die.
It is the most common cause of dementia – a gradual decline in memory, thinking, behavior and social skills – affecting a person’s overall ability to function. Alzheimer’s is characterized by fragments of a protein called amyloid beta, which accumulate in the spaces between nerve cells. These protein fragments can clump together to form amyloid plaques, which is thought to be a factor in aging.
“Although the precise mechanisms underlying Alzheimer’s disease are not fully understood, there is evidence that a build-up of amyloid beta peptides in the brain plays a role in the development of the disease,” said Kurowski.
“Specifically, it is thought that the aggregation of amyloid beta in plaques may disrupt communication between neurons and eventually lead to cell death.” He added that the relationship between amyloid beta plaques and Alzheimer’s disease is complex, and other factors such as inflammation and the accumulation of another protein called tau are also thought to be involved.
“Amyloid peptides, including amyloid beta, are known to interact with lipids in the brain,” Kurowski said. “These interactions may play a role in the formation of amyloid plaques and in the pathophysiology of Alzheimer’s disease.” form of amyloid beta. “This suggests that the interaction may be particularly important with respect to the harmful effects of amyloid beta in Alzheimer’s disease,” he said.