A new study sheds light on the potential mechanism linking a diet high in saturated fat to Alzheimer’s disease. Researchers have identified specific changes in small RNA molecules, called microRNAs, that act as markers and regulators of disease, shedding light on how dietary habits can influence the onset of neurodegenerative diseases. The results were published in the journal Nutrients.
“The results of this study constitute an advance in our understanding of this disease and could explain the relationship between obesity, type 2 diabetes and the onset of Alzheimer’s disease. The results also offer new targets for possible prevention and treatment of the disease,” said researcher Mònica Bulló.
Alzheimer’s disease is a progressive neurodegenerative disease characterized by the progressive loss of cognitive functions, including memory, thinking and reasoning. It is the most common cause of dementia in older people. The disease usually begins with mild memory loss, but can progress to serious problems with communication, behavior and the ability to carry out daily activities.
The main pathological features of Alzheimer’s disease include the accumulation of β-amyloid plaques and tau protein tangles in the brain, which disrupt neuronal function and lead to cell death. These changes are accompanied by inflammation and a reduction in brain volume, further contributing to cognitive decline.
Researchers conducted this new study to investigate the underlying mechanisms that link dietary habits, particularly a diet high in saturated fat, to the development of Alzheimer’s disease. Previous studies have established that metabolic conditions such as obesity and type 2 diabetes are important risk factors for Alzheimer’s disease, with these conditions often preceding or exacerbating the onset of the disease.
However, the exact biological pathways linking these metabolic disorders to Alzheimer’s disease were not well understood. Focusing on the role of microRNAs, small RNA molecules that regulate gene expression, researchers sought to uncover how diet-induced metabolic changes might influence brain health and accelerate neurodegeneration.
The researchers were particularly interested in microRNAs linked to insulin regulation and Alzheimer’s pathology. Insulin resistance, a common feature of obesity and type 2 diabetes, has been linked to the development of Alzheimer’s disease. By studying changes in microRNA levels in the blood and brain tissue of mice on a high-fat diet, researchers hoped to identify specific molecular markers that could explain the link between a high-fat diet and Alzheimer’s disease. .
The study was conducted using mouse models genetically predisposed to developing Alzheimer’s disease in adulthood. The researchers compared these mice to healthy wild mice, with the two groups divided into two diets: one with conventional food and the other with a diet high in saturated fat. The high-fat diet, rich in palmitic acid from hydrogenated coconut oil, accounted for 60% of the mice’s daily intake.
The mice were monitored for six months, during which their body weight, glucose tolerance and insulin response were measured. Blood and brain tissue samples were collected at the end of the study to analyze the expression of 15 specific miRNAs. These miRNAs were chosen based on their known roles in insulin regulation and neurodegenerative processes.
The researchers observed that mice on a high-fat diet showed marked metabolic deterioration, including significant weight gain and impaired glucose and insulin responses. These metabolic changes are similar to those seen in conditions such as obesity and type 2 diabetes, both of which are known risk factors for Alzheimer’s disease.
One of the key findings was the change in levels of specific microRNAs in the blood and brain tissue of mice. The study identified significant changes in the expression of 15 insulin-related microRNAs. Notably, miR-19a-3p was consistently upregulated in the blood, cortex, and hippocampus of mice fed a high-fat diet. This consistent upregulation suggests that miR-19a-3p may play a central role in the link between peripheral metabolic disturbances and central neurodegenerative processes.
The researchers also found that the modified microRNAs were associated with key pathological processes in Alzheimer’s disease. These include the accumulation of β-amyloid plaques, excess tau protein production, and increased brain inflammation.
For example, miR-29c-3p, another microRNA upregulated in the brain and blood of mice fed a high-fat diet, is known to downregulate β-secretase (BACE1), an enzyme involved in the production of β-amyloid. plates. The upregulation of miR-29c-3p could be a counter-regulatory response to the harmful effects of the high-fat diet, aiming to attenuate the formation of these plaques.
The study highlighted the potential of microRNAs as biomarkers and therapeutic targets. The consistent changes in specific microRNAs in different tissues suggest that they could serve as early indicators of Alzheimer’s disease-related changes induced by dietary factors. This opens the possibility of developing non-invasive diagnostic tools based on blood tests to detect the first molecular signs of Alzheimer’s disease. Targeting these microRNAs through dietary interventions or pharmacological approaches could offer new strategies to prevent or slow the progression of Alzheimer’s disease.
The study represents a significant advance in understanding the influence of dietary habits on the risk of Alzheimer’s disease, but the translation of these results to humans requires additional studies. Clinical trials are needed to confirm the role of these microRNAs in Alzheimer’s disease in human populations and to test possible dietary interventions.
“In summary, our results support the role of specific insulin-related miRNAs in the development of specific features of Alzheimer’s disease and indicate the potential of a high-fat diet to aggravate neurodegenerative processes. Notably, miR-19a-3p and miR-29c-3p showed similar changes in peripheral and central levels after high-fat food consumption, suggesting their potential role not only as therapeutic targets for Alzheimer’s disease, but also as peripheral biomarkers of disease. » concluded the researchers.
The study titled “Effects of a high-fat diet on insulin-related miRNAs in plasma and brain tissues in APPSwe/PS1dE9 and Wild-Type C57BL/6J mice” was authored by Melina Rojas-Criollo , Nil Novau-Ferré, Laia Gutierrez. -Tordera, Miren Ettcheto, Jaume Folch, Christopher Papandreou, Laura Panisello, Amanda Cano, Hamza Mostafa, Javier Mateu-Fabregat, Marina Carrasco, Antoni Camins and Mònica Bulló.
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