In a recent review published in Nutrients, researchers reviewed the existing data on the interactions between the gut microbiome, lipids, and Alzheimer’s disease (AD), providing valuable information to inform the prevention and management of AD.
survey: Lipids, gut microbiota and the complex relationship with Alzheimer’s disease: A narrative review. Image Credit: Atthapon Rakshaput/Shutterstock.com
Background
AD is a chronic neurological disease associated with aging. Modifiable risk factors can reduce Alzheimer’s disease morbidity and mortality. Aging causes gut dysbiosis, leading to an increase in pro-inflammatory bacteria and a decrease in anti-inflammatory bacteria, causing neuroinflammation and damage.
The gut-brain microbiota axis (GBMA) has a major impact on neurodegenerative diseases. High consumption of saturated and trans fats increases cortisol release, but low consumption of omega-3 polyunsaturated fatty acids (PUFA) is associated with neurological disorders.
About the review
In the current review, researchers described the interaction between the gut microbiome, dietary lipids, and Alzheimer’s disease.
The Web of Science, Scopus, Embase, Cochrane Central Register of Controlled Trials (CENTRAL) and Medical Literature Retrieval and Analysis Online (MEDLINE) databases were searched for relevant records published in English, Spanish or Portuguese. Papers not specifically related to Alzheimer’s disease were excluded.
Alzheimer’s disease and the gut microbiome
Gut microbiota can influence the development and progression of neurodegenerative diseases such as Alzheimer’s disease. The GBMA is a two-way communication channel between the digestive tract and the central nervous system (CNS) and may contribute to Alzheimer’s disease (AD) in imbalanced situations.
The CNS regulates gastrointestinal permeability, secretion, motility, and immunity through autonomic neural networks. Vagal circuits connect the GBMA to the tenth cranial nerve (vagus) via efferent and afferent pathways.
Breakdowns in this communication can affect the immune system’s ability to fight infections, avoid chronic inflammation, and keep the CNS healthy. Gut dysbiosis contributes to Alzheimer’s disease through pathways that promote amyloid plaque formation and neuroinflammation.
A healthy gut microbiota can influence behavior by creating monoamines and short-chain fatty acids (SCFAs), including butyrate, gamma-aminobutyric acid (GABA), serotonin, and dopamine, which improve cognition and memory. Understanding GBMA is critical to creating new treatment options for Alzheimer’s disease.
Dietary lipids and Alzheimer’s disease
Lipids are vital macromolecules in the human body, especially in the brain, with critical functions in cell membranes and signal transduction. Alterations in lipid metabolism contribute to Alzheimer’s disease because lipid oxidation occurs early in the disease. Increased amounts of free cholesterol and reduced sphingomyelin in the middle frontal gyrus of Alzheimer’s disease patients are associated with the membrane oxidative stress that drives the disease.
Inadequate availability of cholesterol to neurons can impair synaptic plasticity and neural signal transmission, leading to tau disease and neurodegeneration.
Specific lipids in the blood can affect BBB permeability, possibly altering the availability of fatty acids and other lipids in brain cells. Lipid microdomains, which are membrane structures composed of sphingolipids, cholesterol, and saturated and polyunsaturated fatty acids, play an important role in the pathology of Alzheimer’s disease, including the formation of amyloid beta (Aβ), and allow interactions between A, apolipoprotein (APOE), and tau proteins.
Saturated fat consumption is associated with systemic inflammation, as evidenced by increased oxidative stress, reactive oxygen species (ROS) levels, and proinflammatory cytokine production, exacerbating neurodegeneration in people with Alzheimer’s disease.
The gut microbiome and dietary lipids
Sphingolipids present in wheat, soy, eggs and dairy products are beneficial for gut health and play a crucial role in the composition and diversity of gut microbiota. On the contrary, high-fat foods can negatively affect the gut microbiota by promoting dysbiosis, affecting intestinal permeability and increasing the number of gram-negative bacteria that generate LPS. These lipids can also mimic LPS effects, causing pro-inflammatory processes and weakening of the mucus layer.
Dysbiosis is characterized by reduced Lactobacillus and Bacteroidetes abundance and increased Clostridium abundance. In addition, Alzheimer’s patients have decreased Bifidobacterium, Castellaniella, Rosuria, Erysipelotrichaceae, Lactobacillaceae, Monoglobusand tutzerella numbers.
Western diets high in saturated and trans fatty acids are associated with an increased risk of Alzheimer’s disease and hypercholesterolemia, possibly due to the accumulation of oxysterols in the brain.
PNMCs are necessary for brain growth and function in Alzheimer’s disease, and omega-3 supplements may slow progression.
Plant-based diets, on the other hand, such as the Mediterranean diet, are advocated as a worldwide healthy dietary pattern due to their anti-inflammatory qualities. These diets include vital functional nutrients that have antioxidant, anti-inflammatory and free radical-fighting properties that benefit gut and brain health.
Conclusions
Based on review findings, gut microbiota, lipids, and Alzheimer’s disease are linked, with dietary lipids potentially promoting AD pathogenesis. Fatty acids are critical for brain inflammation, synaptic plasticity and memory.
A healthy diet, such as Mediterranean meals rich in monounsaturated and polyunsaturated fats, can help reduce symptoms and improve gut health and blood-brain barrier function. Conversely, Western diets high in saturated and trans fats may accelerate the development of Alzheimer’s disease.
Further research is needed to understand the lipid composition of the brain, to discover lipid biomarkers, and to investigate dietary therapies that alter the composition of the gut microbiota.
