Table 1.
Effects of metabolic disorders, diet, and gut microbiota on Alzheimer’s disease (AD).
| Harmful | Protective | |
|---|---|---|
| Metabolism | ||
| Obesity | Human: risk in midlife. Mice: memory loss, Aβ deposition and gliosis. |
|
| Diabetes | Human and mice: defects in insulin/IGF-1 pathway in brains. | |
| Dyslipidaemia | Human: risk in midlife. Mice: correlates with burden of Aβ pathology. |
|
| MAFLD | Human: impaired cognition. Mice: AD-like pathology. |
|
| Diet | ||
| Fat intake | Human: saturated fat. Mice: high-fat diet worsens severity in AD-mice. |
Human and mice: ω-3 PUFAs protect neurons, reduce inflammation and vascular damage. |
| Antioxidants | Human and mice: counteract ROS production, lipid peroxidation, DNA damage. | |
| Dietary patterns | Human: MeD. Human and mice: caloric restriction. |
|
| Microbiota | ||
| Composition | Opportunistic gram-negative bacteria | SCFA-producing bacteria. |
| Mechanisms | Endotoxin exposure, IEB permeability, gut inflammation. | SCFAs supply to gut and brain |
| Gut-brain axis | Aβ deposition in the gut of animal models. Bacterial amyloids may aid in cross-seeding. Gut-to-brain transport after prolonged time. |
|
| Gut microbiota-based Therapy | Improve metabolic markers. Efficacy on cognition is limited. |
|