2024.01.29 | David Medina-Julio, Mariana M. Ramírez-Mejía, Jacqueline Cordova-Gallardo, Emilio Peniche-Luna, Carlos Cantú-Brito, Nahum Mendez-Sanchez
Metabolic dysfunction-associated fatty liver disease (MAFLD/MASLD) is a common chronic liver condition affecting a large portion of the global population, linked to metabolic syndrome, insulin resistance, and systemic inflammation. Beyond its impact on liver function, MAFLD/MASLD is associated with cognitive impairment, which is an intermediate stage between normal aging and dementia. Studies show that individuals at risk of liver fibrosis have impaired executive function and global cognitive decline. The cognitive impairment in MAFLD/MASLD is influenced by factors such as insulin resistance, lipotoxicity, and systemic inflammation, which contribute to neuroinflammation and cognitive dysfunction. The brain-gut-liver axis plays a crucial role in this process, with disruptions in gut microbiota and increased intestinal permeability leading to systemic inflammation and cognitive decline. The liver, connected to the gut via the portal vein, is involved in the pathophysiology of MAFLD/MASLD and its impact on cognitive function. Potential treatments include GLP-1 agonists, PPARγ agonists, and omega-3 fatty acids, which may improve cognitive function. Future research aims to better understand the complex mechanisms linking MAFLD/MASLD and cognitive impairment, leading to improved diagnostic tools and therapeutic strategies. The relationship between MAFLD/MASLD and cognitive impairment highlights the need for integrated approaches to address both metabolic and neurological health.Metabolic dysfunction-associated fatty liver disease (MAFLD/MASLD) is a common chronic liver condition affecting a large portion of the global population, linked to metabolic syndrome, insulin resistance, and systemic inflammation. Beyond its impact on liver function, MAFLD/MASLD is associated with cognitive impairment, which is an intermediate stage between normal aging and dementia. Studies show that individuals at risk of liver fibrosis have impaired executive function and global cognitive decline. The cognitive impairment in MAFLD/MASLD is influenced by factors such as insulin resistance, lipotoxicity, and systemic inflammation, which contribute to neuroinflammation and cognitive dysfunction. The brain-gut-liver axis plays a crucial role in this process, with disruptions in gut microbiota and increased intestinal permeability leading to systemic inflammation and cognitive decline. The liver, connected to the gut via the portal vein, is involved in the pathophysiology of MAFLD/MASLD and its impact on cognitive function. Potential treatments include GLP-1 agonists, PPARγ agonists, and omega-3 fatty acids, which may improve cognitive function. Future research aims to better understand the complex mechanisms linking MAFLD/MASLD and cognitive impairment, leading to improved diagnostic tools and therapeutic strategies. The relationship between MAFLD/MASLD and cognitive impairment highlights the need for integrated approaches to address both metabolic and neurological health.