Abstract
Non-alcoholic fatty liver disease (NAFLD) has emerged as the hepatic component of the metabolic syndrome and now seemingly affects one-fourth of the world population. Features associated with NAFLD and the metabolic syndrome have frequently been linked to cognitive dysfunction, i.e. systemic inflammation, vascular dysfunction, and sleep apnoea. However, emerging evidence suggests that NAFLD may be a cause of cognitive dysfunction independent of these factors. NAFLD in addition exhibits dysbiosis of the gut microbiota and impaired urea cycle function, favouring systemic ammonia accumulation and further promotes systemic inflammation. Such disruption of the gut–liver–brain axis is essential in the pathogenesis of hepatic encephalopathy, the neuropsychiatric syndrome associated with progressive liver disease. Considering the growing burden of NAFLD, the morbidity from cognitive impairment is expected to have huge societal and economic impact. The present paper provides a review of the available evidence for cognitive dysfunction in NAFLD and outlines its possible mechanisms. Moreover, the clinical challenges of characterizing and diagnosing cognitive dysfunction in NAFLD are discussed.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is the hepatic component associated with the metabolic syndrome and constitutes a major global health burden, affecting an alarming one-fourth of the general population worldwide [1,2,3]
NAFLD patients had poor performance on the SDLT (β, 95% CI: 0.105 to 1.347) and worse performance on the SRTT and SDST, but non-significantly so after adjusting for life-style related confounders
Poor performance on the SDST and SDLT scores were associated with increasing blood transaminases
Summary
Non-alcoholic fatty liver disease (NAFLD) is the hepatic component associated with the metabolic syndrome and constitutes a major global health burden, affecting an alarming one-fourth of the general population worldwide [1,2,3]. These are all features linked with NAFLD [22,23], but it is unclear if NAFLD in itself gives rise to and contributes to cognitive dysfunction Adding to these features, NAFLD exhibits disruption of the gut microbiota and impairment of urea synthesis in the liver, leading to ammonia accumulation even in precirrhotic stages [24,25]. NAFLD exhibits disruption of the gut microbiota and impairment of urea synthesis in the liver, leading to ammonia accumulation even in precirrhotic stages [24,25] These disturbances, compounded by systemic inflammation, are central elements of the gut–liver–brain axis and acknowledged as significant in the pathogenesis of hepatic encephalopathy (HE), the neuropsychiatric syndrome associated with progressive liver injury [26,27,28,29]. The clinical challenges of characterization and diagnostic testing are discussed
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