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BACKGROUND: We assessed the relationship of liver fibrosis score with incident dementia in a large, national sample. METHODS: For this retrospective cohort study, data of dementia‐free individuals aged 40‐69 years were derived from electronic records of the largest healthcare provider in Israel. The association between liver fibrosis score (FIB‐4), assessed from routine laboratory measurements, and incident dementia was explored through multivariate cox regression models. RESULTS: Of the total sample (N = 826,578, mean age 55 ± 8 years at baseline), 636,967 (77%) had no fibrosis, 180,114 (21.8%) had inconclusive fibrosis status and 9497 (1.2%) had high risk for advanced fibrosis. Over a median follow‐up of 17 years, 41,089 dementia cases were recorded. Inconclusive liver fibrosis and advanced fibrosis were associated with increased dementia risk (HR = 1.09, 95%CI: 1.07–1.11 and HR = 1.18, 95%CI: 1.10–1.27, respectively). This association remained robust through seven sensitivity analyses. CONCLUSIONS: Liver fibrosis assessed through a serum‐based algorithm may serve as a risk factor for dementia in the general population. Highlights: Liver fibrosis may predict dementia diagnosis in the general population.Inconclusive liver fibrosis was associated with 9% increased dementia risk.Advanced liver fibrosis was associated with 18% increased dementia risk.Findings remained robust in sensitivity analyses and after adjustments. [ABSTRACT FROM AUTHOR]

Background: Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver condition. Accumulating evidence points to an association of NAFLD with cognitive impairment, brain aging and decreased brain activity, yet the association with Alzheimer's disease is unclear. Evidence suggests that liver fibrosis, rather than the existence of hepatic steatosis per se, is a strong prognostic factor for long‐term extra‐hepatic complications. We examined whether NAFLD and risk for advanced fibrosis assessed using a non‐invasive index, are associated with in vivo quantification of brain amyloid and tau pathology. Method: The study sample included participants from the Offspring and Third generation of the Framingham Study. We included participants who underwent positron emission tomography (PET) imaging for assessment of amyloid and tau deposition who do not consume excessive amount of alcohol. Additionally, we included those with information on NAFLD from CT imaging (n=169) or those with all components of the FIB‐4 index (i.e. age, platelets count, aspartate aminotransferase and alanine aminotransferase; n=177). Linear regression models were performed to assess the relationship of NAFLD and risk of advanced fibrosis with amyloid FLR and amyloid and tau regional measures, adjusting for age, sex, time between exposure and PET, and camera, and additionally for body mass index, alcohol consumption, systolic blood pressure, smoking, cardiovascular disease, physical activity, C‐reactive protein, cholesterol, insulin resistance, diabetes, hypertension and visceral adipose tissue. Result: Of the subsample with NAFLD information (mean age 52±9y; 57% males), 57 (34%) had NAFLD. Prevalent NAFLD was not associated with PET amyloid and tau. Of the subsample with information on liver fibrosis (mean age 50±10y; 51% males), 34 (19%) had increased risk of advanced fibrosis (FIB4>1.3). One unit increment of FIB‐4 index (but not advanced fibrosis) was significantly associated with increased tau in the inferior temporal, parahippocampal, entorhinal and rhinal brain regions (table 1). Among individuals with prevalent NAFLD (n=57), liver fibrosis (both continuous and using the 1.3 cutoff) was related to all amyloid and tau measures except for entorhinal amyloid (table 2). Conclusion: This pioneering study suggests a possible association between liver fibrosis and early Alzheimer's disease markers, independently of vascular risk factors. [ABSTRACT FROM AUTHOR]

Background: Ultra‐processed foods (UPF) are ready‐to‐eat/heat foods that derive from a series of industrial processes. These products constitute a large and increasing amount of the food supply in high and middle‐income countries. Accumulating evidence point to an association of UPF intake with increased mortality and adverse health outcomes, including cardiovascular and metabolic diseases. However, whether UPF consumption is associated with cognitive function is not clear. We investigated the associations between UPF intake and cognitive decline, in a cohort of older adults at high‐risk for dementia due to type‐2 diabetes (T2D). Method: The study sample included initially non‐demented T2D older adults (≥65y), from the Israel Diabetes and Cognitive Decline (IDCD) study, who had complete information on nutrition at baseline and at least three cognitive assessments (mean follow‐up 5.3±1.5y). Nutritional intake was evaluated by a validated Food‐Frequency Questionnaire and foods were categorized as UPF based on NOVA classification. Percent of calories from UPF were calculated from total caloric consumption, first as overall UPF intake and then for specific food groups. Global cognitive functioning and four cognitive domains (episodic memory, working memory/attention, semantic categorization, and executive functions) were assessed. Mixed effect models were used to examine the link between UPF intake (top vs. bottom quartiles) and change in cognitive function while adjusting for age, sex, education, smoking, physical activity, BMI, HbA1C, duration of diabetes, total cholesterol and blood pressure. Result: Of the total sample (N=578; mean age at baseline 71.3±4.5y, 61% men), 144 (top quartile) consumed >31% kcal from UPF out of total kcal. Total UPF consumption was not related to cognitive function. However, consumption of ultra‐processed fat (e.g. mayonnaise) was associated with faster decline in global cognition, executive function and memory (ß=‐0.028±0.010; p=0.009, ß=‐0.031±0.014; p=0.022 and ß=‐0.035±0.017; p=0.046, respectively). Additionally, increased intake of ultra‐processed meat (e.g. sausages) was associated with a faster decline in executive functions (ß=‐0.029±0.013; p=0.031). UPF derived from dairy products and carbohydrates were not associated with cognitive change. Conclusion: This pioneering study suggests a possible association of ultra‐processed meat and fat intake with accelerated cognitive decline in older individuals with T2D, independently of sociodemographic, lifestyle, cardiovascular and T2D‐related factors. [ABSTRACT FROM AUTHOR]