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Nonalcoholic steatohepatitis (NASH) is a progressive form of nonalcoholic fatty liver disease (NAFLD) and is strongly associated with type 2 diabetes mellitus (T2DM). Patients with both T2DM and NASH have increased risk for adverse clinical outcomes, leading to higher risk for mortality and morbidity. We built a Markov model with 1-year cycles and 20-year horizon to estimate the economic burden of NASH with T2DM in the U.S. RESEARCH DESIGN AND METHODS Cohort size was determined by population size, prevalence of T2DM, and prevalence and incidence of NASH in 2017. The model includes 10 health statesdNAFL, NASH fibrosis stages F0 through F3, compensated and decompensated cirrhosis, hepatocellular carcinoma, 1 year post-liver transplant, and post-liver transplantdas well as liver-related, cardiovascular, and background mortality. Transition probabilities were calculated from meta-analyses and literature. Annual costs for NASH and T2DM were taken from literature and billing codes. RESULTS We estimated that there were 18.2 million people in the U.S. living with T2DM and NAFLD, of which 6.4 million had NASH. Twenty-year costs for NAFLD in these patients were $55.8 billion. Over the next 20 years, NASH with T2DM will account for 65,000 transplants, 1.37 million cardiovascular-related deaths, and 812,000 liver-related deaths. CONCLUSIONS This model predicts significant clinical and economic burden due to NASH with T2DM over the next 20 years. In fact, this burden may be greater since we assumed conservative inputs for our model and did not increase costs or the incidence of T2DM over time. It is highly likely that interventions reducing morbidity and mortality in NASH patients with T2DM could potentially reduce this projected clinical and economic burden. Nonalcoholic fatty liver disease (NAFLD) is characterized by hepatic steatosis (.5%) in the absence of excessive alcohol consumption or other causes of fatty liver disease and chronic liver disease (1). NAFLD ranges from simple steatosis (NAFL), which has a low likelihood of progression to advanced liver disease, to nonalcoholic steatohepatitis (NASH), which has greater potential for progression. NAFLD is recognized as one of the most common causes of chronic liver disease in the U.S. and worldwide (1-3). NAFLD is

Objective: Data from the Einstein Aging Study (EAS) were used to prospectively evaluate the free recall score from the Free and Cued Selective Reminding Test (FCSRT-FR) and Logical Memory I immediate recall (LM-IR) subtest of the Wechsler Memory Scale-Revised for prediction of incident Alzheimer disease (AD) dementia among individuals from a community-based cohort with memory complaints.Methods: Analyses included 854 participants, age $70 years, who initially had no dementia, and had memory complaints. Clinic evaluations were completed annually and AD dementia was diagnosed using standard criteria (n 5 86 cases; average follow-up 4.1 years). Time-dependent receiver operating characteristic analysis was used to evaluate the prognostic ability of FCSRT-FR and LM-IR for incident AD over various durations of follow-up.Results: For identifying those with memory complaints who will develop incident AD dementia over 2-4 years, the FCSRT-FR had better operating characteristics than LM-IR. APOE e4 status, age, and education did not affect cut points; however, positive predictive values were higher among APOE e4-positive individuals.Conclusions: For follow-up intervals of 2-4 years, the FCSRT-FR is more predictive than the LM-IR for identifying individuals with memory complaints who will develop incident AD. APOE e4 status improves positive predictive value, but does not affect the choice of optimal cuts. Neurology Diagnostic guidelines for Alzheimer disease (AD) have been revised to reflect the view of the disease as a continuum.1,2 The long preclinical course of AD dementia suggests the potential for preventive measures aimed at the preclinical stages, and the search for biomarkers to identify asymptomatic individuals at high risk is underway. In the absence of definitive biomarkers to facilitate primary prevention, secondary prevention trials target persons without dementia with memory impairment and aim to delay or prevent onset of clinical AD dementia.1,2 A critical step in the design of these trials is the ability to discriminate between those with memory complaints attributable to underlying AD and those with impairment due to other causes. 325 There are different approaches to conceptualizing the symptomatic predementia phase of AD. Definitions of mild cognitive impairment (MCI) rely on norming cognitive performance relative to an age-and education-matched sample. However, if the goal is to identify individuals with high probability of developing AD dementia, the ideal cognitive cut scores for cognitive screening could be determined prospectively based on ability to predict incident AD dementia. Demographic and genetic covariates might enhance the predictive ability of these longitudinally derived screening cut scores. Because intervention studies may involve various

In subjects with MCI and evidence of amyloid pathology, the injury markers CSF t-tau and p-tau and hippocampal atrophy can predict further cognitive decline.