Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 and has rapidly escalated into a global pandemic.¹ Severe illness of COVID-19 predominantly occurs in individuals with underlying medical comorbidities.^2-5 Patients with cancer have weakened immune status; often have multiple comorbid conditions, including type 2 diabetes, obesity, and cardiovascular diseases; and are more likely to get infections.^6-11 Reports from China and the US described clinical characteristics and outcomes of patients with cancer and COVID-19 and examined risk factors for mortality in this population; they suggested a higher rate of death due to COVID-19 and severe outcomes in patients with cancer.^12-16 However, there is a knowledge gap regarding the susceptibility of patients with cancer to COVID-19 and its severe outcomes in the US. It remains unknown how race and other demographic factors such as age and sex affect the risk of COVID-19 infection and outcomes among patients with cancer, given that the cancer burden in the US varies by race and other demographic factors.

Thirteen human malignant neoplasms have been identified as obesity-associated cancers (OAC), ie, the presence of excess body fat is associated with increased risk of developing cancer and worse prognosis in patients with these specific tumors.¹ Obesity also contributes to insulin resistance and type 2 diabetes (T2D), which may further increase the risk and worsen the prognosis of the OACs.^2,3

Introduction: At present, there is limited data on the risks, disparity, and outcomes for COVID‐19 in patients with dementia in the United States.Methods: This is a retrospective case‐control analysis of patient electronic health records (EHRs) of 61.9 million adult and senior patients (age ≥ 18 years) in the United States up to August 21, 2020.Results: Patients with dementia were at increased risk for COVID‐19 compared to patients without dementia (adjusted odds ratio [AOR]: 2.00 [95% confidence interval (CI), 1.94–2.06], P < .001), with the strongest effect for vascular dementia (AOR: 3.17 [95% CI, 2.97–3.37], P < .001), followed by presenile dementia (AOR: 2.62 [95% CI, 2.28–3.00], P < .001), Alzheimer's disease (AOR: 1.86 [95% CI, 1.77–1.96], P < .001), senile dementia (AOR: 1.99 [95% CI, 1.86–2.13], P < .001) and post‐traumatic dementia (AOR: 1.67 [95% CI, 1.51–1.86] P < .001). Blacks with dementia had higher risk of COVID‐19 than Whites (AOR: 2.86 [95% CI, 2.67–3.06], P < .001). The 6‐month mortality and hospitalization risks in patients with dementia and COVID‐19 were 20.99% and 59.26%, respectively.Discussion: These findings highlight the need to protect patients with dementia as part of the strategy to control the COVID‐19 pandemic.

INTRODUCTION: Emerging preclinical evidence suggests that semaglutide, a glucagon‐like peptide receptor agonist (GLP‐1RA) for type 2 diabetes mellitus (T2DM) and obesity, protects against neurodegeneration and neuroinflammation. However, real‐world evidence for its ability to protect against Alzheimer's disease (AD) is lacking.METHODS: We conducted emulation target trials based on a nationwide database of electronic health records (EHRs) of 116 million US patients. Seven target trials were emulated among 1,094,761 eligible patients with T2DM who had no prior AD diagnosis by comparing semaglutide with seven other antidiabetic medications. First‐ever diagnosis of AD occurred within a 3‐year follow‐up period and was examined using Cox proportional hazards and Kaplan–Meier survival analyses.RESULTS: Semaglutide was associated with significantly reduced risk for first‐time AD diagnosis, most strongly compared with insulin (hazard ratio [HR], 0.33 [95% CI: 0.21 to 0.51]) and most weakly compared with other GLP‐1RAs (HR, 0.59 [95% CI: 0.37 to 0.95]). Similar results were seen across obesity status, gender, and age groups.DISCUSSION: These findings support further studies to assess semaglutide's potential in preventing AD.Highlights: Semaglutide was associated with 40% to 70% reduced risks of first‐time AD diagnosis in T2DM patients compared to other antidiabetic medications, including other GLP‐1RAs. Semaglutide was associated with significantly lower AD‐related medication prescriptions. Similar reductions were seen across obesity status, gender, and age groups. Our findings provide real‐world evidence supporting the potential clinical benefits of semaglutide in mitigating AD initiation and development in patients with T2DM. These findings support further clinical trials to assess semaglutide's potential in delaying or preventing AD.