Race is a social construct with profound consequences on health. Although race does not always segregate with genetic ancestry, some genetic variants are more frequently found in certain self-identified racial and ethnic groups. Differences in the epidemiology and the pathophysiology of Alzheimer disease (AD) and other neurodegenerative conditions have been described in certain racial groups. Unfortunately, most studies in the field of AD have mainly included non-Hispanic White (NHW) participants, with an underrepresentation of other populations. In the past few years, however, research on race and ethnic differences in AD has grown rapidly. Some studies indicate that African Americans (AA) have a greater risk for AD than NHW.1 The reasons hypothesized to account for this higher risk are certain genetic risk factors associated with AA, the higher prevalence of vascular risk factors in AA, and socioeconomic factors.2 In addition, some studies have reported a different pathophysiology and pattern of AD biomarkers. There is evidence that AA have lower concentrations of total-Tau, phosphorylated Tau, and neurofilament light in the CSF compared with NHW.3 The differences in AD pathophysiology in racial groups can be due to various factors, such as genetic variants associated with that race, but also with other environmental factors such as socioeconomic status, diet, or medical comorbidities. Another factor that could play a role in this association is a different innate immune response to AD pathology.