There is currently no disease-modifying treatment for Alzheimer's disease (AD) and the need is great as the number of people diagnosed with AD is predicted to steadily increase. Inflammation is associated with AD, and is predictive of more advanced disease pathology and cognitive impairment. Moreover, preventing inflammation reduces the risk of developing AD. However, clinical trials with anti-inflammatory treatment have not been successful. One reason may be that there is diversity in the immune response and reducing immune activity with anti-inflammatories is not appropriate in all conditions. Recently, we have begun to apply categorizations, used to characterize the peripheral immune response, to the immune processes of the brain. When we do this, we are able to describe an individual's inflammatory profile within this spectrum. We have observed that patients with early AD are distributed across two broad categories of immune activation. If we recognize the diversity within this cohort of individuals with early AD and use information about immune phenotypes to guide the choice of treatment, then we may expect better clinical outcomes.