It is hypothesized that NSAID use would be associated with greater volume in brain regions typically affected by AD pathology, and analyses were restricted to the hippocampus and parahippocampal gray matter, as these regions are known to be profoundly affected in AD.
phagocytize pathogens. However, even slight perturbations in the CNS can induce activation and endocytic damage (Banati et al., 1993). A post mortem study of a subset of brains donated by participants in the Religious Orders Study did not show brain differences between NSAID-users and non-users (Arvanitakis et al., 2008); yet only plaque and tangle burdens were compared, but not activated microglia nor other indices of neuroinflammation (Mackenzie and Munoz, 1998; Mackenzie, 2000). The results of a recent brain imaging study suggest a neuroprotective effect of anti-inflammatory drugs on brain volume (Walther et al., 2009). Walther et al. (2009) examined gray and white matter volume in a group of participants ranging in age from 65 to 93 years who were taking NSAIDs or other anti-inflammatory medications. Anti-inflammatory drugs were associated with widespread attenuated age-related volume decline. In the present study, we extended upon the findings of Walther et al. (2009) by examining participants ranging in age from 42 to 75 years of age, who were NSAID users or non-user controls. Since NSAIDs protect against AD and are involved in preservation of memory function, we hypothesized that NSAID use would be associated with greater volume in brain regions typically affected by AD pathology. Analyses were restricted to the hippocampus and parahippocampal gray matter, as these regions are known to be profoundly affected in AD (Hyman et al., 1984; de Leon et al., 1989) and are also known to be affected by risk factors for AD such as APOE Based on previous findings indicating that NSAIDs modify cognitive and brain aging trajectories