Alzheimer's disease (AD) has been hypothesized to be an inflammatory c
ondition. We hypothesized that anti-inflammatory cytokines, such as tr
ansforming growth factor beta (TGF-beta), counteract the inflammatory
process. In the present study, we found that TGF-beta levels were elev
ated in both cerebrospinal fluid and serum samples obtained from AD pa
tients <6 h after death. Serum TGF-beta levels were also markedly elev
ated before death. These results suggest that elevated TGF-beta levels
in AD may represent a protective host response to immunologically med
iated neuronal injury.