 Alzheimers disease AD is characterized pathologically by the presence of beta-amyloid plaques in brain. A substantial body of research indicates that the presence of increased beta -amyloid peptide is neurotoxic, and may initiate further pathology observed in AD including neurofibrillary tangles, synaptic loss and dysfunction, and neurodegeneration. There are multiple binding sites available on beta-amyloid plaques. Three clearly identified sites are Congo-red type, Thioflavin-T type, and FDDNP type. Radioligands currently under development using positron emission tomography PET for studying beta-amyloid in clinical research or drug development are based on Thioflavin-T site, such as 11CPIB and 11CSB-13. Though variously effective, these radioligands have one or more drawbacks with respect to measuring relative regional beta-amyloid densities. Therefore, we have recently developed 11CMeS-IMPY as an alternative radioligand for imaging beta-amyloid, which will allow a more accurate quantification of amyloid plaques in AD brain. In the current protocol, we wish to evaluate 11CMeS-IMPY in both healthy subjects and AD patients to determine the kinetics of brain imaging beta-amyloid plaques in AD patients. 