Clinical studies have demonstrated a strong correlation between increased [11C]PK11195 binding and the presence of amyloid deposits in AD patients, inflammatory lesions in MCI patients, and reduced glucose metabolism in patients with multiple neurodegenerative disorders.380 Although the positive results of [11C]PK11195 in human studies have been confirmed, its clinical use has been hampered by various limitations, including low binding affinity and selectivity for human TSPO, a short half-life of 11C (20 min), difficulty in crossing the BBB and poor in vivo stability. This evidence concerns the gene TSPO and Alzheimer disease.