Alzheimers disease is treated by attacking hyperactive microglia preferably before excessive beta amyloid is built up by administering tin-117m-DOTA annexin V. This compound in low radioactive doses selectively binds to the aged hyperactive microglia and emits a conversion electron which effectively induces apoptosis in the hyperactive microglia. A follow-up treatment of tin-annexin Al can be administered to repair the blood brain barrier. The annexin Al assists in the repair of the blood-brain barrier and the associated tin-117m will induce apoptosis in aged hyperactive microglia associated with the blood brain barrier.