The precise trigger mechanisms for the initiation of Alzheimer's Disease (AD) remain unidentified. However, disturbances to the balance of thyroid hormone begin in the pre-clinical stage of Alzheimer's disease. Key elements of molecular pathology in AD can be correlated with a paucity of thyroid hormone activity in the brain. A method for reversing and/or slowing progression of AD and a method for formulation of a therapeutic agent for AD are presented herein wherein an active form of thyroid hormone, T3, is formulated into an extended release dose and administered to a patient safely normalizing key elements of molecular pathology of Alzheimer's Disease.
