Disclosed is a method of treating memory disorders and cognitive decline, e.g., age-related cognitive decline, in a primate by administering thereto a therapeutically effective amount of an alpha-2 agonist having a high affinity for the alpha-2I subtype, e.g., guanfacine and guanabenz or a nontoxic, pharmaceutically acceptable salt thereof. Particularly preferred is the use of alpha-2I selective agonists such as guanfacine.
Disclosed is a method of treating disorders which have prominent symptoms of behavioral disinhibition (e.g., Attention-Deficit Hyperactivity Disorder, Conduct Disorder, Oppositional Defiant Disorder, Tourette's Syndrome, Lesch-Nyhan Syndrome, or the disinhibitory symptoms accompanying Post-traumatic Stress Disorder or dementia) in a primate with minimal sedative side effects by administering thereto a therapeutically effective amount of guanfacine.
This invention provides for a method of raising extracellular brain acetylcholine levels to improve cognition by the administration to a warm-blooded animal of a pharmaceutical composition comprising an effective amount of a dopamine D.sub.1 agonist.
