Chapter 55: Pharmacotherapy of Alzheimer disease: new drugs and novel strategies

Publisher Summary Four major and distinct therapeutic interventions for the treatment of Alzheimer disease (AD) have been envisioned in order to: (1) achieve a symptomatic improvement without attenuation of the pathology by acting on one or several neurotransmitter systems; (2) slow down the progression of amyloid formation in individuals with a diagnosed Alzheimer condition; this might also slow down the disease course; (3) prevent, slow down or reverse the accumulation of the P-amyloid protein in cerebral blood vessels and/or neuritic plaques in individuals genetically at risk for the disease; this group of patients is relatively small (0.7%–5 %) ; (4) develop a curative therapy by means of a causal approach. Approach (1) is discussed in detail in this chapter. Approaches (2) and (3) are important, although P-amyloid deposition is probably not the primary cause of the disease. Approach (4) is theoretical since the etiology of the disease is unknown. With regard to approach (1), one should keep in mind that AD is not a “mono-neurotransmitter disease.” In younger patients, a deficiency of norepinephrine (NE) in the central nervous system (CNS) seems to be frequent. There is also evidence that the concentration of other neurotransmitters, besides acetylcholine (ACh) and NE, is lower than normal. Glutamate and serotonin are also reduced in cerebral cortex.