Abel_2008_Vertex_19 Suppl_39

This chapter will focus in the currently treatments for Alzheimer Disease. The meeting points in the proposed pathogenesis of the disease are the cholinergic and the cascade amyloid hypothesis based mainly in postmortem brain changes: 1- Pathological based on greater density of neuritic plaques and the characteristic presence of neurofibrillary tangles associated with neuronal loss, synaptic alterations and evidence for chronic inflammatory reactions, 2) Biochemical based on major depletion of cortical cholinergic innervation, dramatic loss in levels of biochemically determined choline acetyltransferase, accumulation of beta-amyloid peptide, oxidation, glutamatergic excitotoxicity and activation of the apoptotic cascade. The currently available therapies based on the hypothesized pathophysiology of AD are: Acetylcholinesterase inhibitors (donepezil, rivastigmine and galantamine) and the NMDA receptor inhibitor Memantine. None of the "head to head" analyses done with cholinesterase inhibitors (CI) were able to demonstrate a between group effect for efficacy. However the treatment planning is based on their differences, their titration phase to reach the therapeutic doses, interactions and side effects. The non pharmacological treatment in the early and late stages of the disease, the different cognitive stimulation techniques and available prevention trials are also addressed and discussed.