title: [Treatment of Alzheimer's disease].
abstract: OBJECTIVE
  To review the experience of the last twenty years in the treatment of Alzheimer s disease (AD).
  
  
  METHODS
  Literature review.
  
  
  RESULTS
  The neuropathological bases of AD are centered on two important pathophysiological mechanisms: 1) Structural damage (e.g., senile plaques, neurofibrillary tangles, neuronal loss, inflammatory processes), and 2) Loss of cholinergic neurons (and acetylcholine depletion) in the nucleus basalis of Meynert, which sends cholinergic projections to all areas of the neocortex, especially the temporal lobes and frontal and parietal association areas. The indemnity of this system is essential for normal cognitive functioning. At this moment, the only long term treatment available for AD are acetylcholinesterase inhibitors (CEIs) (e.g., tacrine, donepezil, rivastigmine, galanthamine). There are being investigated several treatments that may alter the development of neurofibrillary tangles and neuritic plaques (e.g., peripherally administered antibodies against beta amyloid proteins). Nerve growth factors may have the capability of improving neuronal survival, although their form of administration remains a problem. Amelioration of oxidative stress and CNS inflammatory processes may slow dawn the rate of neurodegeneration.
  
  
  CONCLUSIONS
  All suspected mechanisms of the metabolic cascade of AD have been explored with specific and non specific treatments. Current treatments (e.g., CEIs) still have to prove that their effects can last for long periods of time. With the advent of further understanding of the neurodegenerative processes that cause AD, new treatments that may slow down the progression of the disease will be available.
authors.affiliation: Departamento de Nurología. Escuela de Medicina. Universitdad de Pettsburgh, Pennsylvania, EE.UU. lopezol@msx.upmc
authors.forename: O L
authors.initials: OL
authors.lastname: López
authors.forename: J T
authors.initials: JT
authors.lastname: Becker
mesh_terms: D000109:Acetylcholine / Q000378:metabolism*; D000544:Alzheimer Disease / Q000188:drug therapy*; D000975:Antioxidants / Q000627:therapeutic use; D001921:Brain / Q000473:pathology; D018679:Cholinergic Agonists / Q000627:therapeutic use; D002800:Cholinesterase Inhibitors / Q000627:therapeutic use; D003072:Cognition Disorders / Q000188:drug therapy*; D004967:Estrogens / Q000627:therapeutic use; D006801:Humans; D008996:Monoamine Oxidase Inhibitors / Q000627:therapeutic use; D020932:Nerve Growth Factor / Q000627:therapeutic use; D018696:Neuroprotective Agents / Q000627:therapeutic use; D018697:Nootropic Agents / Q000627:therapeutic use; D018384:Oxidative Stress; D008517:Phytotherapy
chemical_list: D000975:Antioxidants; D018679:Cholinergic Agonists; D002800:Cholinesterase Inhibitors; D004967:Estrogens; D008996:Monoamine Oxidase Inhibitors; D018696:Neuroprotective Agents; D018697:Nootropic Agents; D020932:Nerve Growth Factor; D000109:Acetylcholine