The neurobiology and pharmacotherapy of Alzheimer's disease.
Alzheimer's disease (AD), the most common cause of dementia, has become a major public health concern as our population ages. In recent years, AD has attracted the attention of a wide range of biological disciplines, and substantial progress has been made in understanding the mechanisms of neurodegeneration in AD. Four different genes have now been associated with AD and are providing insights into the pathogenesis of the disease. The roles of beta-amyloid, tau, hormonal changes, inflammation, and oxidative stress in the neurodegeneration of AD are also being delineated. Based on these discoveries, rational therapeutic strategies are developing rapidly. The authors review these and other recent advances in the neurobiology and pharmacotherapy of AD.
Felician
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Department of Neurology, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA.
Sandson
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TA
D000109:Acetylcholine / Q000378:metabolism; D000544:Alzheimer Disease / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000235:genetics / Q000378:metabolism; D001057:Apolipoproteins E / Q000235:genetics; D001921:Brain / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D002799:Cholinergic Fibers / Q000502:physiology; D002800:Cholinesterase Inhibitors / Q000627:therapeutic use; D002888:Chromosomes, Human, Pair 19; D004967:Estrogens / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D008870:Microtubules / Q000378:metabolism; D008959:Models, Neurological; D016874:Neurofibrillary Tangles / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress / Q000502:physiology; D058225:Plaque, Amyloid / Q000235:genetics / Q000378:metabolism / Q000473:pathology