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Semin Neurol 2006; 26(5): 499-506
DOI: 10.1055/s-2006-951622
Published 2006 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA.

Alzheimer's Disease

R. Scott Turner1 , 2 , 3
  • 1Neurology Service, VA Ann Arbor Healthcare System, Michigan
  • 2Research Scientist, VA Geriatric Research Education and Clinical Center, Ann Arbor, Michigan
  • 3Associate Professor, Department of Neurology, University of Michigan, Ann Arbor, Michigan
Further Information

Publication History

Publication Date:
17 October 2006 (online)

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ABSTRACT

Alzheimer's disease (AD) is the most commonly diagnosed etiology of dementia and may be caused by the progressive accumulation and deposition of neurotoxic Aβ/amyloid plaques and aggregates in brain with aging-the amyloid hypothesis of AD. However, Aβ/amyloid deposition is likely necessary but not sufficient to cause AD, and other putative downstream pathologies, including the aggregation of phospho-tau in neurofibrillary tangles, synaptic and neuronal loss, and glial and inflammatory responses, are likely equally important to AD pathogenesis. The majority of AD is sporadic (> 95%) but the discovery of rare early onset familial forms of AD has been pivotal to our understanding of its pathogenesis and in developing novel therapeutic strategies. Currently available drugs for patients with AD provide modest, temporary, and palliative benefits, but they consistently demonstrate safety and efficacy on cognitive, functional, behavioral, and global outcome measures. Novel potential disease-modifying therapies now in preclinical research or clinical trials may be more effective in preventing or arresting the progressive dementia of AD and will provide a test of the amyloid hypothesis.

KEYWORDS

Aβ - Alzheimer's disease - amyloid plaque - dementia - mild cognitive impairment - presenilin - tau - neurofibrillary tangle - acetylcholinesterase inhibitor - memantine

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R. Scott TurnerM.D. Ph.D. 

VA Ann Arbor Healthcare System, GRECC (11G)

2215 Fuller Road, Ann Arbor, MI 48105

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