Pathologic correlates of nondemented aging, mild cognitive impairment, and early-stage alzheimer’s disease

Article

DOI: 10.1385/JMN:17:2:101

Cite this article as:
Morris, J.C. & Price, J.L. J Mol Neurosci (2001) 17: 101. doi:10.1385/JMN:17:2:101

Abstract

The results of studies from the Washington University Alzheimer Disease (AD) Research Center and those from other centers and investigators regarding the neuropathologic correlates of normal aging and early-stage AD are reviewed. We conclude that widespread amyloid plaques in the neocortex best distinguishes very early stage AD, including “MCI” stage, and preclinical stages, from healthy brain aging. Other AD lesions, including increased formation of neurofibrillary tangles and neuronal degeneration appear to result from the amyloid-initiated pathologic process, although they may have a more immediate effect on expression and severity of dementia. These data provide strong support for anti-amyloid intervention as a preventive therapy for AD. It is now critical to develop methods to detect preclinical AD during life.

Index Entries

Aging mild cognitive impairment Alzheimer’s disease amyloid plaques 

Copyright information

© Humana Press Inc 2001

Authors and Affiliations

  1. 1.Department of NeurologyWashington University School of MedicineSt. Louis
  2. 2.Department of Pathology and ImmunologyWashington University School of MedicineSt. Louis
  3. 3.Department of Anatomy and NeurobiologyWashington University School of MedicineSt. Louis
  4. 4.the Alzheimer Disease Research CenterWashington University School of MedicineSt. Louis

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