Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Site Tools

  • AAAS
  • Subscribe
  • Feedback

Site Search

Search Advanced

Science 19 July 2002:
Vol. 297. no. 5580, pp. 353 - 356
DOI: 10.1126/science.1072994
Prev | Table of Contents | Next

Review

The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics

John Hardy,1 Dennis J. Selkoe2*

It has been more than 10 years since it was first proposed that the neurodegeneration in Alzheimer's disease (AD) may be caused by deposition of amyloid beta -peptide (Abeta ) in plaques in brain tissue. According to the amyloid hypothesis, accumulation of Abeta in the brain is the primary influence driving AD pathogenesis. The rest of the disease process, including formation of neurofibrillary tangles containing tau protein, is proposed to result from an imbalance between Abeta production and Abeta clearance.

1 Laboratories of Neurogenetics, National Institute on Aging, Bethesda, MD 20892, USA.
2 Center for Neurologic Diseases, Harvard Medical School, Brigham and Women's Hospital, Boston, MA 02115, USA.
*   To whom correspondence should be addressed. E-mail: selkoe{at}cnd.bwh.harvard.edu

Read the Full Text

ADVERTISEMENT
Click Me!

ADVERTISEMENT
Click Me!

To Advertise     Find Products

Science. ISSN 0036-8075 (print), 1095-9203 (online)