AUTHOR CONTACT:
Todd Golde
Mayo Clinic, Jacksonville, Florida, USA.
Phone: 904-953-2538
Fax: 904-953-7370
Email: tgolde@mayo.edu

View the PDF of this article at: https://www.the-jci.org/press/18162.pdf

ACCOMPANYING COMMENTARY:
Amyloid-beta and Alzheimer disease therapeutics: The devil may be in the details

AUTHOR CONTACT:
David M. Holtzman
Washington University School of Medicine, St. Louis, Missouri, USA.
Phone: 314-747-0286
Fax: 314-362-2826
Email: holtzman@neuro.wustl.edu

View the PDF of this commentary at: https://www.the-jci.org/press/19420.pdf

Immune response to Alzheimer diseaserelated protein changes as we age

Alzhemier disease (AD) is characterized by the progressive accumulation of amyloid beta protein (Abeta) in areas of the brain serving cognitive functions such as memory and language. Active immunization with Abeta peptides has been shown to decrease Abeta-related lesions in the brain in mouse models of AD. Unfortunately, the first clinical trials for Abeta vaccination in humans were halted due to side-effects experienced by a small subset of subjects. However, these immunization strategies remain a viable concept in developing treatments for AD.

In the August 1 issue of the Journal of Clinical Investigation Howard Weiner and colleagues from Harvard Medical School and Brigham and Women's Hospital in Boston, Massachusetts, have further characterized the immune response to Abeta in humans, and revealed intriguing reactions of the elderly human body to Abeta. The authors found that some healthy, elderly individuals, as well as those with AD, contained elevated levels of T ce
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Contact: Brooke Grindlinger
science_editor@the-jci.org
212-342-9006
Journal of Clinical Investigation
1-Aug-2003