Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comment
. 2003 Aug;112(3):321-3.
doi: 10.1172/JCI19420.

Amyloid beta and Alzheimer disease therapeutics: the devil may be in the details

John R Cirrito  1 , David M Holtzman
Affiliations
Comment

Amyloid beta and Alzheimer disease therapeutics: the devil may be in the details

John R Cirrito et al. J Clin Invest. 2003 Aug.

Abstract

Alzheimer 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. The first of two separate reports (see the related articles beginning on pages 415 and 440) reveals that intrinsic T cell reactivity to the self-antigen Abeta exists in many humans and increases with age. This finding has implications for the design of Abeta vaccines. The second report demonstrates that a number of FDA- approved nonsteroidal anti-inflammatory drugs are capable of lowering Abeta levels in mice. The work suggests that further testing of the therapeutic utility of these types of compounds for the potential treatment of AD is warranted.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Model of how certain NSAIDs decrease Aβ42 production. NSAIDs may directly bind to the γ-secretase complex and alter APP processing to decrease Aβ42 production and also change production of other Aβ species.
See this image and copyright information in PMC

Comment on

References

    1. Schenk D, et al. Immunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouse. Nature. 1999;400:173–177. - PubMed
    1. DeMattos RB, et al. Peripheral anti-A beta antibody alters CNS and plasma A beta clearance and decreases brain A beta burden in a mouse model of Alzheimer’s disease. Proc. Natl. Acad. Sci. U. S. A. 2001;98:8850–8855. - PMC - PubMed
    1. Bard F, et al. Peripherally administered antibodies against amyloid β-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease. Nat. Med. 2000;6:916–919. - PubMed
    1. Monsonego A, et al. Increased T cell reactivity to amyloid β protein in older humans and patients with Alzheimer disease. J. Clin. Invest. 2003;112:415–422. doi:10.1172/JCI200318104. - PMC - PubMed
    1. Eriksen JL, et al. NSAIDs and enantiomers of flurbiprofen target γ-secretase and lower Aβ42 in vivo. J. Clin. Invest. 2003;112:440–449. doi:10.1172/JCI200318162. - PMC - PubMed

MeSH terms

Substances