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
Review
. 2004 Oct 5;101 Suppl 2(Suppl 2):14657-62.
doi: 10.1073/pnas.0404866101. Epub 2004 Aug 5.

Immunotherapy for Alzheimer's disease

Affiliations
Review

Immunotherapy for Alzheimer's disease

David S Gelinas et al. Proc Natl Acad Sci U S A. .

Abstract

The utility of vaccine strategies to treat neurodegenerative diseases such as Alzheimer's disease (AD) may still hold promise. Both active and passive immunization strategies reduced AD-like pathology and restored cognitive deficits in transgenic mice. These results were initially met with considerable optimism; however, phase IIa clinical trials were halted because of a small but significant occurrence of meningoencephalitis. Knowledge gained from studies on amyloid-beta peptide (A beta) immunotherapy will allow optimization of new-generation vaccines, targeting highly specific epitopes while reducing undesired side effects. In harnessing and steering the immune system, an effective response can be generated against A beta. If this proves successful, A beta vaccination could provide the first definitive treatment for AD.

PubMed Disclaimer

Figures

Fig. 1.
Fig. 1.
Aβ42-immunized TgCRND8 mice have a 50% reduction in plaque burden than untreated TgCRND8 mice. Representative pictures of the distribution of Aβ plaques labeled by Dako 6F/3D anti-Aβ antibody in the hippocampus (A and B) and cortex (C and D) of control peptide-immunized (A and C) and Aβ42-immunized TgCRND8 mice (B and D). (Scale bars = 100 μm.)
Fig. 2.
Fig. 2.
Aβ42-immnized TgCRND8 mice have reduced microglial activation in comparison with control peptide-immunized TgCRND8 mice. Representative pictures of the distribution of activated microglia as labeled by anti-CD68 IgG in the hippocampus (A and B) of control peptide-immunized (A and C) and Aβ42-immunized TgCRND8 mice (B and D). Higher magnification reveals that activated microglia have similar morphology under both immunization paradigms (C and D). [Scale bars = 75 μm (A and B) and 5 μm (C and D).]
Fig. 3.
Fig. 3.
The sequence of B and T cell epitopes within the Aβ1–42 amino acid sequence as determined by mathematical algorithms.

Similar articles

Cited by

References

    1. Citron, M. (2002) Nat. Neurosci. 5, Suppl., 1055-1057. - PubMed
    1. Davis, K. L. & Samuels, S. C. (1998) in Pharmacological Management of Neurological and Psychiatric Disorders, eds. Enna, S. J. & Coyle, J. T. (McGraw–Hill, New York), pp. 267-316.
    1. Selkoe, D. (2001) Physiol. Rev. 81, 741-766. - PubMed
    1. McLaurin, J., Yang, D. S., Yip, C. M. & Fraser, P. E. (2000) J. Struct. Biol. 130, 259-270. - PubMed
    1. Pike, C. J., Walencewicz, A. J., Glabe, C. G. & Cotman, C. W. (1991) Brain Res. 573, 311-314. - PubMed

Publication types