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Nat Rev Neurol. 2010 Feb;6(2):108-19. doi: 10.1038/nrneurol.2009.219.

Can Alzheimer disease be prevented by amyloid-beta immunotherapy?

Author information

1
Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, New Research Building 636F, Boston, MA 02115, USA. clemere@rics.bwh.harvard.edu

Erratum in

  • Nat Rev Neurol. 2010 Apr;6(4):183.
  • Nat Rev Neurol. 2010 Jun;6(6):296.

Abstract

Alzheimer disease (AD) is the most common form of dementia. The amyloid-beta (Abeta) peptide has become a major therapeutic target in AD on the basis of pathological, biochemical and genetic evidence that supports a role for this molecule in the disease process. Active and passive Abeta immunotherapies have been shown to lower cerebral Abeta levels and improve cognition in animal models of AD. In humans, dosing in the phase II clinical trial of the AN1792 Abeta vaccine was stopped when approximately 6% of the immunized patients developed meningoencephalitis. However, some plaque clearance and modest clinical improvements were observed in patients following immunization. As a result of this study, at least seven passive Abeta immunotherapies are now in clinical trials in patients with mild to moderate AD. Several second-generation active Abeta vaccines are also in early clinical trials. On the basis of preclinical studies and the limited data from clinical trials, Abeta immunotherapy might be most effective in preventing or slowing the progression of AD when patients are immunized before or in the very earliest stages of disease onset. Biomarkers for AD and imaging technology have improved greatly over the past 10 years and, in the future, might be used to identify presymptomatic, at-risk individuals who might benefit from Abeta immunization.

PMID:
20140000
PMCID:
PMC2864089
DOI:
10.1038/nrneurol.2009.219
[Indexed for MEDLINE]
Free PMC Article

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