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Cited by 351Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Can Alzheimer disease be prevented by amyloid-β immunotherapy?

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Lemere, Cynthia A., Masliah, Eliezer·2010·Nature Reviews Neurology
DOI 10.1038/nrneurol.2009.219PMC PMC2864089
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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.

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Authors
Lemere, C. A., & Masliah, E.
Affiliations
  • Brigham and Women's Hospital (US)
  • University of California San Diego (US)
Corresponding author
Lemere, Cynthia A.
ORCID
Venue
Nature Reviews Neurology
Publisher
Springer Science and Business Media LLC
Published
2010-02
Volume
6
Issue
2
Pages
108-119
ISSN
  • 1759-4758 (ISSN-L)
  • 1759-4766
DOI
10.1038/nrneurol.2009.219
PMC
PMC2864089
OpenAlex
W2060851420
Cited by
351
References
21
Citations by year
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FWCI
4.61
Type
journal article
Language
en
Update notices
Open access
Licence
Locations
  • Nature Reviews Neurology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute on Aging (P01AG010435, R01AG020159, R37AG018440, R01AG018440, P50AG005131, AG-5131, AG 18440, AG02074, R01 AG20159, AG10435)
  • National Institute of Neurological Disorders and Stroke (R01NS136122)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
Alzheimer's disease, amyloid-beta, immunotherapy, active immunization, passive immunization, meningoencephalitis, amyloid plaques, clinical trials, disease prevention, presymptomatic biomarkers, early-stage disease
MeSH terms
Alzheimer Disease, Animals, Clinical Trials as Topic, Humans, Immunotherapy, Amyloid beta-Peptides

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