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A beta peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease.
Nature. 2000 Dec 21-28; 408(6815):979-82.Nat

Abstract

Much evidence indicates that abnormal processing and extracellular deposition of amyloid-beta peptide (A beta), a proteolytic derivative of the beta-amyloid precursor protein (betaAPP), is central to the pathogenesis of Alzheimer's disease (reviewed in ref. 1). In the PDAPP transgenic mouse model of Alzheimer's disease, immunization with A beta causes a marked reduction in burden of the brain amyloid. Evidence that A beta immunization also reduces cognitive dysfunction in murine models of Alzheimer's disease would support the hypothesis that abnormal A beta processing is essential to the pathogenesis of Alzheimer's disease, and would encourage the development of other strategies directed at the 'amyloid cascade'. Here we show that A beta immunization reduces both deposition of cerebral fibrillar A beta and cognitive dysfunction in the TgCRND8 murine model of Alzheimer's disease without, however, altering total levels of A beta in the brain. This implies that either a approximately 50% reduction in dense-cored A beta plaques is sufficient to affect cognition, or that vaccination may modulate the activity/abundance of a small subpopulation of especially toxic A beta species.

Authors+Show Affiliations

Centre for Research in Neurodegenerative Diseases, Department of Medicine, University of Toronto, Ontario, Canada.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

11140685

Citation

Janus, C, et al. "A Beta Peptide Immunization Reduces Behavioural Impairment and Plaques in a Model of Alzheimer's Disease." Nature, vol. 408, no. 6815, 2000, pp. 979-82.
Janus C, Pearson J, McLaurin J, et al. A beta peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease. Nature. 2000;408(6815):979-82.
Janus, C., Pearson, J., McLaurin, J., Mathews, P. M., Jiang, Y., Schmidt, S. D., Chishti, M. A., Horne, P., Heslin, D., French, J., Mount, H. T., Nixon, R. A., Mercken, M., Bergeron, C., Fraser, P. E., St George-Hyslop, P., & Westaway, D. (2000). A beta peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease. Nature, 408(6815), 979-82.
Janus C, et al. A Beta Peptide Immunization Reduces Behavioural Impairment and Plaques in a Model of Alzheimer's Disease. Nature. 2000 Dec 21-28;408(6815):979-82. PubMed PMID: 11140685.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - A beta peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease. AU - Janus,C, AU - Pearson,J, AU - McLaurin,J, AU - Mathews,P M, AU - Jiang,Y, AU - Schmidt,S D, AU - Chishti,M A, AU - Horne,P, AU - Heslin,D, AU - French,J, AU - Mount,H T, AU - Nixon,R A, AU - Mercken,M, AU - Bergeron,C, AU - Fraser,P E, AU - St George-Hyslop,P, AU - Westaway,D, PY - 2001/1/5/pubmed PY - 2001/2/28/medline PY - 2001/1/5/entrez SP - 979 EP - 82 JF - Nature JO - Nature VL - 408 IS - 6815 N2 - Much evidence indicates that abnormal processing and extracellular deposition of amyloid-beta peptide (A beta), a proteolytic derivative of the beta-amyloid precursor protein (betaAPP), is central to the pathogenesis of Alzheimer's disease (reviewed in ref. 1). In the PDAPP transgenic mouse model of Alzheimer's disease, immunization with A beta causes a marked reduction in burden of the brain amyloid. Evidence that A beta immunization also reduces cognitive dysfunction in murine models of Alzheimer's disease would support the hypothesis that abnormal A beta processing is essential to the pathogenesis of Alzheimer's disease, and would encourage the development of other strategies directed at the 'amyloid cascade'. Here we show that A beta immunization reduces both deposition of cerebral fibrillar A beta and cognitive dysfunction in the TgCRND8 murine model of Alzheimer's disease without, however, altering total levels of A beta in the brain. This implies that either a approximately 50% reduction in dense-cored A beta plaques is sufficient to affect cognition, or that vaccination may modulate the activity/abundance of a small subpopulation of especially toxic A beta species. SN - 0028-0836 UR - https://www.unboundmedicine.com/medline/citation/11140685/A_beta_peptide_immunization_reduces_behavioural_impairment_and_plaques_in_a_model_of_Alzheimer's_disease_ L2 - https://doi.org/10.1038/35050110 DB - PRIME DP - Unbound Medicine ER -