Active immunization trial in Aβ42-injected P301L tau transgenic mice

Kulic, Luka, Kurosinski, Pascal, Chen, Feng, Tracy, Jay, Mohajeri, M. Hasan, Li, Hong, Nitsch, Roger M. and Gotz, Juergen (2006) Active immunization trial in Aβ42-injected P301L tau transgenic mice. Neurobiology of Disease, 22 1: 50-56. doi:10.1016/j.nbd.2005.10.002

Author Kulic, Luka
Kurosinski, Pascal
Chen, Feng
Tracy, Jay
Mohajeri, M. Hasan
Li, Hong
Nitsch, Roger M.
Gotz, Juergen
Title Active immunization trial in Aβ42-injected P301L tau transgenic mice
Formatted title
Active immunization trial in Aβ42-injected P301L tau transgenic mice
Journal name Neurobiology of Disease   Check publisher's open access policy
ISSN 0969-9961
Publication date 2006-04-01
Year available 2005
Sub-type Article (original research)
DOI 10.1016/j.nbd.2005.10.002
Open Access Status Not yet assessed
Volume 22
Issue 1
Start page 50
End page 56
Total pages 7
Place of publication Maryland Heights, MO, United States
Publisher Academic Press
Language eng
Formatted abstract
Amyloid β-peptide (Aβ) containing plaques and neurofibrillary tangles (NFT) are the two major histopathological hallmarks of Alzheimer's disease (AD). According to the amyloid cascade hypothesis, deposition of Aβ is an initial and essential step in the pathogenesis of AD, and formation of NFT has been proposed to be caused by increased Aβ levels. Several previous studies revealed that Aβ plaque formation can be reduced or even prevented by active immunization with Aβ preparations or by administration of Aβ-specific antibodies. To assess the role of fibrillar preparations of Aβ42 in NFT formation, we previously performed intracerebral (i.c.) injections of Aβ42 into brains of NFT-forming P301L tau transgenic mice which caused significant increases in NFT numbers. To determine whether these increases in NFT can be blocked or reduced by active immunization, P301L tau mice were immunized with intraperitoneal injections of preaggregated Aβ42. Aβ42-specific titers were monitored and the mice injected i.c. with Aβ42. We found that i.c. injection of Aβ42 caused significant increases in NFT formation. However, this induction was not affected by active immunization despite high serum anti-Aβ42 titer levels and binding of anti-Aβ42 antibodies to the injected Aβ42 aggregates. We conclude that active immunization is not sufficient to prevent the effect of Aβ42 on tau aggregation in our model system. Further studies are required to determine whether modifications of our protocol could affect the Aβ42-mediated induction of NFT formation.
Keyword Alzheimer's disease
Amyloid β-peptide
Neurofibrillary tangles
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: Centre for Ageing Dementia Research Publications
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