Conditional neuronal simian virus 40 T antigen expression induces Alzheimer-like tau and amyloid pathology in mice.

Conditional neuronal simian virus 40 T antigen expression induces Alzheimer-like tau and amyloid pathology in mice. Research Abstract Details 

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Conditional neuronal simian virus 40 T antigen expression induces Alzheimer-like tau and amyloid pathology in mice. Abstract Text:

Kevin H J Park,Janice L Hallows,Paramita Chakrabarty,Peter Davies,Inez Vincent,

A large body of evidence has shown the activation of a cohort of cell cycle regulators and the duplication of DNA in degenerating neurons of Alzheimer's disease (AD) brain. Activation of these regulators and duplication of chromosomes precede neurodegeneration and formation of neurofibrillary tangles (NFTs), one of the diagnostic lesions of AD. These findings, in combination with evidence for cell cycle regulation of amyloid precursor protein and tau, has led to the hypothesis that reentry into the cell cycle underlies AD pathogenesis. To test this hypothesis directly, we have created transgenic mice with forced cell cycle activation in postmitotic neurons via conditional expression of the simian virus 40 large T antigen (TAg) oncogene. We show that TAg mice recapitulate the cell cycle changes seen in AD and display a neurodegenerative phenotype accompanied by tau pathology and NFT-like profiles. Moreover, plaque-like amyloid deposits, similar to those seen in AD, are also observed in the brains of TAg mice. These data provide support for an essential role of ectopic cell cycle activation in the generation of the characteristic pathological hallmarks of AD. Furthermore, our TAg mice are the first model to develop NFTs and amyloid pathology simultaneously and in the absence of any human transgenes. These mice will be useful for further defining the nongenetic mechanisms in AD pathogenesis and for the development of cell cycle-based therapies for AD.

Conditional neuronal simian virus 40 T antigen expression induces Alzheimer-like tau and amyloid pathology in mice. Publishing Authors By Initials

KH Park,JL Hallows,P Chakrabarty,P Davies,I Vincent,

For similar microtubule-associated proteins: tau proteins research abstracts see: microtubule-associated proteins: tau proteins research

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Conditional neuronal simian virus 40 T antigen expression induces Alzheimer-like tau and amyloid pathology in mice. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: The Journal of neuroscience : the official journal

VOLUME: 27

Page Numbers: 2969-78

Journal Abbreviation: J. Neurosci.

ISSN: 1529-2401

DAY: 14

MONTH: Mar

YEAR: 2007

Conditional neuronal simian virus 40 T antigen expression induces Alzheimer-like tau and amyloid pathology in mice. Information

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LANGUAGE: eng

NlmUniqueID: 8102140

Conditional neuronal simian virus 40 T antigen expression induces Alzheimer-like tau and amyloid pathology in mice. Keywords Mesh Terms:

KEYWORDS: tau Proteins

MESH TERMS: physiology

Chemical & Substance for Abstract: Conditional neuronal simian virus 40 T antigen expression induces Alzheimer-like tau and amyloid pathology in mice. Information

Substance Name: tau Proteins

Registry Number: 0

Grant and Affiliation Information for Conditional neuronal simian virus 40 T antigen expression induces Alzheimer-like tau and amyloid pathology in mice.

AFFILIATION: Centre for Molecular Medicine and Therapeutics, Department of Pediatrics, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada, V5Z 4H4.

Country: United States

AGENCY: United States PHS

GRANT: T32 00057

ACRONYM: AG

MEDLINETA: J Neurosci

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