Activation of Cell Cycle Proteins in Transgenic Mice in Response to Neuronal Loss but not Amyloid-β and Tau Pathology

Lopes, Joao P.; Blurton-Jones, Mathew; Yamasaki, Tritia R.; Agostinho, Paula; LaFerla, Frank M.

doi:10.3233/jad-2009-0993

Cited by 32Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsNeurogenesis and neuroplasticity mechanisms

Activation of Cell Cycle Proteins in Transgenic Mice in Response to Neuronal Loss but not Amyloid-β and Tau Pathology

Lopes, Joao P., Blurton-Jones, Mathew, Yamasaki, Tritia R., Agostinho, Paula, LaFerla, Frank M.·2009·Journal of Alzheimer's Disease

DOI 10.3233/jad-2009-0993

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Abstract

Cell cycle proteins are elevated in the brain of patients and in transgenic models of Alzheimer's disease (AD), suggesting that aberrant cell cycle re-entry plays a key role in this disorder. However, the precise relationship between cell cycle reactivation and the hallmarks of AD, amyloid-beta (Abeta) plaques and tau-laden neurofibrillary tangles, remains unclear. We sought to determine whether cell cycle reactivation initiates in direct response to Abeta and tau accumulation or whether it occurs as a downstream consequence of neuronal death pathways. Therefore, we used a triple transgenic mouse model of AD (3xTg-AD) that develops plaques and tangles, but does not exhibit extensive neuronal loss, whereas to model hippocampal neuronal death a tetracycline-regulatable transgenic model of neuronal ablation (CaM/Tet-DT(A) mice) was used. Cell-cycle protein activation was determined in these two models of neurodegeneration, using biochemical and histological approaches. Our findings indicate that Cdk4, PCNA and phospho-Rb are significantly elevated in CaM/Tet-DT(A) mice following neuronal death. In contrast, no significant activation of cell-cycle proteins occurs in 3xTg-AD mice versus non-transgenic controls. Taken together, our data indicate that neuronal cell cycle reactivation is not a prominent feature induced by Abeta or tau pathology, but rather appears to be triggered by acute neuronal loss.

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Similar types of studies did not detect robust neuronal loss in aged 3xTg animals.
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Authors: Lopes, J. P., Blurton-Jones, M., Yamasaki, T. R., Agostinho, P., & LaFerla, F. M.
Affiliations: Center for Neuroscience and Cell Biology, Faculty of Medicine, Biochemistry Institute, University of Coimbra, Coimbra, Portugal
University of California, Irvine (US)
Centro de Neurociências e Biologia Celular (PT)
ORCID: Blurton-Jones, Mathew
Yamasaki, Tritia R.
Agostinho, Paula
LaFerla, Frank M.
Venue: Journal of Alzheimer's Disease
Publisher: SAGE Publications
Published: 2009-03-09
Volume: 16
Issue: 3
Pages: 541-549
ISSN: 1387-2877 (ISSN-L)
1875-8908
DOI: 10.3233/jad-2009-0993
OpenAlex: W1583540109
Cited by: 32
References: 38
Citations by year: 2024: 1 · 2021: 2 · 2020: 1 · 2019: 1 · 2018: 1 · 2017: 1 · 2015: 4 · 2014: 1 · 2013: 6 · 2012: 4
FWCI: 3.09
Type: journal article
Language: en
Open access: closed
Locations: Journal of Alzheimer s Disease (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute on Aging (R01AG027544)
Topics: Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Keywords: cell cycle re-entry, Alzheimer's disease
MeSH terms: Alzheimer Disease, Animals, Denervation, Disease Models, Animal, Histones, Mice, Transgenic, Neurons, Tetracycline, Retinoblastoma Protein, Amyloid beta-Peptides, tau Proteins, Cell Death, Cell Cycle Proteins, Proliferating Cell Nuclear Antigen, Cyclin-Dependent Kinase 4, Mice

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Activation of Cell Cycle Proteins in Transgenic Mice in Response to Neuronal Loss but not Amyloid-β and Tau Pathology

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