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Genetically augmenting tau levels does not modulate the onset or progression of Abeta pathology in transgenic mice.
J Neurochem. 2007 Aug; 102(4):1053-63.JN

Abstract

The two hallmark pathologies of Alzheimer's disease (AD) are amyloid plaques, composed of the small amyloid-beta (Abeta) peptide, and neurofibrillary tangles, comprised aggregates of the microtubule binding protein, tau. The molecular linkage between these two lesions, however, remains unknown. Based on human and mouse studies, it is clear that the development of Abeta pathology can trigger tau pathology, either directly or indirectly. However, it remains to be established if the interaction between Abeta and tau is bidirectional and whether the modulation of tau will influence Abeta pathology. To address this question, we used the 3xTg-AD mouse model, which is characterized by the age-dependent buildup of both plaques and tangles. Here we show that genetically augmenting tau levels and hyperphosphorylation in the 3xTg-AD mice has no effect on the onset and progression of Abeta pathology. These data suggest that the link between Abeta and tau is predominantly if not exclusively unidirectional, which is consistent with the Abeta cascade hypothesis and may explain why tauopathy-only disorders are devoid of any Abeta pathology.

Authors+Show Affiliations

Oddo S
Department of Neurobiology and Behavior, Institute for Brain Aging and Dementia, University of California, Irvine, California, USA.
Caccamo A
No affiliation info available
Cheng D
No affiliation info available
Jouleh B
No affiliation info available
Torp R
No affiliation info available
LaFerla FM
No affiliation info available

MeSH

Age FactorsAlzheimer DiseaseAmyloid Precursor Protein SecretasesAmyloid beta-PeptidesAnimalsAntibodies, MonoclonalDisease Models, AnimalDisease ProgressionEnzyme-Linked Immunosorbent AssayGene Expression Regulation, EnzymologicHumansMiceMice, TransgenicMicroscopy, Electron, TransmissionNeurofibrillary TanglesPhosphoprotein PhosphatasesPhosphorylationPlaque, Amyloidtau Proteins

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17472708

Citation

Oddo, Salvatore, et al. "Genetically Augmenting Tau Levels Does Not Modulate the Onset or Progression of Abeta Pathology in Transgenic Mice." Journal of Neurochemistry, vol. 102, no. 4, 2007, pp. 1053-63.
Oddo S, Caccamo A, Cheng D, et al. Genetically augmenting tau levels does not modulate the onset or progression of Abeta pathology in transgenic mice. J Neurochem. 2007;102(4):1053-63.
Oddo, S., Caccamo, A., Cheng, D., Jouleh, B., Torp, R., & LaFerla, F. M. (2007). Genetically augmenting tau levels does not modulate the onset or progression of Abeta pathology in transgenic mice. Journal of Neurochemistry, 102(4), 1053-63.
Oddo S, et al. Genetically Augmenting Tau Levels Does Not Modulate the Onset or Progression of Abeta Pathology in Transgenic Mice. J Neurochem. 2007;102(4):1053-63. PubMed PMID: 17472708.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Genetically augmenting tau levels does not modulate the onset or progression of Abeta pathology in transgenic mice. AU - Oddo,Salvatore, AU - Caccamo,Antonella, AU - Cheng,David, AU - Jouleh,Bahareh, AU - Torp,Reidun, AU - LaFerla,Frank M, Y1 - 2007/04/30/ PY - 2007/5/3/pubmed PY - 2007/10/5/medline PY - 2007/5/3/entrez SP - 1053 EP - 63 JF - Journal of neurochemistry JO - J Neurochem VL - 102 IS - 4 N2 - The two hallmark pathologies of Alzheimer's disease (AD) are amyloid plaques, composed of the small amyloid-beta (Abeta) peptide, and neurofibrillary tangles, comprised aggregates of the microtubule binding protein, tau. The molecular linkage between these two lesions, however, remains unknown. Based on human and mouse studies, it is clear that the development of Abeta pathology can trigger tau pathology, either directly or indirectly. However, it remains to be established if the interaction between Abeta and tau is bidirectional and whether the modulation of tau will influence Abeta pathology. To address this question, we used the 3xTg-AD mouse model, which is characterized by the age-dependent buildup of both plaques and tangles. Here we show that genetically augmenting tau levels and hyperphosphorylation in the 3xTg-AD mice has no effect on the onset and progression of Abeta pathology. These data suggest that the link between Abeta and tau is predominantly if not exclusively unidirectional, which is consistent with the Abeta cascade hypothesis and may explain why tauopathy-only disorders are devoid of any Abeta pathology. SN - 0022-3042 UR - https://www.unboundmedicine.com/medline/citation/17472708/Genetically_augmenting_tau_levels_does_not_modulate_the_onset_or_progression_of_Abeta_pathology_in_transgenic_mice_ DB - PRIME DP - Unbound Medicine ER -