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Expression of aquaporins in a transgenic mouse model of Alzheimer's disease

Cerebrospinal Fluid Research
Springer (Biomed Central Ltd.)
Publication Date
DOI: 10.1186/1743-8454-7-s1-s31
  • Oral Presentation
  • Biology
  • Chemistry
  • Medicine


Expression of aquaporins in a transgenic mouse model of Alzheimer's disease ORAL PRESENTATION Open Access Expression of aquaporins in a transgenic mouse model of Alzheimer’s disease Sic L Chan*, Meenu Madan, Srinu Chigurupati, Jogi V Pattisapu From 54th Annual Meeting of the Society for Research into Hydrocephalus and Spina Bifida Vancouver, Canada. 7-10 July 2010 Background Several studies reported altered expression of the water channels, aquaporins (AQPs), in brains of Alzheimer’s dis- ease (AD) but the relevance of the observed changes with respect to the neuropathology of AD is poorly understood. Because aberrant processing of the amyloid precursor pro- tein (APP) to amyloid beta-peptide (A-beta), the principle component of amyloid plaques, is central to the pathogen- esis of AD, we sought to determine the temporal and spa- tial expression of AQPs in the cortex and hippocampus of the triple transgenic mouse model of Alzheimer’s disease (3xTg-AD) and to elucidate whether AQPs contribute directly to the aberrant processing of APP into A-beta. Materials and methods We used a mutant strain 3xTg AD mice, which harbor the human presenilin1 (PS1 M146V), APP (APPSwe) and tau (tauP301L) transgenes and develop age-dependent accumulation of both plaques and tangle pathologies in a pattern consistent with AD. Cortex and hippocampus (free of choroid plexus) were harvested from 2, 6 and 14 month-old 3xTg AD and wild type (C57) mice. AQP1 and AQP4 protein expression was quantified by immu- noblotting, and immunohistochemistry was performed on frozen sections probed with anti-AQP1 and anti- AQP4 antibodies. AQP1 and AQP4 mRNA expression was measured by real-time PCR. Results AQP1 but not AQP4 was detected at significantly higher levels in 3xTg-AD mice at 12 months when compared with younger mice at 2 and 6 months of age. No significant changes in the expression of AQP1 and AQP4 were observed at any ages in non-transgenic control mice. Immunohistochemical analyses to deter- mine co-loc

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