Neural Regeneration Research ›› 2014, Vol. 9 ›› Issue (4): 394-401.doi: 10.4103/1673-5374.128243

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Characterization of hippocampal Cajal-Retzius cells during development in a mouse model of Alzheimer’s disease (Tg2576)

Dongming Yu1, Wenjuan Fan2, Ping Wu1, Jiexin Deng1, Jing Liu1, Yanli Niu1, Mingshan Li1, Jinbo Deng1   

  1. 1 Institute of Neurobiology, School of Life Science, Henan University, Kaifeng, Henan Province, China
    2 Laboratory of Molecular Medicine, Luohe Medical College, Luohe, Henan Province, China
  • Received:2014-01-22 Online:2014-02-25 Published:2014-02-25
  • Contact: Jinbo Deng, Ph.D., Institute of Neurobiology, School of Life Science, Henan University, Kaifeng 475004, Henan Province, China
  • Supported by:

    This work was supported by the National Natural Science Foundation of China, No. 31070952, 81071029; the Joint Funds of the NSFC with Henan Provence Government for Fostering Talents, No. U1204809, and the Henan Province Science Research Project, No. 132102310111.

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Abstract:

Cajal-Retzius cells are reelin-secreting neurons in the marginal zone of the neocortex and hippocampus. The aim of this study was to investigate Cajal-Retzius cells in Alzheimer’s disease pathology. Results revealed that the number of Cajal-Retzius cells markedly reduced with age in both wild type and in mice over-expressing the Swedish double mutant form of amyloid precursor protein 695 (transgenic (Tg) 2576 mice). Numerous reelin-positive neurons were positive for activated caspase 3 in Tg2576 mice, suggesting that Cajal-Retzius neuronal loss occurred via apoptosis in this Alzheimer’s disease model. Compared with wild type, the number of Cajal-Retzius cells was significantly lower in Tg2576 mice. Western blot analysis confirmed that reelin levels were markedly lower in Tg2576 mice than in wild-type mice. The decline in Cajal-Retzius cells in Tg2576 mice was found to occur concomitantly with the onset of Alzheimer’s disease amyloid pathology and related behavioral deficits. Overall, these data indicated that Cajal-Retzius cell loss occurred with the onset and development of Alzheimer’s disease.

Key words: nerve regeneration, neurodegeneration, Alzheimer’s disease, Cajal-Retzius cells, hippocampus, development, neuronal apoptosis, reelin, Tg2576 mice, NSFC grant, neural regeneration