Chu Yanan,Song Chong,He Guiqiong,Liu Gang,Wang Lingxi,Zhou Zefen.Expression and distribution of presenilin enhancer-2 in brain of APP/PS1 double transgenic mice[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(24):2479-2483.
Chu Yanan,Song Chong,He Guiqiong,Liu Gang,Wang Lingxi,Zhou Zefen.Expression and distribution of presenilin enhancer-2 in brain of APP/PS1 double transgenic mice[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(24):2479-2483.DOI:
Objective To examine the expression and distribution of presenilin enhancer-2 (Pen-2)
an essential component of γ-secretase complex
in the brain of APP/PS1 double transgenic mice
so as to clarify the relationship between Pen-2 and Alzheimer’s disease (AD). Methods Offspring which were bred by APP/PS1 double transgenic AD mice were genotyped. Immunohistochemical staining was used to check the distribution and expression of Pen-2 in the brain of 8-month-old APP/PS1 double transgenic AD model mice and its age-matched wild-type littermates. Results Pen-2 was widely expressed throughout almost all the regions of brain in APP/PS1 double transgenic mice
including the cerebral cortex
hippocampus
basal nuclei
rhinencephalon
cerebellum
brainstem
and so on. While senile plaques (SP) were selectively distributed in the cerebral cortex
hippocampus
and rhinencephalon. The distribution of Pen-2 was much more extensive than that of SP in the brain of AD model mice. Meanwhile
Pen-2-positive neurons in AD model mice (2.09±0.33) was more dark-stained than that in wildtype controls (1.29±0.31); Furthermore
both the cell membrane and cytoplasm of Pen-2-positive neurons were heavily stained in the AD mice
while in the wildtype littermates
only membrane and its surrounding of Pen-2-positive neurons were relatively dark-stained
and the cytoplasma was mildly or not stained. Conclusion Distribution and expression of Pen-2 in the brain of APP/PS1 double transgenic mouse model is different from its wildtype littermates. These differences may indicate that Pen-2 is tightly related to SP formation and AD pathogenesis.