Li Shijie. Dynamic changes of hippocampal neuron mitochondria in APP/PS1 double transgenic Alzheimer’s disease mice at different months[J]. Journal of Chongqing Medical University, 2021,46(10):1141-1146.
Li Shijie. Dynamic changes of hippocampal neuron mitochondria in APP/PS1 double transgenic Alzheimer’s disease mice at different months[J]. Journal of Chongqing Medical University, 2021,46(10):1141-1146. DOI: 10.13406/j.cnki.cyxb.002904.
Objective: To detect the dynamic changes of mitochondria in hippocampal neurons of APP/PS1 double transgenic Alzheimer’s disease (AD) mice at different months and explore its significance. Methods: Twenty male APP/PS1 double transgenic AD mice were selected and divided into 3-month-old group
6-month-old group
9-month-old group and 12-month-old group
with C57 mice as the control group. The morphological changes of mitochondria in hippocampal neurons were observed by electron microscope. Western blot was used to detect the expression levels of autophagy-related proteins LC3 and P62
the expression levels of mitochondrial autophagy-related proteins PINK1
Parkin and Miro1
and the expression levels of mitochondrial outer membrane protein Tom20. Results: Electron microscopy study showed that the pathological changes of mitochondria damage in hippocampus neurons of APP/PS1 double transgenic AD mice were gradually aggravated with the increase of months
namely that
mitochondria showed obviously edema
transparent and irregularly arranged
broken or even disappeared cristae. Western blot results showed that compared with the wild mouse group
the expression levels of LC3
P62
PINK1 and Parkin protein were significantly increased in 6-month-old
9-month-old and 12-month-old mice (P<0.05)
while Miro1 protein was significantly decreased (P<0.05)
and the expression level of Tom20 had no statistical significance (P>0.05). Conclusion: With the increase of age
the pathological changes of mitochondria in hippocampal neurons are dynamic in APP/PS1 double transgenic AD mice. Mitophagy is dynamically enhanced but accompanied by mitochondrial clearance obstacles.