AD模型 z-bio 2021-08-10 555

　　OBJECTIVE: To observe the relationship between changes in hippocampal metabolites of APP/PS1 transgenic mice and ultramicroscopic pathological changes, so that genetic mice can be used more effectively for experimental research on Alzheimer's disease (AD).

　　Method: Through a new object recognition experiment, the learning and memory abilities of wild mice of the same age and background as APP/PS1 transgenic mice were compared. Comparing the two groups of hippocampal N-acetylaspartic acid (NAA); nerve cells and stars by hydrogen proton magnetic resonance spectroscopy (1HMRS), inositol (mI), choline (Cho), glutamic acid (Glu) and other metabolites The ultrafine structure of glial cells was observed with a transmission electron microscope.

　　Result: Compared with wild mice, the learning and memory ability of transgenic mice was decreased, and the difference between the two groups was statistically significant (Pu003c0.05). The ratio of AA to creatine (Cr) in the hippocampus is significantly reduced. (Pu003c0.05), increased mI/Cr and Cho/Cr (Pu003c0.05); mitochondrial degeneration and phagocytosis of neurons and astrocytes, increased number of secondary lysosomes, excessive activation of astrocytes , Malnutrition synaptic phagocytosis.

　　Conclusion: The changes of NAA, mI, Cho and other metabolites in the hippocampus of APP/PS1 transgenic mice show the pathological characteristics of abnormal inflammation and synaptic structure destruction caused by β-amyloid during AD. The PS1 gene mouse may reflect that it is better used to provide an experimental basis for AD research.