动物造模,基因AD模型 z-bio 2021-01-18 284

　　OBJECTIVE: To observe the relationship between changes in hippocampal metabolites of APP/PS1 transgenic mice and ultramicroscopic pathological changes, so as to provide evidence for genetic mice to be better used in 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. We compared the two groups of hippocampal N-acetylaspartic acid (NAA) by hydrogen proton magnetic resonance spectroscopy (1HMRS). ), inositol (mI), choline (Cho), glutamate (Glu) and other metabolites; the superstructure of nerve cells and stellate cells was observed under a transmission electron microscope. Compared with wild mice, the learning and memory abilities of transgenic mice were decreased, and the difference between the two groups was statistically significant (P\u003c0.05); the ratio of hippocampal creatine (Cr) AA and AA was significantly reduced (P \u003c0.05), increased mI/Cr and Cho/Cr (P\u003c0.05); mitochondrial degeneration and neuron and stellate impetigo, increased number of secondary lysosomes, excessive activation of stellate cells, and nutrition Phagocytosis of bad synapses.

　　 Conclusion: The changes of NAA, mI, Cho and other metabolites in the hippocampus of APP/PS1 transgenic mice are the pathological features of abnormal inflammation and synaptic structure induced by β-amyloid in the pathological process of AD.