Objective To identify co-expressed genes and potential comorbidity mechanisms between Alzheimer's disease(AD)and epilepsy with publicly available single-cell transcriptome sequencing data from human brains,fol-lowed by functional validation in APP/PS1 double transgenic AD mouse models expressing the chimerical Mo/HuAPP695swe amyloid precursor protein and mutant PS1-dE9 presenilin 1.Methods The single-cell transcriptome sequencing data of brain tissue from AD and epilepsy patients were collected from gene expression omnibus(GEO)database followed by cell clustering,differential expression analysis and gene ontology(GO)func-tional enrichment analysis using R-based tools such as Seurat and cluster Profiler and video electroencephalogram (vEEG)monitoring and Western blot experiments.Results A total of eight major brain cell types were identified,with neurons and glial cells exhibiting shared differentially expressed genes between AD and epilepsy.These co-ex-pressed genes were significantly clustered in pathways related to metal ion homeostasis,synaptic transmission,oxi-dative stress,and immune activation,which suggested common pathological mechanisms involving in synaptic dys-function and neuro-inflammation in both disorders.The vEEG recordings of APP/PS1 mouse model of AD showed 30％of mice exhibited high-frequency epileptic seizures,while 70％showed low-frequency seizure activity.Subse-quent validation in the prefrontal cortex of AD mice confirmed up-regulated expression of key molecular markers(HES5,c-FOS,and RPL10A)identified through single-cell sequencing analysis.Conclusions AD and epilepsy share gene co-expression profiles and functional pathways in specific cell types.The results of research provide a theoretical support for further elucidating their comorbidity mechanisms and developing targeted therapeutic strategy.

[Objective] To observe the curative effects and the influence of activity of Superoxide dismutase(SOD) and contents of Maleic dialdehyde(MDA) of Qingchangyukui Gel in Rats with Experimental Ulcerative Colitis. [Method]Ulcerative Colitis model was established in Wistar rats by injecting trinitro-benzene-sulfonic acid (TNBS)into anus, and then treated with Qingchangyukui Gel and salisy-lazosulfa-pyridine(SASP) respectively. Isolating the colon and measuring the SOD and MDA after treating for two weeks. [Results]Colon mucous membrane in the model group had serious erosion, ulcer, damaging of glandular organ, high inflammation grade; activity of SOD in model group was significantly lower than in normal group and contents of MDA increased. The other groups, especially in Qingchangyukui Gel group, had different levels of inflammation repairing, ulcer healing, increasing of SOD and reducing of MDA. [Conclusion]TNBS can cause Colon mucous membrane inflammation and ulcer, reducing of SOD and increasing of MDA , which are the typical pathological change of Ulcerative Colitis; the Qingchangyukui Gel has the effects of increasing the activity of SOD and reducing contents of MDA, therefore it can effectively treat the UC rat.