课题组成立后发表的第一份研究工作，报道COVID-19恢复后一定时期内，老年人群大脑海马及内嗅皮层出现类似AD样的tau蛋白磷酸化水平升高、胶质激活及炎症因子表达增加现象，提示老年人群感染COVID-19可能会增加AD患病风险。齐雪涛、袁书路、丁九阳（贵州医科大学）为共同第一作者。

Coronavirus disease 2019 (COVID-19) has been suggested to increase the risk of memory decline and Alzheimer’s disease (AD), the main cause of dementia in the elderly. However, direct evidence about whether COVID-19 induces AD-like neuropathological changes in the brain, especially post recovery from acute infection, is still lacking. Here, using postmortem human brain samples, we found abnormal accumulation of hyperphosphorylated tau protein in the hippocampus and medial entorhinal cortex 4~13 months post clinically recovery from acute COVID-19, together with prolonged activation of glia cells and increases in inflammatory factors, even though no SARS-COV-2 invasion was detected in these regions. By contrast, COVID-19 did not change beta-amyloid deposition and hippocampal neuron number, and had limited effects on AD-related pathological phenotypes in olfactory circuits including olfactory bulb, anterior olfactory nucleus, olfactory tubercle, piriform cortex and lateral entorhinal cortex. These results provide neuropathological evidences linking COVID-19 with prognostic increase of risk for AD.

原文：Qi X#, Yuan S#, Ding J#, Sun W, Shi Y, Xing Y, Liu Z, Yao Y, Fu S, Sun B, Qi X, Xia B, Liu F, Yi M, Mao J, Wan Y*, Zheng J*. Emerging signs of Alzheimer-like tau hyperphosphorylation and neuroinflammation in the brain post recovery from COVID-19. Aging Cell. 2024. 00, e14352. https://doi.org/10.1111/acel.14352