Emerging signs of Alzheimer‐like tau hyperphosphorylation and neuroinflammation in the brain post recovery from COVID‐19
Xuetao Qi, Shulu Yuan, Jiuyang Ding, Weiqi Sun, Yajiao Shi, Yuanwei Xing, Zilong Liu, Yun Yao, Su Fu, Baofei Sun, Xiaolan Qi, Bing Xia, Fengyu Liu, Ming Yi, Jian Mao, You Wan, Jie Zheng
Abstract
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 within 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.