Publications by authors named "Xuetao Qi"

Postoperative cognitive dysfunction (POCD) is common in the aged population and associated with poor clinical outcomes. Irisin, an endogenous molecule that mediates the beneficial effects of exercise, has shown neuroprotective potential in several models of neurological diseases. Here we show that preoperative serum level of irisin is reduced in dementia patients over the age of 70.

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  • COVID-19 may heighten the risk of memory decline and Alzheimer's disease, but direct evidence of its impact on brain changes is still limited.
  • A study of postmortem brain samples revealed abnormal levels of hyperphosphorylated tau protein and prolonged glial activation in key brain areas months after COVID-19 recovery, despite no evidence of the virus in those regions.
  • While COVID-19 didn't significantly affect beta-amyloid levels or neuron counts, the findings suggest a potential link between post-COVID neurological changes and an increased risk of Alzheimer's disease.
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  • Over-generalized fear is an inappropriate reaction to non-threatening situations, common in PTSD and anxiety disorders, and linked to specific brain cells in the dorsal dentate gyrus (dDG).
  • Research using advanced imaging techniques shows that fear engram cells in the dDG are more actively involved in generalized fear responses in similar contexts.
  • The study suggests that modifying these fear memories or activating a specific neuronal pathway can reduce fear generalization, shedding light on the underlying brain mechanisms involved.
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A large proportion of patients with chronic pain experience co-morbid anxiety. The medial prefrontal cortex (mPFC) is proposed to underlie this comorbidity, but the molecular and neuronal mechanisms are not fully understood. Here, we reported that impaired neuronal macroautophagy in the prelimbic cortical (PrL) subregion of the mPFC paralleled the occurrence of anxiety-like behaviors in rats with chronic spared nerve injury (SNI).

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Chronic pain is a significant health problem worldwide. Recent evidence has suggested that the ventral hippocampus is dysfunctional in humans and rodents, with decreased neuronal excitability and connectivity with other brain regions, parallel pain chronicity, and persistent nociceptive hypersensitivity. But the molecular mechanisms underlying hippocampal modulation of pain remain poorly elucidated.

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Chronic pain is one of the most significant medical problems throughout the world. Recent evidence has confirmed the hippocampus as an active modulator of pain chronicity, but the underlying mechanisms remain unclear. Using in vivo electrophysiology, we identify a neural ensemble in the ventral hippocampal CA1 (vCA1) that shows inhibitory responses to noxious but not innocuous stimuli.

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Pain chronicity involves unpleasant experience in both somatosensory and affective aspects, accompanied with the prefrontal cortex (PFC) neuroplastic alterations. However, whether specific PFC neuronal ensembles underlie pain chronicity remains elusive. Here we identify a nociceptive neuronal ensemble in the dorsomedial prefrontal cortex (dmPFC), which shows prominent reactivity to nociceptive stimuli.

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A genome editing technique based on the clustered regularly interspaced short palindromic repeats (CRISPR)-associated endonuclease Cas9 enables efficient modification of genes in various cell types, including neurons. However, neuronal ensembles even in the same brain region are not anatomically or functionally uniform but divide into distinct subpopulations. Such heterogeneity requires gene editing in specific neuronal populations.

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