| First Author | Wang X | Year | 2024 |
| Journal | Brain Res | Volume | 1825 |
| Pages | 148711 | PubMed ID | 38092296 |
| Mgi Jnum | J:344451 | Mgi Id | MGI:7572205 |
| Doi | 10.1016/j.brainres.2023.148711 | Citation | Wang X, et al. (2023) Asthma aggravates alzheimer's disease by up-regulating NF- kappaB signaling pathway through LTD4. Brain Res 1825:148711 |
| abstractText | Clinical studies have shown that asthma is a risk factor for dementia or Alzheimer's disease (AD). To investigate whether asthma aggravates AD in APP/PS1 mice and explore the potential mechanisms, an asthma model was established using six-month-old APP/PS1 mice, and montelukast was used as a therapeutic agent in APP/PS1 mice with asthma. The Morris water maze test showed that asthma aggravates spatial learning and memory abilities. Asthma also upregulates the NF-kappaB inflammatory pathway in APP/PS1 mice and promotes the expression of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), amyloid-beta (Abeta) deposition, neuronal damage, synaptic plasticity deficiency, activation of microglia and astrocytes. The level of LTD4 and its receptor CysLT1R in the hippocampus of APP/PS1 mice after the asthma modeling was established was higher than that in APP/PS1 mice, suggesting that asthma may affect the pathology of AD through LTD4 and its receptor Cys-LT1R. Montelukast ameliorates these pathological changes and cognitive impairment. These results suggest that asthma aggravates AD pathology and cognitive impairment of APP/PS1 mice via upregulation of the NF-kappaB inflammatory pathway, and montelukast ameliorates these pathological changes. |
