当前位置：
X-MOL 学术
›
Aging Cell
›
论文详情
Our official English website, www.x-mol.net, welcomes your
feedback! (Note: you will need to create a separate account there.)
Anti-inflammatory treatment rescues memory deficits during aging in nfkb1-/- mice.
Aging Cell ( IF 8.0 ) Pub Date : 2020-09-11 , DOI: 10.1111/acel.13188 Edward Fielder 1 , Clare Tweedy 2 , Caroline Wilson 3 , Fiona Oakley 3 , Fiona E N LeBeau 2 , João F Passos 4, 5 , Derek A Mann 3 , Thomas von Zglinicki 1 , Diana Jurk 1, 4, 5
Aging Cell ( IF 8.0 ) Pub Date : 2020-09-11 , DOI: 10.1111/acel.13188 Edward Fielder 1 , Clare Tweedy 2 , Caroline Wilson 3 , Fiona Oakley 3 , Fiona E N LeBeau 2 , João F Passos 4, 5 , Derek A Mann 3 , Thomas von Zglinicki 1 , Diana Jurk 1, 4, 5
Affiliation
|
Chronic inflammation is a common feature of many age‐related conditions including neurodegenerative diseases such as Alzheimer's disease. Cellular senescence is a state of irreversible cell‐cycle arrest, thought to contribute to neurodegenerative diseases partially via induction of a chronic pro‐inflammatory phenotype. In this study, we used a mouse model of genetically enhanced NF‐κB activity (nfκb1−/−), characterized by low‐grade chronic inflammation and premature aging, to investigate the impact of inflammaging on cognitive decline. We found that during aging, nfkb1−/− mice show an early onset of memory loss, combined with enhanced neuroinflammation and increased frequency of senescent cells in the hippocampus and cerebellum. Electrophysiological measurements in the hippocampus of nfkb1−/− mice in vitro revealed deficits in gamma frequency oscillations, which could explain the decline in memory capacity. Importantly, treatment with the nonsteroidal anti‐inflammatory drug (NASID) ibuprofen reduced neuroinflammation and senescent cell burden resulting in significant improvements in cognitive function and gamma frequency oscillations. These data support the hypothesis that chronic inflammation is a causal factor in the cognitive decline observed during aging.
中文翻译：
抗炎治疗可挽救 nfkb1-/- 小鼠衰老过程中的记忆缺陷。
慢性炎症是许多与年龄相关的疾病的共同特征，包括阿尔茨海默病等神经退行性疾病。细胞衰老是一种不可逆的细胞周期停滞状态，被认为部分通过诱导慢性促炎症表型而导致神经退行性疾病。在这项研究中，我们使用基因增强的 NF-κB 活性 ( nfκb1 −/− ) 小鼠模型（以低度慢性炎症和过早衰老为特征）来研究炎症对认知能力下降的影响。我们发现，在衰老过程中， nfkb1 −/−小鼠表现出较早出现的记忆丧失，同时神经炎症增强，海马和小脑中衰老细胞的频率增加。体外nfkb1 −/−小鼠海马体的电生理测量显示伽马频率振荡缺陷，这可以解释记忆能力的下降。重要的是，使用非甾体抗炎药（NASID）布洛芬治疗可减少神经炎症和衰老细胞负担，从而显着改善认知功能和伽马频率振荡。这些数据支持这样的假设：慢性炎症是衰老过程中认知能力下降的一个致病因素。
更新日期：2020-10-23
中文翻译：
抗炎治疗可挽救 nfkb1-/- 小鼠衰老过程中的记忆缺陷。
慢性炎症是许多与年龄相关的疾病的共同特征，包括阿尔茨海默病等神经退行性疾病。细胞衰老是一种不可逆的细胞周期停滞状态，被认为部分通过诱导慢性促炎症表型而导致神经退行性疾病。在这项研究中，我们使用基因增强的 NF-κB 活性 ( nfκb1 −/− ) 小鼠模型（以低度慢性炎症和过早衰老为特征）来研究炎症对认知能力下降的影响。我们发现，在衰老过程中， nfkb1 −/−小鼠表现出较早出现的记忆丧失，同时神经炎症增强，海马和小脑中衰老细胞的频率增加。体外nfkb1 −/−小鼠海马体的电生理测量显示伽马频率振荡缺陷，这可以解释记忆能力的下降。重要的是，使用非甾体抗炎药（NASID）布洛芬治疗可减少神经炎症和衰老细胞负担，从而显着改善认知功能和伽马频率振荡。这些数据支持这样的假设：慢性炎症是衰老过程中认知能力下降的一个致病因素。
京公网安备 11010802027423号