ER stress and UPR in Alzheimer's disease: mechanisms, pathogenesis, treatments.
ER stress and UPR in Alzheimer's disease: mechanisms, pathogenesis, treatments.
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DOI：
10.1038/s41419-022-05153-5
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发表时间：
2022-08-15
影响因子：
9
通讯作者：
Pratico, Domenico
中科院分区：
文献类型：
--
作者：
Ajoolabady, Amir;Lindholm, Dan;Ren, Jun;Pratico, Domenico
阿尔茨海默病（AD）是一种毁灭性的神经退行性疾病，其特征是记忆和认知功能逐渐丧失，给全球医疗保健系统带来沉重负担。目前干扰 AD 潜在疾病过程的疗法仍在开发中。尽管许多努力都集中在 Aβ 的毒性形式上以有效治疗 AD，但考虑到迄今为止的结果并不令人满意，检查其他靶点和治疗方法也至关重要。内质网 (ER) 应激是指内质网内未折叠或错误折叠蛋白质的积累，从而扰乱内质网和细胞稳态。新的证据表明，内质网应激会导致 AD 的发生和发展。彻底阐明 AD 病理学中的 ER 应激机制可能有助于开辟新的治疗途径来管理这种破坏性病症，以缓解认知痴呆症状。在此，我们的目的是破译 ER 应激在 AD 发病机制中的独特作用，回顾主要发现和现有争议，试图总结 AD 病理生理学管理中合理的治疗干预措施。
Alzheimer’s disease (AD) is a devastating neurodegenerative disorder characterized by gradual loss of memory and cognitive function, which constitutes a heavy burden on the healthcare system globally. Current therapeutics to interfere with the underlying disease process in AD is still under development. Although many efforts have centered on the toxic forms of Aβ to effectively tackle AD, considering the unsatisfactory results so far it is vital to examine other targets and therapeutic approaches as well. The endoplasmic reticulum (ER) stress refers to the build-up of unfolded or misfolded proteins within the ER, thus, perturbing the ER and cellular homeostasis. Emerging evidence indicates that ER stress contributes to the onset and development of AD. A thorough elucidation of ER stress machinery in AD pathology may help to open up new therapeutic avenues in the management of this devastating condition to relieve the cognitive dementia symptoms. Herein, we aim at deciphering the unique role of ER stress in AD pathogenesis, reviewing key findings, and existing controversy in an attempt to summarize plausible therapeutic interventions in the management of AD pathophysiology.
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影响因子：
2.9
作者：
Ajoolabady A;Aslkhodapasandhokmabad H;Henninger N;Demillard LJ;Nikanfar M;Nourazarian A;Ren J
通讯作者：
Ren J
影响因子：
3.8
作者：
de la Monte SM
通讯作者：
de la Monte SM
影响因子：
4.8
作者：
Duran-Aniotz C;Martínez G;Hetz C
通讯作者：
Hetz C
影响因子：
4
作者：
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通讯作者：
Scheper, Wiep
影响因子：
5.6
作者：
Elvira, Rosalie;Cha, Sun Joo;Han, Jaeseok
通讯作者：
Han, Jaeseok