Brain inflammaging in the pathogenesis of late-life depression.

IF 3.4 3区生物学 Q3 CELL BIOLOGY

Human Cell Pub Date : 2024-10-26 DOI:10.1007/s13577-024-01132-4

Toshiaki Ishizuka, Wataru Nagata, Keiichi Nakagawa, Sayaka Takahashi

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Abstract

Late-life depression (LLD) is a prevalent mental disorder among older adults. Previous studies revealed that many pathologic factors are associated with the onset and development of LLD. However, the precise mechanisms that cause LLD remain elusive. Aging induces chronic inflammatory changes mediated by alterations of immune responses. The chronic systemic inflammation termed "inflammaging" is linked to the etiology of aging-related disorders. Aged microglia induce senescence-associated secretory phenotype (SASP) and transition to M1-phenotype, cause neuroinflammation, and diminish neuroprotective effects. In addition, there is an age-dependent loss of blood-brain barrier (BBB) integrity. As the BBB breakdown can lead to invasion of immune cells into brain parenchyma, peripheral immunosenescence may cause microglial activation and neuroinflammation. Therefore, it is suggested that these mechanisms related to brain inflammaging may be involved in the pathogenesis of LLD. In this review, we described the role of brain inflammaging in LLD. Pharmacologic approaches to prevent brain inflammaging appears to be a promising strategy for treating LLD.

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晚年抑郁症发病机制中的大脑炎症。

晚年抑郁症（LLD）是老年人中普遍存在的一种精神障碍。以往的研究表明，许多病理因素与晚年抑郁症的发病和发展有关。然而，导致晚年抑郁症的确切机制仍然难以捉摸。衰老会诱发由免疫反应改变介导的慢性炎症变化。被称为 "炎症老化 "的慢性全身性炎症与衰老相关疾病的病因有关。衰老的小胶质细胞会诱导衰老相关分泌表型（SASP）并向 M1 表型转变，引起神经炎症并削弱神经保护作用。此外，血脑屏障（BBB）的完整性也会随着年龄的增长而丧失。由于血脑屏障的破坏会导致免疫细胞侵入脑实质，外周免疫衰老可能会引起小胶质细胞活化和神经炎症。因此，有人认为这些与脑部炎症相关的机制可能与 LLD 的发病机制有关。在这篇综述中，我们描述了脑部炎症在 LLD 中的作用。预防脑部炎症的药物治疗方法似乎是治疗 LLD 的一种有前途的策略。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Human Cell CELL BIOLOGY-

CiteScore

5.90

自引率

2.30%

发文量

176

审稿时长

4.5 months

期刊介绍： Human Cell is the official English-language journal of the Japan Human Cell Society. The journal serves as a forum for international research on all aspects of the human cell, encompassing not only cell biology but also pathology, cytology, and oncology, including clinical oncology. Embryonic stem cells derived from animals, regenerative medicine using animal cells, and experimental animal models with implications for human diseases are covered as well. Submissions in any of the following categories will be considered: Research Articles, Cell Lines, Rapid Communications, Reviews, and Letters to the Editor. A brief clinical case report focusing on cellular responses to pathological insults in human studies may also be submitted as a Letter to the Editor in a concise and short format. Not only basic scientists but also gynecologists, oncologists, and other clinical scientists are welcome to submit work expressing new ideas or research using human cells.