徳島大学 教育・研究者情報データベース(EDB)

1. 藤田 浩司([徳島大学.大学院医歯薬学研究部.医学域.先端医学教育研究プロジェクト]/[徳島大学.大学院医歯薬学研究部.医学域.医科学部門.内科系.臨床神経科学]/[徳島大学.病院.診療科.内科.脳神経内科])

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2. 和泉 唯信([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.内科系.臨床神経科学]/[徳島大学.病院.診療科.内科.脳神経内科])

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3. 梶 龍兒([徳島大学.研究支援・産官学連携センター])

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(英) [Inflammatory mechanisms in amyotrophic lateral sclerosis].

(英) Neuroinflammation is a pathological hallmark in human amyotrophic lateral sclerosis (ALS) patients and in the transgenic models of the disease. The importance of glial cell activation and pro-inflammatory cytokines in ALS has been confirmed by numerous studies. For instance, tumor necrosis factor- (TNF-), a major pro-inflammatory cytokine, activates microglia and cause neurotoxicity in motor neurons. More recently, the relationship of nuclear factor-B (NF-B) and motor neuron degeneration has garnered attention since optineurin (OPTN) mutations were reported in familial ALS. OPTN negatively regulates TNF--induced NF-B activation, but OPTN mutations can lead to dysinhibition of NF-B-induced neurotoxicity. Notably, OPTN-positive inclusions are observed not only in familial ALS with OPTN mutation but also in sporadic ALS and in familial ALS with SOD1 and fused in sarcoma mutations, suggesting that OPTN- and NF-B-related pathways are relevant to the general pathomechanisms of ALS. In this review, we discuss inflammatory aspects of ALS comprising the roles of cytokines, glial cells, and T cells.

1. (英) Amyotrophic Lateral Sclerosis
2. (英) Animals
3. (英) Chemokines
4. 細胞質分裂(cytokinesis)
5. (英) Humans
6. 炎症(inflammation)
7. (英) NF-kappa B
8. (英) Transcription Factor TFIIIA

1. (英) Article.Affiliation: Department of Clinical Neuroscience, The University of Tokushima Graduate School, Japan.

2. (英) Article.PublicationTypeList.PublicationType: English Abstract

3. (英) Article.PublicationTypeList.PublicationType: Journal Article

4. (英) Article.PublicationTypeList.PublicationType: Review