アミロイドβタンパク質
別名:アミロイドβタンパク、アミロイドβ蛋白、アミロイドβ蛋白質、アミロイドβ、βアミロイド、βアミロイドタンパク、βアミロイドタンパク質、βアミロイド蛋白、βアミロイド蛋白質
英語:amyloid beta protein、amyloid β protein、Aβ、Beta amyloid
アミロイドβタンパク質
36-43個のペプチドからなる、βシート構造を含む異常タンパク質。アミロイドβタンパク質は、アルツハイマー型認知症(アルツハイマー病)の原因となるか、あるいは少なくとも深く関与することが知られている。
アミロイドβタンパク質は、アミロイド前駆体タンパク質(APP)という正常なタンパク質が、酵素によって分解されることにより生じる異常タンパク質である。アミロイドβタンパク質は凝集してアミロイド線維を形成し、神経細胞の外に沈着、蓄積する性質を持つ。アミロイド線維は神経細胞に対して強い毒性を持ち、細胞死を引き起こすことが知られている。
アミロイドβタンパク質の沈着が起こった箇所は、脳の切片を染色すると「老人斑」として確認される。老人斑は健常者でも加齢に伴い増加するが、アルツハイマー型認知症の患者の脳内ではより多く、脳の全体にわたって確認される。アミロイドβタンパク質は中性エンドペプチダーゼという酵素によって分解を受けるが、アルツハイマー型認知症の患者では、その酵素の活性が弱くなる傾向が見られる。
アルツハイマー型認知症の主要な原因としてアミロイドβタンパク質を挙げる説は「アミロイド仮説(アミロイド・カスケード仮説)」と呼ばれており、最も有力な説ともいわれている。アミロイド前駆体タンパク質(APP)のコード遺伝子を持つ21番染色体に異常があるダウン症候群の患者は、アルツハイマー型認知症をほぼ確実に発症することが知られており、それがアミロイド仮説の根拠の一つとされている。また、アルツハイマー病の治療薬には、アミロイド仮説に基づき、アミロイドβタンパク質の生成阻害を目標とした薬が多い。
2014年2月に大阪大学の研究グループは、アミロイドβタンパク質の蓄積が「KLC1E遺伝子」という遺伝子によって制御されていることを示唆する論文を発表した。この論文では、従来アミロイドβタンパク質の蓄積による結果だと考えられていた細胞内輸送の異常が、結果ではなく原因であることも明らかになった。
関連サイト:
アルツハイマー病とは? - 理化学研究所
アルツハイマー病の原因を制御する遺伝子KLC1Eを発見 - 大阪大学
アミロイド‐ベータ【amyloid beta/amyloid β】
読み方:あみろいどべーた
アミロイドβ
出典: フリー百科事典『ウィキペディア(Wikipedia)』 (2023/02/26 08:56 UTC 版)
アミロイドβ(アミロイドベータ、英: Amyloid beta、略称: Aβ)は、アルツハイマー病患者の脳に見られるアミロイド斑の主成分として、アルツハイマー病に重大な関与を行う36–43アミノ酸のペプチドである[2]。このペプチドはアミロイド前駆体タンパク質 (amyloid precursor protein, APP) に由来し、β-セクレターゼとγ-セクレターゼによる切断によって産生される。Aβ分子は凝集し、いくつかの形態の柔軟な可溶性のオリゴマーを形成する。現在では、特定の誤ったフォールディング(ミスフォールディング)をしたオリゴマー(「シード」として知られる)が他のAβ分子のミスフォールドを誘導し、プリオンの感染と類似した連鎖反応が引き起こされると考えられている。このオリゴマーは神経細胞に対する毒性がある[3]。アルツハイマー病への関与が示唆される他のタンパク質であるタウタンパク質も同様にプリオン様のミスフォールドオリゴマーを形成し、ミスフォールドしたAβがタウのミスフォールドを誘導するという証拠も存在する[4][5]。
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- 1 アミロイドβとは
- 2 アミロイドβの概要
- 3 遺伝学
- 4 アミロイドβの計測
- 5 関連項目
- アミロイドβのページへのリンク