Complement pathway in Alzheimer’s pathology and retinal neurodegenerative disorders – the road ahead
Mehdi Mirzaei
Liting Deng
Veer Bala Gupta
Stuart Graham
Vivek Gupta
摘要：Chronic inflammation has increasingly been acknowledged as a hallmark feature of several progressive neurodegenerative disor-ders. Accruing evidence indicates that sustained inflammation compromises the core neuroprotective mechanisms underlying neural injury in Alzheimer’s disease (AD) and retinal neurodegen-erative disorders. Innate immunity and activation of the classical complement pathways are suggested to play important roles in nor-mal central nervous system physiology and complex tissue remod-eling during the disease process (Gasque et al., 2000). The pathway is implicated in normal brain development and is also involved in the inflammatory response in a wide range of neurodegenerative conditions either directly or indirectly through recruitment and activation of immune cells. The classical, alternative and lectin complement pathways, together encompass about 30 plasma and membrane-bound proteins. The classical pathway is comprised of about 20 proteins including several serine proteinases and protein-ase inhibitors connected as part of an amplifying cascade. Activa-tion of the classical pathway is triggered once C1q is attached to the immune complexes containing IgG or IgM leading to production of the C3 convertase (Merle et al., 2015).
机标关键词：
论文发表日期：2020-01-01
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：2( 257-258 )