Neuroinflammation and Proteostasis are Modulated by Endogenously Biosynthesized Neuroprotectin D1

被引:19
作者
Bazan, Nicolas G. [1 ]
机构
[1] Louisiana State Univ, Neurosci Ctr Excellence, Hlth Sci Ctr, New Orleans, LA 70112 USA
关键词
Misfolding; Retinal degenerations; Alzheimer's disease; Huntington's disease; Epilepsy; Docosahexaenoic acid; Ataxin-1; Huntingtin; CAG repeats; APP; Bcl-2; proteins; DOCOSAHEXAENOIC ACID; OXIDATIVE STRESS; CELL-SURVIVAL; ALZHEIMERS; MECHANISMS; APOPTOSIS; DISEASE; BRAIN;
D O I
10.1007/s12035-012-8322-5
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
Neurodegenerative diseases encompass complex cell signaling disturbances that initially damage neuronal circuits and synapses. Due to multiple protective mechanisms enacted to counteract the onset of neurodegenerative diseases, there is often a prolonged period without noticeable impairments during their initiation. Since severe cognitive deficit or vision loss takes place after that period there is an opportunity to harness endogenous protective mechanisms as potential therapeutic approaches. The activation of the biosynthesis of the docosanoid mediator neuroprotectin D1 (NPD1) is an early response to the upsurge of protein misfolding and other neuroinflammatory events. This overview discusses the potent neuroprotective and inflammation-modulating bioactivity of NPD1. This lipid mediator represents an early response to neurodegenerations, aiming to restore homeostasis.
引用
收藏
页码:221 / 226
页数:6
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