Complement pathway in Alzheimer's pathology and retinal neurodegenerative disorders - the road ahead

Complement activation has, interestingly, been reported in a wide range of retinal and brain disorders including AD, depression, seizures, multiple sclerosis, age related macular degeneration, diabetic retinopathy, uveoretinitis and glaucoma. Multiple reports highlighting involvement of complement p...

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Bibliographic Details
Published in:Neural regeneration research 2020-02, Vol.15 (2), p.257-258
Main Authors: Mirzaei, Mehdi, Deng, Liting, Gupta, Veer, Graham, Stuart, Gupta, Vivek
Format: Article
Language:English
Subjects:
Advertising executives
Alzheimer's disease
Amyloid beta-protein
Brain research
Care and treatment
Central nervous system
Chronic illnesses
Clinical trials
Development and progression
Diabetic retinopathy
Glaucoma
Health aspects
Homeostasis
Inflammation
Inflammatory diseases
Macular degeneration
Neurodegeneration
Neurodegenerative diseases
Neurophysiology
Open access publishing
Pathology
Proteins
Retina
Retinal diseases
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Summary:Complement activation has, interestingly, been reported in a wide range of retinal and brain disorders including AD, depression, seizures, multiple sclerosis, age related macular degeneration, diabetic retinopathy, uveoretinitis and glaucoma. Multiple reports highlighting involvement of complement pathway proteins in animal models of AD and human subjects has resulted in growing interest in manipulating the complement pathway, in particular, the classical pathway in the brain to improve function or restore homeostasis. C3 levels were also observed in the retinal ganglion cells in experimental glaucoma models and post-mortem human eyes and enhanced expression of C3 was evident in the retinal ganglion cells in culture under stress induced by serum deprivation of cells. Success in gene therapy to modulate C3 in a glaucoma model and concomitant neuroprotection suggests its promising role in glaucoma (Bosco et al., 2018). [...]we identify consistent beneficial effects of complement inhibition in pre-clinical and clinical trials, it might be difficult to establish whether complement activation is indeed detrimental for neural tissues or if it plays a protective role at least during initial stages of the disease process.
ISSN:1673-5374
1876-7958
DOI:10.4103/1673-5374.265550