Experimental Brain Research

, Volume 232, Issue 11, pp 3363–3377

The role of glial cells and the complement system in retinal diseases and Alzheimer’s disease: common neural degeneration mechanisms

Review

DOI: 10.1007/s00221-014-4078-7

Cite this article as:
Harvey, H. & Durant, S. Exp Brain Res (2014) 232: 3363. doi:10.1007/s00221-014-4078-7

Abstract

Many age-related degenerative diseases of the central nervous system (CNS) increasingly appear to have similarities in their underlying causes. By applying knowledge between disorders, and in particular between degenerative diseases of different components of the CNS (e.g. the eye and the brain), we can begin to elucidate general mechanisms of neural degeneration. Age-related macular degeneration and glaucoma, two diseases of retinal neurons, which have recently been discussed in view of their common mechanisms with Alzheimer’s disease, highlight this perspective. This review discusses the common roles of the complement system (an immunological system) and glial cells (providing, amongst other functions, trophic support to neurons) in these three disorders. A number of facets of these systems would seem to be involved in the mechanisms of degeneration in at least two of the three diseases considered here. Regulatory proteins of the complement system (such as factor H), neurotrophin levels, and the interaction of microglia with the complement system in particular may be general to all three presentations of neural degeneration. Investigating the functioning of these fundamental systems across different diseases exemplifies the importance of considering advances in knowledge across a wider base than specific disease pathology. This may give insights both for understanding the function of these supporting systems and providing an avenue for developing future therapeutic targets general to neural degenerative diseases.

Keywords

Complement systemGliaAlzheimer’s diseaseAge-related macular degenerationGlaucomaNeurodegeneration

Copyright information

© Springer-Verlag Berlin Heidelberg 2014

Authors and Affiliations

  1. 1.Royal HollowayUniversity of LondonEghamUK