An interesting similarity between Glaucoma and other neurodegenerative disorders (such as Parkinson’s and Alzheimer’s) was recently reported in Proceedings of the National Academy of Sciences.  It has been well known for awhile that both Parkinson’s and Alzheimer’s are associated with abnormal protein deposits.  These deposits are associated with decreased cellular function.  Such a protein has recently been discovered to exist in Glaucoma.  Called gamma-synuclein, this is the first evidence that Glacuoma could share a causal mechanism with diseases such as Parkinson’s (which is notable for aggregates of a similar protein called alpha-synuclein).

The article (titled “Myelination Transition Zone Astrocytes are Constitutively Phagocytic and Have Synuclein Dependent Reactivity in Glaucoma“{{1}}) focuses on a type of cell (called astrocyte) that functions as a sort of cellular janitor, mopping up debris within the optic nerve.  What makes this so interesting is that (at least in theory) if we know the protein or cell that is involved in the underlying cause of Glaucoma, potential treatments could be developed that target either gamma-synuclein or the transition zone astrocytes.

Currently, all Glaucoma treatments are targeted toward methods of reducing the intraocular pressure in the eye (IOP) so this new finding could potentially open up an entirely new field of Glacuoma treatment research.


  1. Judy V. Nguyen, Ileana Soto, Keun-Young Kim, Eric A. Bushong, Ericka Oglesby, Francisco J. Valiente-Soriano, Zhiyong Yang, Chung-ha O. Davis, Joseph L. Bedont, Janice L. Son, John O. Wei, Vladimir L. Buchman, Donald J. Zack, Manuel Vidal-Sanz, Mark H. Ellisman, and Nicholas Marsh-Armstrong. Myelination transition zone astrocytes are constitutively phagocytic and have synuclein dependent reactivity in glaucoma. [[1]]

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