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Editors Selection IGR 13-1
Basic research: Myocilin
Comment by Daniel Ju on:
13735 Mitochondrial abnormalities in patients with primary open-angle glaucoma, Abu-Amero KK; Morales J; Bosley TM, Investigative Ophthalmology and Visual Science, 2006; 47: 2533-2541
Mitochondrial abnormalities have been implicated in neurodegenerative disorders including stroke, Parkinson's disease and Alzheimer's disease. However, the precise role of mitochondrial dysfunction in disease pathogenesis remains unknown. Abu-Amero et al. (351) investigated a possible link between mitochondria abnormalities and patients with primary open angle glaucoma (POAG). The authors evaluated 27 patients who met funduscopic, visual field, and anterior segment criteria that defined POAG in contrast to other causes of optic nerve neuropathy. The MYOC and OPTIN genes and the entire mitochondria (mt)DNA coding region were sequenced. Relative mtDNA content and mitochondrial respiratory function were also investigated.
The authors reported three major findings. First, no primary LHON mutations or MYOC and OPTIN nucleotide changes were present in any of the POAG patient. Second, several other mitochondrial abnormalities were present including 27 novel nonsynonymous mtDNA changes in 22 of the POAG patients. These were potentially pathogenic in 14 of these patients. Most mtDNA sequence alterations were transversion-sequence changes that alter purine/pyrimidine orientation. The mtDNA content was relatively increased in patients with POAG. Third, mitochondrial respiratory activity (MRA) was decreased by 21% in patients with POAG.
The authors suggest that mitochondrial abnormalities, increased relative mtDNA content, and reduced MRA levels indicate that oxidative stress and mitochondrial dysfunction may play a role in the pathogenesis of POAG. Further ultrastructural and molecular biological studies for mitochondrial dysfunction are required to confirm this. In addition, studies employing experimental glaucoma models should be considered.
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