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Top-ten 2011 Annual Scientific Congress of the Australian and New Zealand Glaucoma Interest Group
Melbourne, Victoria, February 11-12
- Ivan Goldberg (Sydney, Gillies Lecture), Future priorities for
Glaucoma
To meet our mission to minimize avoidable visual disability from the glaucomas, we seek to diagnose when minimal damage has occurred, to identify and to arrest the mechanism(s) responsible, and to reverse that damage. As well as discovering new knowledge (neuroprotection, neuroregeneration, nutrient delivery and other non-IOP reducing strategies, alternative drug delivery systems, better surgical approaches including wound healing control) we need to apply existing knowledge more effectively: optimization of medical therapy, more effective detection of disease and its progression, and better visual rehabilitation. As the global population grows and ages, the imperative increases exponentially to become more efficient in all these areas of endeavour. - David Mackey (Perth, Keynote Lecture), The I in personalised
genetics
Professor Mackey discussed the advent of direct to consumer DNA testing, giving his own personal experience with particular attention to the risk associated SNPs in the LOXL1 gene. LOXL1 is the main gene associated with risk for development of exfoliation. Although this risk may be of benefit in understanding the risk for XFS it probably doesn't change management of patients. It is likely in the future as more genetic information is acquired that we will be able to build accurate risk profiles for many diseases and tailor our management to that information. We are still in the early days. - Bill Morgan (Perth , Keynote Lecture), Translaminar Pressure
and its effects
The relationship of retrolaminar tissue pressure to CSF pressure, orbital pressure and pia mater characteristics was described. Then magnitude of the translaminar pressure gradient was modelled based upon dog measurements and pial characteristics. Given recent work showing that normal venous endothelial cell alterations are limited to the scleral lamina cribrosa a magnitude of 33mmHg/mm across the scleral lamina is likely to exist in humans with IOP of 15mmHg and CSF pressures of 0mmHg. This is close to the 45mmHg/mm required to retard rapid axonal transport. - Ian Trounce (Melbourne), Is Glaucoma Alzheimer's disease of the
eye?
Alteration of the cellular processing of a protein called the amyloid precursor protein (APP) is thought to underlie Alzheimer's disease, and has recently been suggested to occur in glaucoma. Our research has found that APP can protect nerve cells from toxins that target the mitochondrion, a cellular body that makes energy. Mitochondrial failure is a research focus for both Alzheimer's disease and glaucoma, and we are exploring the hypothesis that loss of APP function in the aging optic nerve may predispose the nerve to mitochondrial failure in glaucoma. - Beverley Lindsell (Sydney), Glaucoma - Frequently asked questions.
What your patients really want to know! The presentation gave an overview from a patient's perspective of being diagnosed, and living with, glaucoma. Topics covered ranged from the patient's feelings, waiting times, some doctors mannerisms, to the cost of visits and treatment. The presentation revealed that patients often communicate more openly with a patient association; articulating views which they believe cannot always be discussed with their treating practitioner. - Jamie Craig (Adelaide), A new genetic locus for congenital glaucoma
Dr Craig reported on work undertaken by Dr Adam Rudkin in blind schools in Cambodia. Several families were found to carry mutations in the CYP1B1 gene. One large consanguineous sibship had 4 individuals severely affected with PCG, and 7 unaffected sibs. Both CYP1B1 and LTBP2 were excluded as the cause in this family. Homozygosity mapping with Illumina Humhap 610 arrays was then used to map a novel genetic locus for autosomal recessive PCG to chromosome 2p25. The investigators are undertaking further studies to identify the third gene for PCG. - Bob Casson (Adelaide), Anterograde axonal transport dysfunction
in experimental glaucoma
Recent research has provided convincing evidence that a labile protein, Nmnat2, is a critical survival factor for axons. If production or transport of Nmnat2 to the axon is inhibited, then the axon undergoes a Wallerian-like degeneration. We have recently shown that anterograde axonal transport is a significant early feature in experimental glaucoma. The implication is that Nmnat2 may be an important part of the pathogenesis of glaucoma. - Paul McMenamin (Melbourne ), The Australian retinal evolution
Little is known of the eye anatomy of many of our fellow mammals so it is hardly surprising that even less is known about the eye of marsupials with which we share a common ancestor 130M yrs ago. Vessels in the central nervous system of marsupials have a paired configuration and do not form anastomotic capillary networks that are seen in mammals and this is the pattern that prevails in species who have developed specialised retinae that require the extra nourishment provided by retinal blood supply. This odd vascular pattern seen in species alive today is likely merely a reflection of the evolutionary constraints inherited from a distant ancestral line, most likely now extinct, which had paired vessels in the nervous system. In all marsupial species investigated to date which have retinal vessels they have been shown to be paired. - Tina Wong (Melbourne), Marked for Failure - the role of tear
cytokines in glaucoma surgery
Chronically medicated patients have higher MCP-1 levels in tears - ie, increased duration on topical medication correlates with increasing MCP-1 detected in tears. Elevated tear MCP-1 correlates with a higher rate of early trabeculectomy failure (6 months) - eyes with a propensity to scar have higher tear MCP-1 at time of surgery - Ecosse Lamoureux (Melbourne), The impact of glaucoma on quality
of life: where to from here
Glaucoma has a substantial impact on patients' functioning, especially in its severe stages. However, our understanding of the full impact of this ocular condition on life dimensions (outside of functioning and mobility) is limited. Future research should develop a glaucoma-specific quality of life scale using modern psychometric methods and accompanying applications such as item banks and computer adaptive testing.