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August 2004 No. 22From the Editor
When you read this the Olympic Games in Athens will be almost over. It must have been a wonderful spectacle to see on TV but even though, for the first time, I was unable to see it, I listened to the commentaries and could get a good idea of the huge crowds and the joy of the athletes when they won a medal for their country. All of them, whether they gained a medal or not, are amazing for the years of dedicated training they undertook, striving to be the best in the world in their chosen sport and are to be congratulated for their performances.
Then In September come the Paralympics, when thousands of disabled athletes from all over the world assemble in Athens to compete at the same venue. They have been training just as hard and long as the able bodied athletes. Retina NZ has a young member, Tim Prendergast, who has already made a name for himself in middle distance running in NZ and at the last Paralympics held in Sydney. We feature him in this issue. Tim will be striving for Gold medals in the 800 and 1500 metres in the stadium in Athens, the capital of Greece, where the Olympic Games began some 2,400 years ago and were revived in 1896 as the modern Olympics.
I have been busy on Retina business lately, representing the Society at the RNZFB Wellington Regional Forum and attending the NZ Visually Impaired Empowering Women's (NZ VIEW) two day conference in Wellington, where I sat next to a woman who had Usher Syndrome (deafness with RP). She was born deaf but could hear with the aid of hearing aids and could lip read. Eventually she was unable to hear or lip read and lived in a silent world, becoming very depressed. She was given a cochlear implant two years ago at the age of 60 and had to learn to hear and interpret speech all over again. Now she has 80% of her hearing restored, has learned to hear and talk again and was representing her area group as well as DeafBlind Inc.
August is Save our Sight month when Retina teams up with the Optometrists' Association and the Foundation of the Blind to promote awareness of blinding eye diseases and how some of them can be treated or prevented. I organised a meeting at my retirement village, having previously mailed Retina information kits containing an Amsler Grid to test your eyesight and our Coping Strategies pamphlet to be mailed to all the residents. An optometrist spoke about Age related macular degeneration (AMD) to the 65 residents who attended and many questions were asked afterwards.
June Ombler, Editor
Apt C16, Rita Angus Village, 66 Coutts Street, Kilbirnie, Wellington
Phone: (04) 387 4553
From the President's Desk
SOS Save Our Sight month being held during August is now well underway. This is a partnership involving the NZ Association of Optometrists, RNZFB and Retina NZ. This year the focus is on Healthy People Healthy Eyes. Creating awareness of the need for everybody to have regular eye checks not just when you know there is something wrong. Also it is about getting vision and eye care specifically incorporated into the NZ primary health care strategy.
Retina NZ is hosting some meetings during August, aimed at the general public to present information about AMD macular degeneration. The first of these held in Paraparaumu on 7 August, attracted 80 people! Double the number expected. Congratulations to the Kapiti VIP support group who organised this event. Our coping strategies pamphlet and Amsler grid cards were included in a pack that went out to all optometrists before the SOS kick off. Hopefully more people will learn that Retina NZ exists, and want to help people with retinal degenerations.
I was privileged to go to the Retina International conference held in Holland at the end of June. Three of us travelled from New Zealand, and spread ourselves around the many different options for workshops and presentations. There will be reports on what we learned in the next newsletter. I was impressed with how well everyone I met could speak English whether they were from Switzerland, Holland, Norway, Japan etc. I am sure learning and conversing in another language must be good for the brain. A large part of being at the biennial conference, is meeting the delegates from other countries and finding out how they go about managing their organisations. By travelling over with Fraser Alexander and Christina van der Wal, I learned how to get treated like VIPs and bypass those endless queues to check passports etc at airports; just ask for blind assistance!
With cheaper airfares making it feasible, I attended the Wellington AGM in May. This was well attended, and they appointed a new chairperson, Gael Hambrook. Denise Keay was appointed as their representative on the national executive. And we welcome her and her perspective of someone who has low vision, but is not a member of the Foundation. Allan Jones retired and we thank him for his contribution to the executive over the last couple of years. He was involved with the Pacific diabetes initiative, supporting Tony Haas.
You already will have received notice of our AGM and conference on the 18 September in Christchurch. We hope to meet as many of you as possible then. The programme was designed to appeal to a broad range of people regardless of vision loss or impairment. So if you haven't already responded to the first mailout, there is still time to come. If you live anywhere near Christchurch, see you there.
Kaye Newton, 8 August 2004
Notes from Dr Dianne Sharp's talk to Auckland Branch at their meeting in Awhina House, Auckland on 30 April 2004
Retinal Degeneration: Inherited retinal dystrophies and macular
* What has happened over recent years?
* What progress has been made?
* Where to from here?
World wide research is aimed at treating, curing and preventing RP and other retinal degenerations including AMD
As we gain understanding of the causes of various types of retinal degeneration, we provide the keys to unlock potential therapies.
A gene defect results in the productions of an abnormal protein balance in the retina leading to destruction of retinal cells. Gene therapy substitutes normal gene material and is introduced by a "courier" or vector. One form of gene therapy is "ribosome technology", being used in a type of Autosomal Dominant retinitis Pigmentosa (ADRP). Ribozomes are molecules that can destroy the message that a cell issues to make a protein. In ADRP, cells are producing both right and wrong messages for a crucial protein. A ribosome is engineered to destroy the wrong message, leaving the right message free to act. Gene therapy aims to stop further retinal degeneration rather than restore sight that has been lost.
* This requires identification of gene mutations. The first mutation was identified just over a decade ago. Now 50% of gene mutations leading to retinal degenerations have been identified. 150 genes out of the total human complement of 35,000 genes have been linked to inherited retinal disease.
* Gene therapy research in animals is becoming more common and some clinical trials are in progress or being planned. The major complication of gene therapy is the safety factor of introducing genes and being able to harness a vector (virus or other substance which can transport genetic material), which is reliable over the life time of the host.
Cell transplants - Experimental transplantation of cells into the human retina
1. Retinal Pigment Epithelial (RPE) cells are "nurse" cells, which lie behind the Photoreceptor (P/R) cells, (the light sensitive cells of the retina) and provide essential nutrients and nurture the P/R but RPE cells can be damaged. Replacing these cells with new RPE cells is the focus of several AMD researchers. The major problems are to avoid rejection of the transplanted cells and ensure long term survival. A possible alternative may be to replace RPE cells with cells from the iris of the eye as they are similar. Researchers have had some success into converting them into functioning RPE cells.
2. Current research to replace lost or damaged photoreceptors by implanting sheets of P/R cells grown in tissue culture. They cause less stimulation to the immune response and therefore less rejection but they do not integrate effectively with the retina, i.e. they need to connect to nerve cells to transmit signals to the brain. If this could be overcome they may inhibit further degeneration or even restore some sight by having transplanted cells communicating with surviving cells.
3. Other research involves placing undifferentiated "seed" cells or stem cells in the retina in the hope that they will transform into functioning P/R cells. Retinal stem cells are placed in a diseased retina and induced to take on the characteristics of healthy retinal cells. To develop into photoreceptor cells, the retinal stem cells must be coaxed through a very complex series of stages.
4. Delivery of growth factors by transplanted cells. GFs are naturally occurring health promoting proteins. Schwann cells commonly occur around nerve fibres of skin and muscle and are not normally present in the eye but they produce growth factors that are known to support P/R survival. In animal eyes where the P/R are degenerating, the implanted growth factors producing cells protect the P/R from deterioration. In future it is possible that the patient's own growth factor producing cells could be implanted into the eye to prevent P/R cell death without the problem of the immune rejection.
One of the most exciting areas where progress is being made in treating retinal degenerations is in pharmaceutical therapies. It is recognised that Biotech and pharmaceutical companies have the expertise, manpower and funding to mount clinical trials. Currently a number of companies are proceeding with trials to assess effectiveness. Growth factors (GFs) are
health promoting proteins, which occur naturally in the body. They influence the survival of cells and experimental studies show that certain growth factors are capable of slowing the rate of degeneration of diseased photoreceptors.
* Growth factors have very descriptive names. Vascular Endothelial Growth Factor (VEGF), Fibroblast growth Factor [FGF 2}, Ciliary Neurotrophic factor (CNTF) and Brain Derived Neurotrophic factor (BDNF).
* Research aims:
(i) To discover new growth factors.
(ii) To deliver growth factors to the eye.
(iii) To understand how GFs influence retinal cells particularly in retinal
(iv) To identify and overcome potential side effects.
Research is active and much of the work, which is currently being done to find treatments for AMD, will pave the way for other degenerative disorders. Products in the pipeline will hopefully not only halt the events that cause disease, e.g. abnormal blood vessel growth in wet AMD, but also remove the abnormal blood vessels that have already developed.
Some of the companies that are developing pharmaceutical products:
* Novartis with an anti VEGF agent called Lucentis to control or even reverse the progress of new blood vessels in wet AMD.
* Eyetech with another anti VEGF compound called Macugen .
* Retaine (anecortave acetate) another agent to stop or slow the growth of new blood vessels in wet AMD and another trial that is commencing to assess its effectiveness in slowing the conversion of dry to wet AMD in patients who already have wet AMD in one eye.
* GenVec uses a modified virus to deliver a therapeutic gene to increase the production of a protein (PEDF) that is produced by the eye and normally inhibits new blood vessels forming.
* Neurotech are investigating Encapsulated Cell Technology (ECT): A device is implanted inside the eye where it slowly releases a therapeutic substance such as a growth factor [CNTF] for the treatment of RP. This particular GF is a nerve protecting substance or "survival factor". It does not correct the defect responsible for the degeneration but slows and ideally stops premature P/R death. While several drugs have shown effectiveness in lab conditions, their safety and effectiveness in humans are still being evaluated.
Electronic chips have already achieved impressive results for some deaf people through cochleal implants. Now researchers are developing the use of electronic chips that respond to light to replace P/R. These stimulate the output neurones of the retina to send signals to the brain.
1. Retinal implants. Optobionics in USA have implanted a retinal "chip" and reported positive results in clinical trials. An array type chip is 3 x 3 mm in size and contains 1,000 light sensitive diodes. The main problem with electronic prostheses is in the gain where the electrode is a crude substitute for full thickness retina.
2. Cortical Implants. 12 patients implanted with electrodes reported some visual function but the high currents needed may cause seizures. Further studies are underway looking at micro amp range but safety issues are greater in brain implants than ocular implants. Further requirements are for better electronics and better devices.
What should we be doing?
1. Increase awareness of current treatments.
2. Knowing the extent and nature of gene mutations responsible for retinal degeneration, it is obvious that a number of different treatments will be needed. With clinical trials commencing, Patient Registries are one of the most important elements for rare diseases such as RP and in Age related Macular degeneration; accurate sub grouping of the disorders is essential. This will allow the future matching of cause and therapy.
Some of these concepts seem like science fiction. When will we see them in the treatment and management of retinal degenerations? I was fortunate to have an Easter holiday in the Blue Mountains west of Sydney with my family and we visited the Jenolan Caves where there are magnificent limestone deposits of stalagmites and stalactites similar to Waitomo Caves. These spectacular formations were formed one drop at a time with each drop adding to the next. That seems to illustrate the path in the development of therapies for retinal degenerations. Progress over the past 5, 10 and 20 years has been positive and steady.
Links between fat and Age-Related Macular Degeneration (AMD)
From Macular Degeneration Partnership, 22 June 2004
A very interesting study is published in the June 2004 Archives of Ophthalmology, one of the major professional journals in the field of vision. It's interesting because of what it shows and also because it highlights the issues that surround research results.
The researchers at Harvard Medical School and Brigham and Women's Hospital in Boston looked at very large groups of professional men and women. The subjects were participating in two important studies, the Nurses Health Study and the Health Professionals Follow up Study. Because of the size of the groups, they were able to look at over 118,000 people across a 12 18 year period. These are the kinds of numbers that usually contribute statistically significant findings, as opposed to studies of much smaller groups.
The participants were at least 50 years old at the time they began the study and had no signs of age related macular degeneration. Over the course of the observation, the 77,562 women filled out diet questionnaires up to five times. The 40,866 men completed them three times. They all reported on vitamin and supplement use as well.
During this period 329 women and 135 men were diagnosed with early AMD, while 217 women and 99 men developed wet AMD
So, when they sifted through all the data,what did they find? You probably won't be surprised that they found eating fruit to be protective of wet macular degeneration. We know that antioxidents in food affect the macula and that people who eat large amounts of fruits and vegetables have a lower risk of AMD (from other large studies around the world). In this study, those who consumed three or more servings of fruit a day lowered their risk of getting wet AMD, compared to those who ate less than 1.5 fruits a day. Of particular benefit were bananas and oranges.
What is interesting in this study is that no connection was shown between the amount of vegetables or the use of antioxidant supplements with reduced AMD. This flies in the face of other studies that identify vegetables, especially green leafy vegetables,as protective for AMD.
The data were adjusted for other AMD risk factors, like smoking, obesity, alcohol intake,fish intake,physical activity, history of hypertension and high blood cholesterol levels and postmenopausal hormone use in women. They note, in fact, that the "participants with higher fruit or vegetable intake were less likely to smoke and more likely to be physically active and to consume fish". That information could be important in itself. And, there may be a difference for early AMD, wet AMD and dry AMD.
The authors admit that these "confounding factors" could contribute to the findings in the study. They also note that "A healthy lifestyle may also be associated with more medical screening, including eye examination, and thus increase the chance of being diagnosed" with AMD. They recommend that further studies be conducted to confirm their findings and to identify the content of fruits that could have caused the results of this research.
So, should you rush right out and start eating quantities of oranges and bananas and skip the spinach? Probably not. It just makes sense to eat a well rounded diet high in fruits AND vegetables. The other food studies continue to point to antioxidents and caretenoids in foods like dark green leafy vegetables. A wise course would be to continue to eat a varied diet with all the colours of the rainbow.
A second gene discovered for Age-Related Macular Degeneration
From U.S. Foundation Fighting Blindness, 23 July 2004
The New England Journal of Medicine issue of 22nd July 2004 reports a second gene has been discovered for Age related Macular Degeneration (AMD). The gene's relationship to AMD was found by a team of researchers at the U.S. FFB funded Research Center for Macular Degeneration and Allied Retinal Diseases at the University of Iowa. The Center's Director and lead author
on the report, is Edwin M. Stone, MD, PhD. Dr Stone is a member of the FFB Scientific Advisory Board.
Age related macular degeneration affects over 9 million people in the U.S. It is the most common cause of irreversible vision loss in the western world. As baby boomers in the U.S. reach a vulnerable age for AMD, the numbers are expected to increase. Researchers are realizing that AMD is not caused by a single gene defect but that many variables, and perhaps multiple genes, are involved. Environmental influences, like smoking, sun exposure, and diet, may also contribute to AMD.
"The finding that the fibulin 5 gene is involved in AMD is a big step forward," says Timothy Schoen, Ph.D., director of FFB's medical therapy program. "The more we know about genes causing retinal degenerative disease, the more closely treatments can be tailored to individual patients." Such gene directed therapy is bound to replace standard one size fits all conventional medical treatments.
By continuing to find genetic links to the possibility of inherited risks for AMD, this reinforces the need to support more research for causes and treatments that will help not only today's patients but also their children.
The fibulin 5 gene is normally involved in the production of a protein called elastin. The protein is made in cells and extruded into extracellular spaces where it helps form elastic fibers. Elastic fibers help maintain the integrity of tissues like skin and blood vessels. They are also found in Bruch's membrane, which underlies the retinal pigment epithelium (RPE) of the retina. We know that cells of the retina rest on the RPE and depend on the RPE and Bruch's membrane for support and nourishment.
How did the researchers find that the fibulin 5 gene is involved in AMD?
They compared DNA in blood samples from 402 patients who had been diagnosed with AMD based on eye examinations to a nearly equal number of age matched control subjects without AMD. The DNA was screened for variations of the amino acid sequence in five different members of the fibulin family of genes. But it was only in the fibulin 5 gene that variations occurred solely in AMD patients.
The variations (mutations) occurred only in seven of the 402 patients, but the finding was scientifically significant, statistically and practically. The fibulin 5 finding is a genetic clue that researchers will use to understand the causes of AMD and for developing treatments or preventive strategies for patients whose gene tests reveal that they may be at risk.
The gene, elastin, and drusen
The researchers believe that there may be a link between the elastin fibers and drusen, which are a hallmark of AMD. The yellowish protein and fat containing drusen form in Bruch's membrane. It is possible that reduced amounts of the fibulin 5 protein in Bruch's membrane, or an aberrant fibulin 5 protein, affects the normal assembly of elastin and somehow sets the stage for drusen formation.
"The Foundation Fighting Blindness believes that the finding by Dr Stone and his group is a significant step toward the prevention and treatment of age related macular degeneration," says Schoen. "We are discovering that AMD is not a disease with a single cause and FFB is working closely with researchers to further this understanding."
Your Questions Answered
I have inherited the autosomal dominant form of RP (ADRP) from my father and my daughter has inherited it from me. My son has fortunately not inherited the dystrophy.
My question is "If a child in a family with ADRP does not inherit the condition, could they pass it on to any of their children or even grandchildren?"
I ask this because I have heard about something called reduced prevalence, which I understand means that children of people with ADRP who do not appear to have inherited this form of progressive blindness can inherit it mildly enough so that they are apparently free of the condition, but that it may appear again in the following generations. From A.D. RP Name and address supplied.
Answer From Harry Bradshaw MB ChB and Andrea Vincent, MB ChB, FRANZCO. Departments of Ophthalmology Auckland Hospital and University of Auckland
Retinitis pigmentosa describes a group of hereditary disorders
characterised by progressive loss of photoreceptor and retinal pigment epithelium (RPE) function. It has been described with Autosomal Dominant (AD), Autosomal Recessive (AR), X linked and digenic (caused by more than one gene) inheritance patterns. It is estimated that AD inheritance accounts for 25% of all RP.
Considering the AD forms there are 13 currently recognised genes: RHO, RDS, RP1, RP9, CA4, ROM1, NRL, CRX, FSCN2, HPRP3, IMPDH1, PRPF8, PRPF31. (http://www.sph.uth.tmc.edu/Retnet). Many of the proteins encoded by these genes are expressed in the retina, and involved with photoreceptor (rods/cones) structure and / or function. It is hoped that we will be able to genetically test individuals within the next decade. Clinically, it is very difficult to determine which gene has caused RP in an individual. There is often a large variation in the severity, age of onset, appearance of the retina and progression between individuals, both within the same family, and between families with the same gene mutation. This is called Variable Expressivity (see below).
To answer your question we must briefly consider some genetic terminology; an allele is the actual DNA sequence of genetic information which can be the 'normal' or wild type or mutant (disease related).
In addition there may be many variants of normal that are not disease causing, known as polymorphisms. A genotype is thus the actual sequence of the gene (recollecting there are 2 per chromosome). A phenotype, however is the observable expression of the genotype, i.e. how the disease actually appears clinically. In an AD inherited condition only one abnormal gene is required for the disease to be present. This can be because;
* The normal product of the normal allele (gene) is not enough
* There is interference in function from the abnormal product from the mutant allele or the abnormal product has enhanced function (Dominant negative)
* There is random loss of the other, normal, allele
To begin to explain the variability in autosomal dominant retinitis pigmentosa there are two main factors one of which you have mentioned; Reduced penetrance and variable expressivity. In addition there is a phenomenon called pleiotropy (or allelic heterogeneity).
Penetrance is the probability that an individual with a gene mutation will actually express the disease. It is an all or nothing phenomenon. The disease is present, (and may range from mild to severe phenotype), OR the disease is not present. Penetrance is therefore reduced if this occurs less than all the time (100%). This has been described in RP in a family of known reduced penetrance, with the PRPF31 (RP11) locus on 19q13.4 implicated the conclusion that the wild type alleles from the non carrier parent have major influence.
Expressivity describes the severity of the expression of the phenotype. This reflects the fact that individuals within the same family may carry the same mutation, yet be quite variably affected in terms of age of onset, progression, vision, visual field loss etc. Also individuals in different families who carry the same mutation in the same gene, may have a very different severity of disease. This reflects the fact that many different genes act together, and other genes, which vary between individuals, may modify the effect of a mutation. Environmental factors may also influence the gene expression such as smoking or diet.
Here a single abnormal gene may produce a diverse range of phenotypic effects. This can be seen with some of the genes that cause autosomal dominant RP. For example, RHO (which encodes for Rhodopsin) can cause Autosomal dominant RP, Autosomal recessive RP, and autosomal dominant macular dystrophy. Similarly, mutations in CRX have been shown to cause AD RP. AD cone, rod dystrophy, AR, AD and de novo Lebers Congenital Amaurosis.
Thus if your father passed the trait to you who, which your daughter subsequently inherited, autosomal dominant seems the most likely inheritance pattern. As you are no doubt aware your son's risk of inheriting the mutant allele was 50% (1:2). If he did have the mutation the chance his children could inherit the mutation would be 50% for each child. If he did not have the mutation, the risk would be almost zero. The risk never becomes zero, as there are so many genes that can cause retinal disease, the child's mother may carry a mutation in another gene, or de novo (new) mutations can occur in the sperm or egg.
Even though your son lacks manifestation of the disease clinically at present, it can be difficult to say absolutely that he may not develop it at a later age. This depends on his age at present, and the average age of onset of the disease in your family. If he had an ERG and this was normal, it is highly likely that he does not carry the mutation. There is still a small chance that with either reduced penetrance or highly variable expressivity, that he still has the mutation, but doesn't appear to have the disease. This could possibly be refined considering the age and severity of onset (manifestation) in the other members of your family, and whether there have been any other occurrences of non penetrance. Unfortunately we are some way off genetic analysis which would answer the question definitively.
Tim Prendergast -- An extraordinary young man
By June Ombler
"My big aim is to be the first vision impaired runner to go under four minutes for the mile", said Retina member Tim Prendergast. This young man has set his sights high. But he is well on the way to achieving his ultimate goal. "I've always had a passion for running as my father and sister both used to compete and just because I wasn't seeing too well didn't mean I was going to give up", he said. Although the mile isn't run as often as it was in the past, it's still a highly sought after mark for middle distance runners. In fact only 28 New Zealanders have ever done the 'sub four' for the 1609 metre journey.
Tim found out that he had Stargardt disease, a hereditary juvenile form of Macular Degeneration when he was eight years old. Born in Taupo he spent five years in Timaru before moving with his parents to Wellington. He attended Papakowhai Primary School and later Wellington College and then completed a degree in English Literature at Victoria University in 2000. Now, at the age of 25, Tim has worked for the Royal NZ Foundation of the Blind in Wellington as their Recreation Advisor for the past three years, a job he really enjoys.
Tim belongs to the Wellington Scottish Athletics Club but his coach for the last 12 years has been Neville Paul, a teacher at Wellington College. His prowess at running was first noticed when, in 1997 he competed in the Open National track and field championships for under 18's and finished third in the 1500 metres, an able bodied event.
In 1998 he represented New Zealand at the International Blind Sports Association (IBSA) World Championships, winning silver medals in both the 800 and 1500 metres and a bronze medal in the 400 metres. In 2000 he was again selected to represent New Zealand at the Paralympic Games, winning Silver medals in both the 800 and 1500 metres.
Two years ago at the Paralympic World Championships, which were again held in France, he achieved the ultimate, winning the Gold medal in the 800 metres, as well as winning a silver in the 1500 metres.
Tim still competes in the able bodied field events and at this year's National track and field championships in Wellington he finished fourth in the men's 800 metre final. "I run unassisted because I still have the use of my peripheral vision. I have good fields, so can still get around OK", he explained. "My night vision isn't great but I still can get by. I just make sure I run in well lit areas when training at night and take care if I'm running on uneven surfaces".
To prepare for his next challenge in September when he is off to Athens for the Paralympics to represent New Zealand in the T13 sight category in the 800 and 1500 metre events, Tim trains every day and twice a day for five days a week. He will be trying to repeat his gold and hopefully upgrading his silver medal winning performance at the Paralympic World Championships in France two years ago and improving his times. Currently his best performances so far are 1 minute 53 seconds for the 800 metres and 3 minutes 52 seconds for the 1500 metres.
"To compete in the able bodied Olympics you need to be running 1 minute 47 seconds for 800 metres and 3 minutes 38 seconds for the 1500 ". "I am a bit off but if I make improvements over the next four years, who knows, I may get to the Olympics in 2008", he said. To dedicate another four years of one's life to shave off a few seconds from each of Tim's middle distance running times takes great determination and perseverance.
Other Awards for Tim Prendergast show that he has what it takes to keep going with training in order to achieve his goal. He was awarded the Blind Achiever's Award in both 1998 and 2002 and became Blind Sportsman of the year in 2002. But he still finds time to enjoy watching lots of different sports, listening to music and "hanging out" with his partner Lisa and his mates.
Tim, I salute you!
EDITOR's NOTE: Tim Prendergast makes his bid for gold medals at the Paralympics in Athens in September. He competes in the 1500 metres on September 21st and the 800 metres on the 27th. If you would like to send him a message of encouragement and wish him good luck, send an Email to <firstname.lastname@example.org>. These races will most likely screen on TV1 in the evenings following his races during their hour of highlights each night between 5 and 6 pm.
We held our Annual General Meeting in May. It was well attended. Allan Jones stood down as chairperson as did committee members Heather Tofts and Terri Greenhalch. Our new chairperson is Gael Hambrook. Denise Keay has become our delegate on the National Executive.
Our main area of responsibility is peer support and Elizabeth East and other branch members have set up the Kapiti VIP Support Group and the Manawatu Support Group in the last twelve months. The Kapiti VIPs meet on the third Monday of each month in the Kapiti Community Centre (contact Gael Hambrook 04 904 3575) and have had an average attendance of 15 at each meeting. The Manawatu Support Group is co ordinated by Alex Thompson (06
356 9611) and it meets quarterly in central Palmerston North.
From Camille Guy
The next Auckland branch public meeting will be held on Sunday 31st October at 1.30 pm. Our speaker will be ophthalmologist Dr Rachel Barnes, who will share any new developments from a conference she is attending in Australia this month. A notice will be sent out to Auckland members early October.
FROM : Robyn Challis
10 Mayo Place
Phone: 03 445 0812
Email : email@example.com
I was diagnosed with Macular Degeneration two and a half years ago and was wondering if there is anyone in the Central Otago area who would like to visit, correspond or chat on the phone. It would be great to be able to share the happenings, support and experiences with someone in the same situation.
Advance Notice of meeting for Waikato members
From Elizabeth East
Retina NZ is intending to hold an early evening meeting in Hamilton on Friday, 29th October, venue to be confirmed. Our President, Kaye Newton from Christchurch will be present as well as one or two other members of the National Executive. Please pencil this date into your diaries and we will write to you nearer the time with the exact details.
Newsletter Editor wanted
We are still open for expressions of interest in taking on the role of editor of our quarterly newsletter. Due to the impending retirement of June Ombler, we are looking for a new editor. This is a crucial role as the newsletter is the main source of support and information for most of our members. For more information about what is required, please contact our National secretary, Janet Palmer, at
REMINDER : National Conference to be held in Christchurch on Saturday 18 September. If you have not already responded, we need to know if you are coming.