Americans rate losing eyesight as having greatest impact on their lives

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Posted on 11th October 2014 by Pacific ClearVision Institute in Cataracts |General

Many Americans across racial and ethnic groups describe losing eyesight as potentially having the greatest impact on their day-to-day life, more so than other conditions including: loss of limb, memory, hearing and speech (57% of African-Americans, 49% of non-Hispanic whites, 43% of Asians and 38% of Hispanics). When asked which disease or ailment is the worst that could happen to them, blindness ranked first among African-Americans followed by AIDS/HIV. Hispanics and Asians ranked cancer first and blindness second, while Alzheimer’s disease ranked first among non-Hispanic whites followed by blindness.

When asked about various possible consequences of vision loss, “quality of life” ranked as the top concern by non-Hispanic whites (73%) and Asians (68%) while African-Americans (66%) and Hispanics (63%) ranked “loss of independence” as number one. These and other findings from a new national public opinion poll commissioned by Research!America and the Alliance for Eye and Vision Research (AEVR) point to various perspectives among racial and ethnic groups regarding eye and vision health.

“Every segment of the population has major concerns about the impact of eye disorders on quality of life,” said Mary Woolley, president and CEO of Research!America. “Individuals realize the importance of good eye health in maintaining productive lives and fear its loss. But the reality is that advances in the prevention and treatment of eye disorders will not be possible without stronger investments in research.”

National support of research that focuses on improving the prevention and treatment of eye and vision disorders is considered a priority among a strong majority of respondents (83% of African-Americans and non-Hispanic whites, 80% of Asians and 79% of Hispanics). When told that the federal government spends on average $2.10 per person each year on such research, half of African-Americans (51%) and Hispanics (50%) say this is not enough followed by non-Hispanic whites (47%) and Asians (35%). About half of all groups believe that non-governmental sectors — industry, patient groups and philanthropies — should also increase funding for eye and vision research (57% of Hispanics, 51% of African-Americans, 49% of Asians and 47% of non-Hispanic whites).

Knowledge about specific eye disorders was uneven among populations. More than half of all groups have heard of cataracts and glaucoma but fewer were aware of age-related macular degeneration (AMD) and diabetic eye disease. Hispanics (35%) and Asians (31%) are more likely to say they have not heard of these conditions compared to 22% of non-Hispanic whites and African-Americans.

As for causes of eye disorders, a majority of all respondents (80% of non-Hispanic whites, 77% of Hispanics, 76% of Asians and 70% of African-Americans) believe that excessive sunlight or ultraviolet radiation is a risk factor for eye disease along with ethnic heritage (64% of Asians, 60% of non-Hispanic whites, 59% of Hispanics and 52% of African-Americans). Chronic exposure of eyes to sunlight can cause cataracts and macular degeneration as well as eye irritation. Minority groups are often at a higher risk for vision impairment and blindness due to higher rates of certain eye conditions such as glaucoma, cataract and diabetic retinopathy.

More than half of Asians (57%), Hispanics and non-Hispanic whites (52%) and a plurality of African-Americans (42%) agree that obesity is also associated with greater risk for eye disease, and 62% of Hispanics, 60% of Asians, 54% of non-Hispanic whites and 48% of African-Americans agree smoking is a risk factor. Research has shown the risks of AMD, diabetic retinopathy, cataract and glaucoma increase with obesity-related systemic diseases such as diabetes or a high body mass index (BMI), abdominal circumference or waist-hip ratio. Smoking also increases the risk of AMD, cataracts, glaucoma, diabetic retinopathy and chronic dry eye.

Looking ahead, many respondents believe health care costs from eye disorders will increase by the year 2050 (62% of non-Hispanic whites, 58% of Asians, 54% of Hispanics and 50% of African-Americans). A June 2014 report by Prevent Blindness estimates that the total cost of vision disorders is expected to reach $717 billion in 2050 compared to the current annual cost of $145 billion.

New DNA test for diagnosing diseases linked to childhood blindness

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Posted on 11th October 2014 by Pacific ClearVision Institute in Cataracts |General

Researchers in the United Kingdom have demonstrated that advanced DNA testing for congenital cataracts can quickly and accurately diagnose a number of rare diseases marked by childhood blindness, according to a study published online in Ophthalmology, the journal of the American Academy of Ophthalmology. Using a single test, doctors were able to tailor care specifically to a child’s condition based on their mutations, reducing the time and money spent on diagnosis and enabling earlier treatment and genetic counseling.

Each year, between 20,000 and 40,000 children worldwide are born with congenital cataracts, a disease that clouds the lens of the eye and often requires surgery and treatment to prevent blindness.[i] The disease can arise following a maternal infection or be inherited as an isolated abnormality. Congenital cataracts can also appear as a symptom of more than 100 rare diseases, making mutations in the 115 genes associated with congenital cataracts useful as diagnostic markers for the illnesses.

Diagnosing these rare diseases previously proved a lengthy, costly and inconclusive process involving numerous clinical assessments and taking a detailed family history. DNA testing, one gene at a time, would have taken years to complete. Employing new DNA sequencing technology, called targeted next-generation sequencing, researchers at the University of Manchester sped up diagnosis to a matter of weeks by testing for mutations in all 115 known congenital cataracts genes at one time.

In 75 percent of the 36 cases tested, the DNA test determined the exact genetic cause of congenital cataracts. In one case, the DNA test helped diagnose a patient with Warburg Micro syndrome, an extremely rare disease that is marked by an abnormally small head and the development of severe epilepsy, among other medical issues. Having a clear diagnosis allowed for genetic counseling and appropriate care to be delivered quicker than previously possible without the test.

“There are many diseases that involve congenital cataracts but finding the exact reason was always difficult,” said Graeme Black, DPhil., professor of genetics and ophthalmology at the University of Manchester and strategic director of the Manchester Centre for Genomic Medicine. “Even with a family history, diagnosing these rare diseases was always a bit of a shot in the dark.”

In the course of their work, done in collaboration with Manchester Royal Eye Hospital, researchers also found previously undescribed mutations linked to cataract formation. “There is hope that our work may one day provide more insight into the development and treatment of age-related cataracts, a leading cause of blindness worldwide,” said Rachel Gillespie, MSc, lead author of the study who designed and developed the test.

The test was made available to U.K. patients through the country’s National Health Service in December 2013. Infants and children who have congenital cataracts can be tested as well as prospective parents with a history of the condition who wish to evaluate the risk to their child. Results generally take about two months. While only available in the U.K., the congenital cataract DNA test can be requested by registered medical facilities through international referral.

As with all genetic testing, the American Academy of Ophthalmology encourages clinicians and patients to consider the benefits as well as the risks. Ophthalmologists who order genetic tests either should provide genetic counseling to their patients themselves, if qualified to do so, or should ensure that counseling is provided by a trained individual, such as a board-certified medical geneticist or genetic counselor. For more information, please see the Academy’s recommendations on genetic testing for inherited eye diseases.

High-precision software developed for diagnosing eye sensitivity

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Posted on 11th October 2014 by Pacific ClearVision Institute in Cataracts |General

Researchers at the University of Alicante have developed high-precision software for diagnosing eye sensitivity. This is a new technology that allows to quantify the degree of opacity in the posterior capsule of the eye caused by the growth of cells in the intraocular lens.

The opacity of the posterior capsule is currently the most important aspect of cataract surgery in modern times, and is the postoperative complication that can still occur months or years after cataract surgery. This is reported to occur between 20% and up to 50% of patients in the period of five years after surgery, and is associated with the decreased of visual acuity, impaired contrast sensitivity and glare problems that involve significant social, medical and economic impact.

According to Dr. Daniel Ruiz Fernández, main researcher and member of the research group in Bioinspired Engineering and Computer Science for Health (IBIS), the problem of quantification of posterior capsule opacity has been addressed in different works and business solutions using different computational techniques. However, these processes entail some drawbacks because they require interaction with experts for them to detect the zones of opacification, with the risk of losing objectivity in the quantification. On the other hand, some of the systems are automated but focused on detecting the lens opacity (cataract origin) and not specifically on the growth of cells in intraocular lens.

The technology developed by the researchers at the UA provides a fully automatic and objective quantification from a digital image of the magnification of the ocular fundus. The process does not require any intervention by specialists, becoming an important tool for diagnosis. Thus, the use of this technology can avoid unnecessary interventions as well as improving diagnostic in those necessary.

This is a high-precision process since it directly analyses the origin of the opacity in the intraocular lens, ie, cells that grow on the lens.

The IBIS group has developed the first prototype of the implementation that has been tested successfully. The group also continues to work on continuous improvement and optimization of the software for better detection of artifacts and cells as well as in reducing the processing time.

Vitamin E, selenium supplements unlikely to affect age-related cataracts in men

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Posted on 11th October 2014 by Pacific ClearVision Institute in Cataracts |General

Taking daily supplements of selenium and/or vitamin E appears to have no significant effect on the development of age-related cataracts in men, writes Author William G. Christen, Sc.D., of Brigham & Women’s Hospital and Harvard Medical School, Boston, and colleagues.

Some research, including animal studies, has suggested that dietary nutrients can have an effect on the onset and progression of cataracts. Vitamin E and selenium are of particular interest.

The authors report the findings for cataracts from the Selenium and Vitamin E Cancer Prevention Trial (SELECT) Eye Endpoints (SEE) Study. The SEE study was an ancillary study of SELECT, a randomized placebo-controlled trial of selenium, vitamin E and a combination of the two in prostate cancer prevention among 35,533 men (50 years and older for black men and 55 years and older for all other men). Men were asked to report cataract diagnosis or removal since entering the SELECT trial. A total of 11,267 SELECT participants took part in the SEE study.

During an average of 5.6 years of treatment and follow-up, there were 389 cases of cataracts. There were 185 cases of cataracts in the selenium group and 204 in the group that didn’t take selenium. There were 197 cases of cataracts in the vitamin E group and 192 in the group without vitamin E. Results were similar for cataract removal.

“These randomized trial data from a large cohort of apparently healthy men indicate that long-term daily supplemental use of vitamin E has no material impact on cataract incidence. The data also exclude any large beneficial effect on cataract for long-term supplemental use of selenium, with or without vitamin E, although a smaller but potentially important beneficial effect could not be ruled out.”

How a single, genetic change causes retinal tumors in young children

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Posted on 11th October 2014 by Pacific ClearVision Institute in General |Retina

Retinoblastoma is a childhood retinal tumor usually affecting children one to two years of age. Although rare, it is the most common malignant tumor of the eye in children. Left untreated, retinoblastoma can be fatal or result in blindness. It has also played a special role in understanding cancer, because retinoblastomas have been found to develop in response to the mutation of a single gene – the RB1 gene — demonstrating that some cells are only a step away from developing into a life-threatening malignancy.

David E. Cobrinik, MD, PhD, of The Vision Center at Children’s Hospital Los Angeles (CHLA), together with colleagues at Memorial Sloan-Kettering Cancer Center, has answered the long-standing question of why mutations to the RB1 gene primarily cause tumors of the retina and not of other cell types. His study -which could reveal new cellular signaling pathways relevant to retinal development, cancer development, and ultimately, the development of novel therapies – is published in this week’s early on line issue of the journal Nature.

“These findings significantly advance our understanding of cancer, not only because they solve the RB riddle, but also because they more generally imply that cancers can develop through the collaboration between a cancer-causing mutation – in this case, inactivation of the RB1 gene – and cell type-specific circuitry,” said Cobrinik, who also an investigator with The Saban Research Institute of CHLA and associate professor of Ophthalmology at USC Eye Institute, Keck School of Medicine at the University of Southern California.

The RB1 gene encodes a tumor suppressor protein, referred to as Rb, which prevents excessive cell growth by inhibiting cell cycle progression until a cell is ready to divide. If both alleles of the RB1 gene are mutated early in life, the Rb protein is inactivated, resulting in development of retinoblastoma cancers. (While the Rb protein regulates proliferation in many cell types, only cells in the retina routinely form cancers when the function of the RB1 gene is lost.)

Cobrinik and colleagues discovered that retinoblastomas originate in cone photoreceptor precursors, and their study explains why retinoblastomas originate in these precursor cells. Cone cells, or cones, are one of the two types of photoreceptor cells in the retina, and are responsible for color vision. A cone precursor is an immature cone cell which is not yet fully differentiated.

The study indicates that cone precursors prominently express key, cancer-related proteins that enable proliferation and suppress apoptosis, or programmed cell death. Meanwhile, the role of the Rb protein is to hold back such proliferation — which means that the loss of Rb alone is sufficient to allow unchecked cell proliferation, causing retinoblastomas to form.

“We showed that the cone precursors’ normal developmental program collaborates with RB1 mutations to deregulate cell growth,” Cobrinik explained. “In other words, loss of the RB1 gene results in abnormal proliferation because the cone precursor cells lack a self-monitoring ‘surveillance system’ – which would normally cause aberrantly proliferating cells to undergo apoptosis. Instead, cells are able to divide uncontrollably and eventually become cancerous.”

Native American ancestry a risk factor for eye disease

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Posted on 11th October 2014 by Pacific ClearVision Institute in General |Retina

New research led by the University of Southern California (USC) Eye Institute, part of Keck Medicine of USC, shows for the first time that Native American ancestry is a significant risk factor for vision-threatening diabetic retinopathy among Latinos with Type 2 diabetes. Diabetic retinopathy is the leading cause of blindness in working-age adults in the United States, affecting more than 4 million Americans age 40 and older.

The research was published online in Investigative Ophthalmology & Visual Science, the peer-reviewed academic journal of The Association for Research in Vision and Ophthalmology.

Diabetic retinopathy occurs when blood vessels in the eye’s retina are damaged. The retina is the light-sensitive tissue at the back of the eye that acts like a film inside a camera; like damaged film, a damaged retina will produce a bad picture. Symptoms may not be noticeable at first, but the disease can get worse over time and lead to vision loss.

“This is the first study, to our knowledge, that examines the contribution of genetic ancestry in vision-threatening diabetic eye disease in Latinos,” said USC Eye Institute Director Rohit Varma, M.D., M.P.H., professor and chair of the Department of Ophthalmology at the Keck School of Medicine of USC and the study’s principal investigator. “Previous research has shown that Latinos have a higher prevalence of diabetic retinopathy than non-Hispanic Whites and African-Americans. Our findings suggest that one contributor to this heavy burden may be due to their Native American ancestry.”

Latinos are a diverse group of people typically with a varying mixture of Native American, European and African ancestry. Varma’s research team examined data from 944 Latinos with Type 2 diabetes from the Los Angeles Latino Eye Study (LALES), the largest population-based study of eye disease in that ethnic group. The participants in the study were 40 years of age or older and hailed from the city of La Puente in Los Angeles County, California. Ninety-five percent of them were of Mexican origin. Of the 944 people with type II diabetes, 135 had vision-threatening diabetic retinopathy while 809 did not.

Using genetic assays and detailed ophthalmologic examinations, the team found that individuals with more than 50 percent Native American ancestry had an 87 percent higher chance of also having vision-threatening diabetic retinopathy compared to those who had less than 50 percent Native American ancestry, even after controlling for known risk factors for the disease.

“Our next steps will be to try to narrow down which genomic locations among those with a Native American origin might be contributing to boosting the risk for developing severe diabetic retinopathy,” said Xiaoyi Gao, the study’s first author who started his research at USC. Gao is now associate professor of ophthalmology in the University of Illinois, Chicago College of Medicine.

To see or not to see: Answering questions about neurons

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Posted on 11th October 2014 by Pacific ClearVision Institute in General |Retina

The brain is a complicated network of small units called neurons, all working to carry information from the outside world, create an internal model, and generate a response. Neurons sense a signal through branching dendrites, carry this signal to the cell body, and send it onwards through a long axon to signal the next neuron. However, neurons can function in many different ways; some of which researchers are still exploring. Some signals that the dendrites receive do not continue to the next neuron; instead they seem to change the way that the neuron handles the subsequent signals. This could help neurons function as part of a large network, but researchers still have many questions. Dr. Sigita Augustinaite, a researcher in the Optical Neuroimaging Unit at the Okinawa Institute of Science and Technology Graduate University, suggested one mechanism explaining how neurons help the network function. Her findings, part of collaboration between the University of Oslo and OIST, were published August 13, 2014 as the cover article in The Journal of Neuroscience.

Dr. Augustinaite studies the visual pathway, where signals from the retina are sent to the visual cortex, where the brain interprets signals from the eye. Between the eye and the visual cortex, the signals must pass through the visual thalamus, that is, through thalamocortical, or TC neurons. These neurons can switch between a “sleeping” state and a “waking” state depending on input they receive from neurons and other brain areas. When an animal is awake, TC neurons transmit the incoming retinal signals on to the cortex, but when the animal is asleep, the neurons block retinal signals.

The visual cortex also sends a massive input back to TC neurons to control retinal signals traveling through the thalamus. But Dr. Augustinaite says that the suggested mechanisms of this control bring more questions than answers. To understand more, she conducted experiments in acute brain slices, small pieces of brain tissue where neurons stay alive and maintain their physiological properties. She added glutamate to dendrites far from the cell body to emulate a feedback signal from the visual cortex. Then she measured the neuron’s response, shown as a voltage difference between inside and outside of the membrane.

Dr. Augustinaite found that stimulating the neurons in this way depolarizes their membranes, creating something called NMDA spike/plateau potentials. If strong enough, depolarization can cause a neuron to fire an action potential, which travels through the axon to activate other neurons. Action potentials look like a sharp, one-millisecond increase in membrane voltage, and they transmit signals from retina to cortex. But if NMDA spike/plateaus induces action potentials, signals from the cortex and signals from the retina would be indistinguishable. With her experiments, Dr. Augustinaite showed that the NMDA spike/plateau potentials in TC neurons do not trigger action potentials. Instead, they lift the voltage of the membrane, changing the neuron’s properties for few hundred milliseconds, creating conditions for reliable signal transmission from retina to cortex.

“The research gives, for the first time, a clear view on what dendritic potentials are good for,” explained Prof. Bernd Kuhn, who leads the lab where Dr. Augustinaite works. “It points directly to the mechanism,” he concluded. Showing how dendritic plateaus function is just one important step toward understanding how neurons function as a network. “This mechanism could also be used in many other neuronal circuits, where one input regulates how another input moves through the network,” Dr. Augustinaite said. “This mechanism is an exciting logical element in the neuronal network, but just the start of putting the puzzle together.”

New therapeutic target may prevent blindness in premature babies at risk of retinopathy

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Posted on 11th October 2014 by Pacific ClearVision Institute in General |Retina

According to a study conducted by pediatricians and researchers at Sainte-Justine University Hospital Research Center (Sainte-Justine) and Université de Montréal published online in the prestigious medical journal Nature Medicine on September 14, 2014, the activation of a receptor that migrates to the nucleus of nerve cells in the retina promotes the growth of blood vessels. The finding opens the possibility of developing new, more selective drugs to control the abnormal growth of blood vessels and prevent blindness including retinopathy of prematurity, a disorder that may result in retinal detachment due to abnormal blood vessel growth in the retina of the eye.

“This study shows that a single receptor may play various roles depending on whether its site of action is in the nucleus or on the cell membrane,” states Dr. Jean-Sébastien Joyal, MD, PhD, a pediatric intensivist at the Sainte-Justine UHC and an assistant professor at the Université de Montréal. The groundbreaking discovery has significant clinical implications, since many drugs act on this family of receptors irrespective of their site of action in the cell. “Our results are extremely encouraging. They indicate that drugs formulated to target this nuclear receptor may one day prevent retinopathy in premature babies,” continued Dr. Sylvain Chemtob, a neonatologist at Sainte-Justine and a full professor in Pediatrics, Ophthalmology and Pharmacology at the Université de Montréal.

Abnormal proliferation of blood vessels may lead to a number of disorders. Therefore, the finding may offer therapeutic potential for other conditions, particularly proliferative diabetic retinopathy and cancer. This potential still needs to be explored.

Changes in eye can predict changes in brain

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Posted on 11th October 2014 by Pacific ClearVision Institute in General |Retina

Researchers at the Gladstone Institutes and University of California, San Francisco have shown that a loss of cells in the retina is one of the earliest signs of frontotemporal dementia (FTD) in people with a genetic risk for the disorder — even before any changes appear in their behavior.

Published in the Journal of Experimental Medicine, the researchers, led by Gladstone investigator Li Gan, PhD and UCSF associate professor of neurology Ari Green, MD, studied a group of individuals who had a certain genetic mutation that is known to result in FTD. They discovered that before any cognitive signs of dementia were present, these individuals showed a significant thinning of the retina compared with people who did not have the gene mutation.

“This finding suggests that the retina acts as a type of ‘window to the brain,’” said Dr. Gan. “Retinal degeneration was detectable in mutation carriers prior to the onset of cognitive symptoms, establishing retinal thinning as one of the earliest observable signs of familial FTD. This means that retinal thinning could be an easily measured outcome for clinical trials.”

Although it is located in the eye, the retina is made up of neurons with direct connections to the brain. This means that studying the retina is one of the easiest and most accessible ways to examine and track changes in neurons.

Lead author Michael Ward, MD, PhD, a postdoctoral fellow at the Gladstone Institutes and assistant professor of neurology at UCSF, explained, “The retina may be used as a model to study the development of FTD in neurons. If we follow these patients over time, we may be able to correlate a decline in retinal thickness with disease progression. In addition, we may be able to track the effectiveness of a treatment through a simple eye examination.”

The researchers also discovered new mechanisms by which cell death occurs in FTD. As with most complex neurological disorders, there are several changes in the brain that contribute to the development of FTD. In the inherited form researched in the current study, this includes a deficiency of the protein progranulin, which is tied to the mislocalization of another crucial protein, TDP-43, from the nucleus of the cell out to the cytoplasm.

However, the relationship between neurodegeneration, progranulin, and TDP-43 was previously unclear. In follow-up studies using a genetic mouse model of FTD, the scientists were able to investigate this connection for the first time in neurons from the retina. They identified a depletion of TDP-43 from the cell nuclei before any signs of neurodegeneration occurred, signifying that this loss may be a direct cause of the cell death associated with FTD.

TDP-43 levels were shown to be regulated by a third cellular protein called Ran. By increasing expression of Ran, the researchers were able to elevate TDP-43 levels in the nucleus of progranulin-deficient neurons and prevent their death.

“With these findings,” said Dr. Gan, “we now not only know that retinal thinning can act as a pre-symptomatic marker of dementia, but we’ve also gained an understanding into the underlying mechanisms of frontotemporal dementia that could potentially lead to novel therapeutic targets.”

Study of noninvasive retinal imaging device presented at Alzheimer’s conference

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Posted on 11th October 2014 by Pacific ClearVision Institute in General |Retina

A noninvasive optical imaging device developed at Cedars-Sinai can provide early detection of changes that later occur in the brain and are a classic sign of Alzheimer’s disease, according to preliminary results from investigators conducting a clinical trial in Australia.

The researchers will present their findings July 15 in an oral presentation at the Alzheimer’s Association International Conference 2014 in Copenhagen, Denmark. They also were invited by conference organizers to participate in a “breaking news” news conference beginning at 7:30 a.m. Sunday, July 13 in Copenhagen, 1:30 a.m. EDT.

“In preliminary results in 40 patients, the test could differentiate between Alzheimer’s disease and non-Alzheimer’s disease with 100 percent sensitivity and 80.6 percent specificity, meaning that all people with the disease tested positive and most of the people without the disease tested negative. The optical imaging exam appears to detect changes that occur 15-20 years before clinical diagnosis. It’s a practical exam that could allow testing of new therapies at an earlier stage, increasing our chances of altering the course of Alzheimer’s disease,” said Shaun Frost, a biomedical scientist and the study manager at the Commonwealth Scientific and Industrial Research Organisation. CSIRO is Australia’s national science agency.

Frost, first author of the AAIC 2014 abstract, will make the oral presentation. He said 120 participants of a full study of 200 had completed testing.

Keith Black, MD, professor and chair of Cedars-Sinai’s Department of Neurosurgery, director of the Maxine Dunitz Neurosurgical Institute and the Ruth and Lawrence Harvey Chair in Neuroscience, said the accumulation of beta-amyloid plaque in the brain is a hallmark sign of Alzheimer’s, but current tests detect changes only after the disease has advanced to late stages. Researchers believe that as treatment options improve, early detection will be critical, but existing diagnostic methods are inconvenient, costly and impractical for routine screening.

“PET scans require the use of radioactive tracers, and cerebrospinal fluid analysis requires that patients undergo invasive and often painful lumbar punctures, but neither approach is quite feasible, especially for patients in the earlier stages of disease,” he said. Positron emission tomography, or PET, is the current diagnostic standard.

“The retina, unlike other structures of the eye, is part of the central nervous system, sharing many characteristics of the brain. A few years ago, we discovered at Cedars-Sinai that the plaques associated with Alzheimer’s disease occur not only in the brain but also in the retina. By ‘staining’ the plaque with curcumin, a component of the common spice turmeric, we could detect it in the retina even before it began to accumulate in the brain. The device we developed enables us to look through the eye — just as an ophthalmologist looks through the eye to diagnose retinal disease — and see these changes.”

This clinical trial was designed to enable researchers to correlate retinal plaque detected by optical imaging with brain plaque detected by PET scans. Studies involved patients diagnosed with Alzheimer’s, a group with mild cognitive impairment and a group of people with no evidence of brain abnormality.

The retinal beta-amyloid plaque findings and optical imaging technology began at Cedars-Sinai with studies in live rodents and the post-mortem investigation of human retinas of people who had died with Alzheimer’s. Maya Koronyo-Hamaoui, PhD, assistant professor of neurosurgery in the Department of Neurosurgery and the Department of Biomedical Sciences, and Yosef Koronyo, a research scientist, were first authors of the original results that were published in a journal and presented at the AAIC in 2010. The Australian study is one of several in progress to determine if similar results can be confirmed in humans living with the disease.

“This large double-blind clinical trial appears to validate our novel human retinal amyloid imaging approach using curcumin labeling. It further demonstrates significant correlation with brain amyloid burden, thereby predicting accumulation of plaques in the brain through the retina,” said Koronyo-Hamaoui, a faculty principal investigator and head of the Neuroimmunology and Retinal Imaging Laboratory at Cedars-Sinai.