Good news for people who lose their foveal vision due to macular diseases

Main Category: Eye Health / Blindness
Also Included In: Seniors / Aging
Article Date: 19 Aug 2013 - 0:00 PDT Current ratings for:
Good news for people who lose their foveal vision due to macular diseases

When something gets in the way of our ability to see, we quickly pick up a new way to look, in much the same way that we would learn to ride a bike, according to a new study published in the Cell Press journal Current Biology.

Our eyes are constantly on the move, darting this way and that four to five times per second. Now researchers have found that the precise manner of those eye movements can change within a matter of hours. This discovery by researchers from the University of Southern California might suggest a way to help those with macular degeneration better cope with vision loss.

"The system that controls how the eyes move is far more malleable than the literature has suggested," says Bosco Tjan of the University of Southern California. "We showed that people with normal vision can quickly adjust to a temporary occlusion of their foveal vision by adapting a consistent point in their peripheral vision as their new point of gaze."

The fovea refers to the small, center-most portion of the retina, which is responsible for our high-resolution vision. We move our eyes to direct the fovea to different parts of a scene, constructing a picture of the world around us. In those with age-related macular degeneration, progressive loss of foveal vision leads to visual impairment and blindness.

In the new study, MiYoung Kwon, Anirvan Nandy, and Tjan simulated a loss of foveal vision in six normally sighted young adults by blocking part of a visual scene with a gray disc that followed the individuals' eye gaze. Those individuals were then asked to complete demanding object-following and visual-search tasks. Within three hours of working on those tasks, people showed a remarkably fast and spontaneous adjustment of eye movements. Once developed, that change in their "point of gaze" was retained over a period of weeks and was reengaged whenever their foveal vision was blocked.

Tjan and his team say they were surprised by the rate of this adjustment. They note that patients with macular degeneration frequently do adapt their point of gaze, but in a process that takes months, not days or hours. They suggest that practice with a visible gray disc like the one used in the study might help speed that process of visual rehabilitation along. The discovery also reveals that the oculomotor (eye movement) system prefers control simplicity over optimality.

"Gaze control by the oculomotor system, although highly automatic, is malleable in the same sense that motor control of the limbs is malleable," Tjan says. "This finding is potentially very good news for people who lose their foveal vision due to macular diseases. It may be possible to create the right conditions for the oculomotor system to quickly adjust," Kwon adds.

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Omega-3 rich oils improve membrane fluidity in retina cells and can help fight age-related eye diseases

Main Category: Eye Health / Blindness
Also Included In: Nutrition / Diet;  Seniors / Aging
Article Date: 19 Aug 2013 - 1:00 PDT Current ratings for:
Omega-3 rich oils improve membrane fluidity in retina cells and can help fight age-related eye diseases

Scientists working at the Research Center on Aging at the Health and Social Services Centre - University Institute of Geriatrics of Sherbrooke (CSSS-IUGS) have been studying strategies for protecting retinal pigment epithelium (RPE) cells. Dysfunction of the RPE is found in retinopathy and age-related macular degeneration, which is the leading cause of blindness of elderly people in developed countries.

Findings published in the Canadian Journal of Physiology and Pharmacology suggest that incubating retinal cells with vegetable oils induces biochemical and biophysical changes in the cell membrane, which may have a beneficial effect in preventing or slowing the development of retinopathy.

"Membrane fluidity, which refers to the viscosity of the lipid bi-layer of a cell membrane, is a marker of the cell function," explained Prof. A. Khalil, professor at the Université de Sherbrooke and principal investigator of the study. "A decrease of membrane fluidity can affect the rotation and diffusion of proteins and other bio-molecules within the membrane, thereby affecting the functions of these molecules. Whereas, an increase in membrane fluidity makes for a more flexible membrane and facilitates the transmission of light through the eye."

The researchers discovered that vegetable oil fatty acids incorporate in retina cells and increase the plasma membrane fluidity. They concluded that a diet low in trans-unsaturated fats and rich in omega-3 fatty acids and olive oil may reduce the risk of retinopathy. In addition, the research suggests that replacing the neutral oil used in eye drops with oil that possesses valuable biological properties for the eye could also contribute to the prevention of retina diseases.

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New culprit identified that may make aging brains susceptible to neurodegenerative diseases

Main Category: Neurology / Neuroscience
Also Included In: Seniors / Aging;  Alzheimer's / Dementia;  Parkinson's Disease
Article Date: 15 Aug 2013 - 0:00 PDT Current ratings for:
New culprit identified that may make aging brains susceptible to neurodegenerative diseases

The steady accumulation of a protein in healthy, aging brains may explain seniors' vulnerability to neurodegenerative disorders, a new study by researchers at the Stanford University School of Medicine reports.

The study's unexpected findings could fundamentally change the way scientists think about neurodegenerative disease.

The pharmaceutical industry has spent billions of dollars on futile clinical trials directed at treating Alzheimer's disease by ridding brains of a substance called amyloid plaque. But the new findings have identified another mechanism, involving an entirely different substance, that may lie at the root not only of Alzheimer's but of many other neurodegenerative disorders - and, perhaps, even the more subtle decline that accompanies normal aging.

The study, published in the Journal of Neuroscience, reveals that with advancing age, a protein called C1q, well-known as a key initiator of immune response, increasingly lodges at contact points connecting nerve cells in the brain to one another. Elevated C1q concentrations at these contact points, or synapses, may render them prone to catastrophic destruction by brain-dwelling immune cells, triggered when a catalytic event such as brain injury, systemic infection or a series of small strokes unleashes a second set of substances on the synapses.

"No other protein has ever been shown to increase nearly so profoundly with normal brain aging," said Ben Barres, MD, PhD, professor and chair of neurobiology and senior author of the study. Examinations of mouse and human brain tissue showed as much as a 300-fold age-related buildup of C1q.

The finding was made possible by the diligence and ingenuity of the study's lead author, Alexander Stephan, PhD, a postdoctoral scholar in Barres' lab. Stephan screened upward of 20,000 antibodies before finding one that binds to C1q and nothing else. (Antibodies are proteins, generated by the immune system, that adhere to specific "biochemical shapes," such as surface features of invading pathogens.)

Comparing brain tissue from mice of varying ages, as well as postmortem samples from a 2-month-old infant and an older person, the researchers showed that these C1q deposits weren't randomly distributed along nerve cells but, rather, were heavily concentrated at synapses. Analyses of brain slices from mice across a range of ages showed that as the animals age, the deposits spread throughout the brain.

"The first regions of the brain to show a dramatic increase in C1q are places like the hippocampus and substantia nigra, the precise brain regions most vulnerable to neurodegenerative diseases like Alzheimer's and Parkinson's disease, respectively," said Barres. Another region affected early on, the piriform cortex, is associated with the sense of smell, whose loss often heralds the onset of neurodegenerative disease.

Other scientists have observed moderate, age-associated increases (on the order of three- or four-fold) in brain levels of the messenger-RNA molecule responsible for transmitting the genetic instructions for manufacturing C1q to the protein-making machinery in cells. Testing for messenger-RNA levels - typically considered reasonable proxies for how much of a particular protein is being produced - is fast, easy and cheap compared with analyzing proteins.

But in this study, Barres and his colleagues used biochemical measures of the protein itself. "The 300-fold rise in C1q levels we saw in 2-year-old mice p equivalent to 70- or 80-year-old humans p knocked my socks off," Barres said. "I was not expecting that at all."

C1q is the first batter on a 20-member team of immune-response-triggering proteins, collectively called the complement system. C1q is capable of clinging to the surface of foreign bodies such as bacteria or to bits of our own dead or dying cells. This initiates a molecular chain reaction known as the complement cascade. One by one, the system's other proteins glom on, coating the offending cell or piece of debris. This in turn draws the attention of omnivorous immune cells that gobble up the target.

The brain has its own set of immune cells, called microglia, which can secrete C1q. Still other brain cells, called astrocytes, secrete all of C1q's complement-system "teammates." The two cell types work analogously to the two tubes of an Epoxy kit, in which one tube contains the resin, the other a catalyst.

Previous work in Barres' lab has shown that the complement cascade plays a critical role in the developing brain. A young brain generates an excess of synapses, creating a huge range of options for the potential formation of new neural circuits. These synapses strengthen or weaken over time, in response to their heavy use or neglect. The presence of feckless connections contributes noise to the system, so the efficiency of the maturing brain's architecture is improved if these underused synapses are pruned away.

In a 2007 paper in Cell, Barres' group reported that the complement system is essential to synaptic pruning in normal, developing brains. Then in 2012, in Neuron, in a collaboration with the lab of Harvard neuroscientist Beth Stevens, PhD, they showed that it is specifically microglia - the brain's in-house immune cells - that attack and ingest complement-coated synapses.

Barres now believes something similar is happening in the normal, aging brain. C1q, but not the other protein components of the complement system, gradually becomes highly prevalent at synapses. By itself, this C1q buildup doesn't trigger wholesale synapse loss, the researchers found - although it does seem to impair their performance. Old mice whose capacity to produce C1q had been eliminated performed subtly better on memory and learning tests than normal older mice did.

Still, this leaves the aging brain's synapses precariously perched on the brink of catastrophe. A subsequent event such as brain trauma, a bad case of pneumonia or perhaps a series of tiny strokes that some older people experience could incite astrocytes - the second tube in the Epoxy kit - to start secreting the other complement-system proteins required for synapse destruction.

Most cells in the body have their own complement-inhibiting agents. This prevents the wholesale loss of healthy tissue during an immune attack on invading pathogens or debris from dead tissue during wound healing. But nerve cells lack their own supply of complement inhibitors. So, when astrocytes get activated, their ensuing release of C1q's teammates may set off a synapse-destroying rampage that spreads "like a fire burning through the brain," Barres said.

"Our findings may well explain the long-mysterious vulnerability specifically of the aging brain to neurodegenerative disease," he said. "Kids don't get Alzheimer's or Parkinson's. Profound activation of the complement cascade, associated with massive synapse loss, is the cardinal feature of Alzheimer's disease and many other neurodegenerative disorders. People have thought this was because synapse loss triggers inflammation. But our findings here suggest that activation of the complement cascade is driving synapse loss, not the other way around."

In 2011, Barres co-founded a company, Annexon, to develop drugs that inhibit the complement cascade to treat Alzheimer's, glaucoma, Parkinson's, stroke, multiple sclerosis and several other neurodegenerative diseases characterized by massive synapse loss. Annexon has licensed multiple associated patent applications from Stanford, which filed them.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our neurology / neuroscience section for the latest news on this subject.

The study was funded by the Ellison Medical Foundation and the National Institute of Drug Addiction (grant DA15403).

Other Stanford co-authors of the study were Daniel Madison, PhD, associate professor of molecular and cellular physiology; Mehrdad Shamloo, PhD, associate professor of comparative medicine; postdoctoral scholars Laurence Coutellier, PhD, and Jose Maria Mateos, PhD; research associate Emilie Lovelett; and graduate student Dominic Berns.

Stanford University Medical Center

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Wild type genetic background affects outcome even for diseases with a simple genetic basis

Main Category: Genetics
Article Date: 05 Aug 2013 - 0:00 PDT Current ratings for:
Wild type genetic background affects outcome even for diseases with a simple genetic basis

If two women have the same genetic mutation that puts them at higher-than-average risk for a disease such as breast cancer, why does only one develop the disease?

In the current issue of PLOS Genetics, Michigan State University genetic scientists have begun to understand how the rest of the genome interacts with such mutations to cause the differences we see among individuals.

"It's been known for a while that genetic mutations can modify each other's effects," said Ian Dworkin, MSU associate professor of zoology and co-author of the paper. "And we also know that the subtle differences in an individual's genome - what scientists call wild type genetic background - also affects how mutations are manifested."

Dworkin and Sudarshan Chari, zoology doctoral student and the paper's lead author, wanted to know how common it was for wild type genetic background to alter the way genetic mutations interact with each other. This is the first time that it's been examined in a systematic manner, Dworkin added.

Using the fruit fly genome, the researchers found that wild type genetic background affected the outcomes of interactions between genetic mutations about 75 percent of the time. This could have huge implications in how scientists construct genetic networks - maps of how genes interact with each other.

"It may be that some crucial portions of genetic networks are missing," he said. "It also seems that network descriptions are more fluid than we thought."

Fruit flies have been called humans with wings, genetically speaking, due to their similarities. By focusing on wings and a genetic mutation that alters them, the researchers demonstrated the influence of wild type genetic background was actually quite common.

The broader implication for humans is that even for diseases with a simple genetic basis, variation in the genome may matter for both understanding and treatment, Dworkin said.

This new insight explains how, in an example like breast cancer, every woman's genetic background is likely influencing how the mutation is expressed, causing different disease outcomes. The research also may help explain why some people benefit from a specific treatment for a disease, while others get no benefits or become resistant to a drug after a short time.

It's likely that most diseases with a suspected genetic component, such as cancer, asthma or Parkinson's, involve reactions between more than one set of genes. For Dworkin and Chari, the next step is to tease apart the intricacies of what's happening.

"Is it just the two pairs of genes that are interacting?" Dworkin asked. "Or is it that the two genes are interacting and then many other genes are modifying that reaction? This will help us understand how much complexity is involved."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our genetics section for the latest news on this subject.

The research is funded by the National Science Foundation grant number MCB 0922344.

Michigan State University

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Health Tips & Info : The End of Common Diseases.

This picture presents the latest available statistics of the World Health Organization regarding the main causes of death in Europe, the United States, and other industrialized countries at the end of the twentieth century. Every year 12 million people worldwide die of the results of atherosclerosis, heart infarctions, and strokes. These are by far the most common causes of death of our time. 
Cellular Medicine has already found an answer to this epidemic: atherosclerosis and its consequences, heart infarction and stroke are early forms of scurvy. Based on this knowledge, coronary heart disease will be reduced to a fraction of the current figures over the next decades. The second-largest common disease is cancer—malignant tumors. Coronary disease and cancer together are responsible for over 80% of all deaths in industrialized countries. Incidences of cancer keep increasing on a global scale. There is only one plausible explanation for this: conventional medicine does not know the causes for cancer nor how this disease spreads. Because of this there is no effective cancer therapy available and the disease can keep expanding on a global scale. The most common diseases and causes of death in developing countries are infectious diseases, including the AIDS epidemic. These serious infectious diseases can only continue spreading the way they do because the knowledge of cellular health has been not efficiently used. This book will also provide the solution for the control of these diseases.From : Cellular Health Series Cancer Book. By Matthias Rath, M.D.

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