“Cognitive biometrics is a novel approach to user authentication and/or identification that utilises the response(s) of nervous tissue,” explains Revett, who is the journal’s academic editor. He explains that cognitive biometrics relies on the response of the subject when they are presented with a particular stimulus such as a familiar photograph, a song, a puzzle, or even a Rorschach ink blot.

The response can be acquired through a variety of techniques, including: electroencephalogram (EEG), an electrocardiogram (ECG), electrodermal response (EDR), blood pulse volume (BVP). Other techniques such as near-infrared spectroscopy (NIR), electromyogram (EMG), eye trackers (pupilometry), hemoencephalography (HEG), and related technologies might also be used. The validation of the user is then based on the matching of their response to the stimulus with a pre-recorded ECG, EEG or other metric. The stimuli are designed to elicit responses that are sensitive to the individual’s genetic predispositions, modulated by subjective experiences.

Revett points out that cognitive biometrics can “provide a more intuitive and arguably a more robust and user-friendly authentication protocol that is suitable for both static and continuous authentication requirements,” he says. It might also be combined with other related biometric techniques such as keystroke and/or mouse dynamics, which would increase the level of security to virtually any desired level. He adds that the inaugural issue of the journal not only introduces the concept of cognitive biometrics in more detail than ever before but also presents several papers that focus on a wide variety of issues, such as security and user adoption, associated with implementing cognitive biometrics. The range of papers focuses on factors such as how easy the data is to acquire, persistence, ease of generalisation and deployment issues, Revett adds.

“Provided the proper stimuli are presented, the stimulus-response paradigm provides a powerful methodology for evaluating the authenticity of the subject requesting authentication,” he concludes.

Normal, non-pathological emmetropic eyes are the most common type amongst the population (43.2%), with a percentage that swings between 60.6% in children from three to eight years and 29% in those older than 66.

Therefore, a study determines their anatomical pattern so that they serve as a model for comparison with eyes that have refractive defects (myopia, hypermetropia and stigmatism) pathological eyes (such as those that have cataracts).

“We know very little about emmetropic eyes even though they should be used for comparisons with myopic and hypermetropic eyes” Juan Alberto Sanchis-Gimeno, researcher at the University of Valencia and lead author of the study explained.

The project, published in the journal ‘Surgical and Radiologic Anatomy’ shows the values by gender for the central corneal thickness, minimum total corneal thickness, white to white distance and pupil diameter in a sample of 379 emmetropic subjects.

“It is the first study that analyses these anatomical indexes in a large sample of healthy emmetropic subjects” Sanchis-Gimeno states. In recent years new technologies have been developed, such as corneal elevation topography, which allows us to increase our understanding of in vivo ocular anatomy.

Although the research states that there are no big differences between most of the parameters analysed, healthy emmetropic women have a wider pupil diameter than men.

“It will be necessary to investigate as to whether there are differences in the anatomical indexes studied between emmetropic, myopic and hypermetropic eyes, and between populations of different ethnic origin” the researcher concludes.

How the human eye works

Light penetrates through the pupil, crosses the crystalline lens and is projected onto the retina, where the photoreceptor cells turn it into nerve impulses, and it is transferred through the optic nerve to the brain. Rays of light should refract so that they can penetrate the eye and can be focused on the retina. Most of the refraction occurs in the cornea, which has a fixed curvature.

The pupil is a dilatable and contractile opening that regulates the amount of light that reaches the retina. The size of the pupil is controlled by two muscles: the pupillary sphincter, which closes it, and the pupillary dilator, which opens it. Its diameter is between 3 and 4.5 millimetres in the human eye, although in the dark it could reach up to between 5 and 9 millimetres.

Marketed by Avedro, Inc., Lasik Xtra is a corneal crosslinking procedure that applies the company’s VibeX riboflavin ophthalmic solution to the eye’s surface (cornea), and then uses Avedro’s KXL System to irradiate the cornea with UV-A rays. Lasik Xtra is an accelerated form of crosslinking — Avedro says it takes two minutes — which makes it more convenient to combine with LASIK.

Avedro said that in April it will report on studies that show the procedure has helped people who received hyperopic LASIK, which tends to regress more than myopic LASIK, to maintain the vision correction they had received from LASIK.

Although corneal crosslinking has not received FDA approval yet, Avedro’s VibeX solution has received orphan drug approvals from the agency. Orphan drug status is usually conferred on treatments for rare medical conditions (in this case, keratoconus, which is a gradual thinning of the cornea).

And in another advance, the retina structures showed the capacity to form layers of cells – as the retina does in normal human development – and these cells possessed the machinery that could allow them to communicate information. (Light-sensitive photoreceptor cells in the retina along the back wall of the eye produce impulses that are ultimately transmitted through the optic nerve and then to the brain, allowing you to see.) Put together, these findings suggest that it is possible to assemble human retinal cells into more complex retinal tissues, all starting from a routine patient blood sample.

Many applications of laboratory-built human retinal tissues can be envisioned, including using them to test drugs and study degenerative diseases of the retina such as retinitis pigmentosa, a prominent cause of blindness in children and young adults. One day, it may also be possible replace multiple layers of the retina in order to help patients with more widespread retinal damage.

“We don’t know how far this technology will take us, but the fact that we are able to grow a rudimentary retina structure from a patient’s blood cells is encouraging, not only because it confirms our earlier work using human skin cells, but also because blood as a starting source is convenient to obtain,” says Dr. David Gamm, pediatric ophthalmologist and senior author of the study. “This is a solid step forward.”

In 2011, the Gamm lab at the UW Waisman Center created structures from the most primitive stage of retinal development using embryonic stem cells and stem cells derived from human skin. While those structures generated the major types of retinal cells, including photoreceptors, they lacked the organization found in more mature retina.

This time, the team, led by Gamm, Assistant Professor of Ophthalmology and Visual Sciences in the UW School of Medicine and Public Health, and postdoctoral researcher and lead author Dr. Joseph Phillips, used their method to grow retina-like tissue from iPS cells derived from human blood gathered via standard blood draw techniques.

In their study, about 16 percent of the initial retinal structures developed distinct layers. The outermost layer primarily contained photoreceptors, whereas the middle and inner layers harbored intermediary retinal neurons and ganglion cells, respectively. This particular arrangement of cells is reminiscent of what is found in the back of the eye. Further, work by Dr. Phillips showed that these retinal cells were capable of making synapses, a prerequisite for them to communicate with one another.

The iPS cells used in the study were generated through collaboration with Cellular Dynamics International (CDI) of Madison, Wis., who pioneered the technique to convert blood cells into iPS cells. CDI scientists extracted a type of blood cell called a T-lymphocyte from the donor sample, and reprogrammed the cells into iPS cells. CDI was founded by UW stem cell pioneer Dr. James Thomson.

“We were fortunate that CDI shared an interest in our work. Combining our lab’s expertise with that of CDI was critical to the success of this study,” added Dr. Gamm.

Other members of the research team include:

– Kyle Wallace, Amelia Verhoeven, Jessica Martin, Lynda Wright, Wei Shen, Elizabeth Capowski and Enio Perez, of the Waisman Center.
– Sarah Dickerson and Michael Miller of CDI.
– E. Ferda Percen of the Faculty of Medicine, Gazi University, Ankara, Turkey.
– Xiufeng Zhong and Maria Canto-Soler, of the Wilmer Eye Institute at Johns Hopkins Univerity.

The research is supported by the Foundation Fighting Blindness, the National Institutes of Health, the Retina Research Foundation, the UW Institute for Clinical and Translational Research, the UW Eye Research Institute and the E. Matilda Ziegler Foundation for the Blind, Inc.

Damage to the retina is called retinopathy. In the study, the damage was mild enough to not cause significant symptoms.

“Problems with the tiny blood vessels in the eye may be a sign that there are also problems with the blood vessels in the brain that can lead to cognitive problems,” said study author Mary Haan, DrPH, MPH, of the University of California, San Francisco. “This could be very useful if a simple eye screening could give us an early indication that people might be at risk of problems with their brain health and functioning.”

The study involved 511 women with an average age of 69. The women took tests of their thinking and memory skills every year for up to 10 years. Their eye health was tested about four years into the study and scans were taken of their brains about eight years into the study.

A total of 39 women, or 7.6 percent, had retinopathy. The women with retinopathy on average had lower scores on the cognitive tests than the women who did not have retinopathy. The women with retinopathy also had more areas of small vascular damage within the brain, with 47 percent larger volumes of areas of damage than women who did not have retinopathy. In the parietal lobe of the brain, the women with retinopathy had 68 percent larger volumes of areas of damage.

The results remained the same even after adjusting for high blood pressure and diabetes, which can be a factor in vascular issues in the eye and the brain.

On a test of visual acuity, the women with retinopathy had similar scores as the women without the disease.

The study was supported by the National Heart, Lung and Blood Institute, the U.S. Department of Health and Human Services, Wyeth Pharmaceuticals and the National Institute on Aging.

The two areas of the brain that are particularly good at reacting to external movements, even during eye movements, are known as V3A and V6. They are located in the upper half in the posterior part of the brain. Area V3A shows a high degree of integration: it reacts to movements around us regardless of whether or not we follow the moving object with our eyes. But the area does not react to visual movements on the retina when eye movements produce them. Area V6 has similar characteristics. In addition, it can perform these functions when we are moving forwards. The calculations the brain has to perform are more complicated in this case: the three-dimensional, expanding forward movement is superimposed onto the two-dimensional lateral movements that are caused by eye movements.

The scientists Elvira Fischer and Andreas Bartels from the Werner Reichardt Centre for Integrative Neuroscience and the Max Planck Institute for Biological Cybernetics have investigated these areas with the help of functional magnetic resonance imaging (fMRI). fMRI is a procedure that can measure brain activity based on local changes in blood flow and oxygen consumption. Participants in the study were shown various visual scenarios whilst undergoing fMRI scanning. For example, they had to follow a small dot with their eyes while it moved across a screen from one side to the other. The patterned background was either stationary or moved at varying speeds, sometimes slower, faster or at the same speed as the dot. Sometimes the dot was stationary while only the background moved. In a total of six experiments the scientists measured brain activity in more than a dozen different scenarios. From this they have been able to discover that V3A and V6, unlike other visual areas in the brain, have a pronounced ability to compare eye movements with the visual signals on the retina. “I am especially fascinated by V3A because it reacts so strongly and selectively to movements in our surroundings. It sounds trivial, but it is an astonishing capability of the brain,” explains Andreas Bartels, project leader of the study.

Whether it is ourselves who move or something else in our surroundings is a problem about which we seldom think, since at the subconscious level our brain constantly calculates and corrects our visual impression. Indeed, patients who have lost this ability to integrate movements in their surroundings with their eye movements can no longer recognize what it is that ultimately is moving: the surroundings or themselves. Every time they move their eyes these patients feel dizzy. Studies such as this bring us one step closer to an understanding of the causes of such illnesses.

The study was a collaboration between the Werner Reichardt Centre for Integrative Neuroscience and the department for Human Perception, Cognition and Action of Heinrich Bülthoff as well as the department for Physiology of Cognitive Processes of Nikos Logothetis at the Max Planck Institute for Biological Cybernetics.

Researchers increased the resistance of optic nerve cells to damage by repeatedly exposing the mice to low levels of oxygen similar to those found at high altitudes. The stress of the intermittent low-oxygen environment induces a protective response called tolerance that makes nerve cells — including those in the eye — less vulnerable to harm.

The study, published online in Molecular Medicine, is the first to show that tolerance induced by preconditioning can protect against a neurodegenerative disease.

Stress is typically thought of as a negative phenomenon, but senior author Jeffrey M. Gidday, PhD, associate professor of neurological surgery and ophthalmology, and others have previously shown that the right kinds of stress, such as exercise and low-oxygen environments, can precondition cells and induce changes that make them more resistant to injury and disease.

Scientists previously thought tolerance in the central nervous system only lasted for a few days. But last year Gidday developed a preconditioning protocol that extended the effects of tolerance from days to months. By exposing mice to hypoxia, or low oxygen concentrations, several times over a two-week period, Gidday and colleagues triggered an extended period of tolerance. After preconditioning ended, the brain was protected from stroke damage for at least 8 weeks.

“Once we discovered tolerance could be extended, we wondered whether this protracted period of injury resistance could also protect against the slow, progressive loss of neurons that characterizes neurodegenerative diseases,” Gidday says.

To find out, Gidday turned to an animal model of glaucoma, a condition linked to increases in the pressure of the fluid that fills the eye. The only treatments for glaucoma are drugs that reduce this pressure; there are no therapies designed to protect the retina and optic nerves from harm.

Scientists classify glaucoma as a neurodegenerative disease based on how slowly and progressively it kills retinal ganglion cells. The bodies of these cells are located in the retina of the eye; their branches or axons come together in bundles and form the optic nerves. Scientists don’t know if damage begins in the bodies or axons of the cells, but as more and more retinal ganglion cells die, patients experience peripheral vision loss and eventually become blind.

For the new study, Yanli Zhu, MD, research instructor in neurosurgery, induced glaucoma in mice by tying off vessels that normally allow fluid to drain from the eye. This causes pressure in the eye to increase. Zhu then assessed how many cell bodies and axons of retinal ganglion cells were intact after three or 10 weeks.

The investigators found that normal mice lost an average of 30 percent of their retinal ganglion cell bodies after 10 weeks of glaucoma. But mice that received the preconditioning before glaucoma-inducing surgery lost only 3 percent of retinal ganglion cell bodies.

“We also showed that preconditioned mice lost significantly fewer retinal ganglion cell axons,” Zhu says.

Gidday is currently investigating which genes are activated or repressed by preconditioning. He hopes to identify the changes in gene activity that make cells resistant to damage.

“Previous research has shown that there are literally hundreds of survival genes built into our DNA that are normally inactive,” Gidday says. “When these genes are activated, the proteins they encode can make cells much less vulnerable to a variety of injuries.”

Identifying specific survival genes should help scientists develop drugs that can activate them, according to Gidday.

Neurologists are currently conducting clinical trials to see if stress-induced tolerance can reduce brain damage after acute injuries like stroke, subarachnoid hemorrhage or trauma.

Gidday hopes his new finding will promote studies of tolerance’s potential usefulness in animal models of Parkinson’s disease, Alzheimer’s disease and other neurodegenerative conditions.

“Neurons in the central nervous system appear to be hard-wired for survival,” Gidday says. “This is one of the first steps in establishing a framework for how we can take advantage of that metaphorical wiring and use positive stress to help treat a variety of neurological diseases.”

From a purely intuitive point of view, it is easy to believe that our ability to actively pay attention to a target is inextricably connected with our capacity to consciously perceive it. However, this proposition remains the subject of extensive debate in the research community, and surprising new findings from a team of scientists in Japan and Europe promise to fuel the debate.

Resolving how these aspects of perception are managed requires a detailed understanding of how the visual centers in our brain process information. A region known as V1 has been investigated as it represents the first portion of the visual cortex to receive and process signals transmitted from the retina.

Many researchers favor a model in which functions pertaining consciousness are widely spread among the whole visual system, including V1. The classical model, which assumes that the neural mechanism of consciousness is integrated into a narrow subset of brain structures, referred to as a homunculus, or ‘little human’, is almost defunct. However, a modern version of this model is under debate. It proposes that the neural mechanism of consciousness is a privileged set of cortical areas, a subpopulation of neurons, or certain neural dynamics (e.g. oscillations); while there are also visual systems that have nothing to do with conscious vision, explains Masataka Watanabe a researcher investigating brain function at the University of Tokyo, Japan.

Watanabe cites studies proposing that visual attention as processed within V1 may be only minimally impacted by conscious perception; but, the experimental data have been contradictory. For example, studies using a technique called functional magnetic resonance imaging (fMRI) to map brain activity have indicated that V1 contributes to both attention and awareness in humans. However, invasive electrophysiological studies in non-human primates yielded different results. “You would find only 10 to 15% of neurons in V1 that are barely modulated by awareness, and 85% or so that are not modulated at all,” says Watanabe. To resolve this ambiguity, he, Kang Cheng from the RIKEN Brain Science Institute, Wako, and their colleagues designed an experiment that examined both processes independently. Surprisingly, their results may lend support the modern homunculus model.

Attentive, but unaware

The results proved striking: for all seven subjects, the shift of attention toward or away from the target had a dramatic effect on brain activity in the region of V1 corresponding to the visual target. However, the ability to consciously perceive the target proved surprisingly unimportant, and shifts in target awareness had no clear or consistent effect on the activity of this subset of neurons. “I was quite surprised that there was zero modulation of awareness in V1,” says Watanabe. “Even in monkey studies where the [animals] showed only 10% of their neurons being modulated, [those researchers] were nevertheless observing modulation.” By comparison, no such awareness effect was observed in the human subjects.

Watanabe and colleagues’ findings indicate that awareness is not a major factor in the earliest stages of visual perception, even though it is clearly a core component of the overall process. Further investigation will be required to determine how consciousness becomes integrated with other visual data. “Scientists are pretty sure that the terminal areas of the visual system, such as the regions that process shape and color or motion, are likely to be heavily modulated by awareness,” says Watanabe. “But where exactly this modulation starts is still an open question.”

Future studies from this research team will seek out the brain structures involved in awareness processing. For now, these data offer surprising support for a still-contested model of visual perception and consciousness. “To tell the truth, three years ago I would not have believed this result,” says Watanabe. “I don’t think the ‘Battle of V1′ is fully settled, but these data could imply that the modern homunculus model may be true.”

The journal is published by Lippincott Williams & Wilkins, a part of Wolters Kluwer Health.

Using detailed information on eye growth and vision changes in children over time, the new research shows “decoupling” of lens adaptation from eye growth about a year before myopia occurs. Donald O. Mutti, OD, PhD, of The Ohio State University College of Optometry, is lead author of the new study.

Growth Imbalance Leads to Myopia…

The researchers analyzed repeated measurements of vision and eye growth performed over several years in children aged 6 to 14. The study focused on the growth of the two key parts of the eye affecting normal vision: the cornea, the transparent front part that lets light into the eye; and the lens, located behind the cornea, which focuses light rays on the retina at the back of the eye.

Myopia or nearsightedness — difficulty seeing objects at a distance — develops in about 34% of American children as they grow. Vision professionals and scientists typically think of myopia as a problem occurring when the eyeball becomes too long (front to back) for the optical power of the cornea and lens.

However, it has been unclear how this imbalance develops in children who previously had normal vision. To answer this question, Dr. Mutti and colleagues compared changes in eye growth for children who developed myopia at different ages versus those whose vision remained normal.

They found that, in children without myopia, the lens grew thinner and flatter to maintain normal vision as the eye grew. This adaptation maintained a normal balance between the optical power of the lens and the increasing length of the eyeball. From age nine months to nine years, eyeball length increased by an average of three millimeters.

…As Lens Stops Responding to Increasing Eye Length

However, in children who developed myopia, the lens stopped changing in response to eye growth. Nearsightedness developed not just because of increases in the length of the eyeball, but rather because the optical power of the lens no longer changed as the eye grew.

The imbalance occurred rather suddenly: about one year before the children became nearsighted. For at least five years after the development of myopia, the eye kept becoming longer but the lens stopped flattening and thinning.

In contrast to the lens, changes in corneal growth showed little or no relation to the development of myopia. The cornea is responsible for about two-thirds of the optical power of the eye, and the lens for the remaining one-third.

The study provides vision professionals with an important new piece of information on why some children develop myopia. However, what’s still unclear is why the lens suddenly stops adapting to continued growth of the eye. More research will be needed to answer that question — one possibility is that an abnormally thick ciliary muscle within the eye forms a mechanical restriction preventing the stretching that thins and flattens the lens as the eye continues to grow.

It is estimated that 6.5% of people over age 40 in the US currently have AMD. There is an inheritable genetic risk factor but risk is also increased for smokers and with exposure to UV light. Genome-wide studies have indicated that genes involved in the innate immune system and fat metabolism are involved in this disease. However none of these prior studies examined gene expression differences between AMD and normal eyes.

In order to address this question, researchers at the University of California Santa Barbara, the University of Utah John Moran Eye Center, and the University of Iowa combined forces and used a human donor eye repository to identify genes up-regulated in AMD. The ability of these genes to recognize AMD was tested on a separate set of samples.

The team discovered over 50 genes that have higher than normal levels in AMD, the top 20 of which were able to ‘predict’ a clinical AMD diagnosis. Genes over-expressed in the RPE-choroid (a tissue complex located beneath the retina) included components of inflammatory responses, while in the retina, the researchers found genes involved in wound healing and the complement cascade, a part of the innate immune system. They found retinal genes with expression levels that matched the disease severity for advanced stages of AMD.

Dr. Monte Radeke, one of the project leaders, explained, “Not only are these genes able to identify people with clinically recognized AMD and distinguish between different advanced types — some of these genes appear to be associated with pre-clinical stages of AMD. This suggests that they may be involved in key processes that drive the disease. Now that we know the identity and function of many of the genes involved in the disease, we can start to look among them to develop new diagnostic methods, and for new targets for the development of treatments for all forms of AMD.”