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I used to flinch at the topic of aging. Is there anything we can do about the inevitable?

But recently I've been digging into a new wave of longevity research that is making it an exciting time to be an aging human which is all of us.

It turns out, we all age at varying rates. Super-agers may have great genes, but research shows our habits and routines everything from what we eat and how we move our bodies to who we spend our time with matter a lot, when it comes to aging well.

Now, the next frontier is to target the basic biology of aging and come up with new interventions to slow it down.

Many scientists are optimistic that we're on the cusp of breakthroughs. Not only to help us live longer, but more importantly to extend the number of years we live with good health.

This is the goal of researchers at the Human Longevity Lab at the Northwestern University Feinberg School of Medicine. They're recruiting study participants so they can test what kinds of interventions may slow the rate of aging. To that end, I decided to roll up my sleeve for science.

When I arrived, the first step was a quick blood draw. The Potocsnak Longevity Institute is housed on the light-filled 21st floor of Northwestern Memorial Hospital, overlooking Lake Michigan. It felt more like a spa than a doctor's office. I didn't anticipate the vast range of data and insights scientists could glean from a battery of tests.

Over a four-hour period, they performed more than two dozen assessments. At first it felt a bit like an annual physical. They checked my blood pressure, weight, glucose and cholesterol.

NPR's Allison Aubrey has her body composition measured inside a BodPod. Several other tests performed at the longevity lab led by Dr. Douglas Vaughan are used to estimate biological age. Jane Greenhalgh/NPR hide caption

NPR's Allison Aubrey has her body composition measured inside a BodPod. Several other tests performed at the longevity lab led by Dr. Douglas Vaughan are used to estimate biological age.

But then, the tests got a lot more interesting. Inside a small exam room, a medical assistant opened the hinge of a BodPod, a capsule that looks like a submersible. The machine assessed my body composition, determining the ratio of fatty mass to lean mass, which includes muscle. Strength is a key marker of healthy aging, helping us fend off frailty and falls.

Next, I was asked to sniff and identify a range of distinct smells from leather to chocolate to test olfactory function. The loss of smell can be an early sign of disease and cognitive decline. They scanned my retina and took digital images of the inside of my eyes, which can also help detect disease. And I took a memory and cognitive function test, called MOCA. Thankfully, all was healthy.

Then I went through a slew of cardiovascular health tests. They measured my endothelial function, which keeps blood flowing smoothly through the body. They looked at my heart rate variability and pulse-wave velocity, which is an indicator of stiffness of the arteries. I had electrodes placed onto my chest for an electrocardiogram.

Midway through I was feeling a bit nervous, and my mind raced to what ifs.

Of all the tests they performed, the most intriguing is the GrimAge test. This test predicts biological age. It's gauging whether your DNA age is younger, or older, than your actual age, known as chronological age. Conjure images of the Grim Reaper? Yep, that's the idea: The test can estimate how quickly, or slowly, you're aging.

To figure this out, researchers use a technique based on DNA methylation, which is a measure of modifications in our DNA. Basically, as we age, compounds called methyl groups attach to some of our DNA molecules, which can turn genes on or off. Researchers have shown that the higher the proportion of methylated DNA in certain locations, the more accelerated a person's biological age. Published research suggests this is a reliable way to predict life span and health span.

No one wants to find out they're aging faster than their peers, right? But here's the exciting part. Our biological age may be malleable. The hope is that we can slow down our rate of aging by making changes to lifestyle. Down the line, there may be anti-aging pills or other interventions.

Dr. Douglas Vaughan and Dr. John Wilkins of the Northwestern University Feinberg School of Medicine and the Potocsnak Longevity Institute. Allison Aubrey/NPR hide caption

Dr. Douglas Vaughan and Dr. John Wilkins of the Northwestern University Feinberg School of Medicine and the Potocsnak Longevity Institute.

For researchers, the GrimAge test isn't just a way to estimate DNA age. It's a tool to study whether interventions can alter it.

"That's the big ray of optimism that comes through all of this the possibility that we can slow down aging and extend the health span of people," says Dr. Douglas Vaughan, director of the Longevity Institute. Health span is the number of years we live with good health. "It can be changed very rapidly in experimental models and probably in people, too," he says.

For example, smoking has a very strong effect on methylation. "Tens of thousands of locations gain methylation when you smoke," explains researcher Steve Horvath, who developed the epigenetic clock used as part of the GrimAge test. People with obesity also exhibit higher methylation at certain locations. "Conversely, if you eat vegetables, if you are lean, if you exercise, that slows methylation age," he explains.

Now, of course, it's long been known that smoking and eating poorly are bad for you. But researchers can now test specific interventions to see if it's possible to move the needle.

Vaughan's deep interest in aging took off when he identified a distinct genetic variant in an Amish community in Indiana. People who have the variant are protected from diabetes and have healthier cardiovascular systems compared to people who don't. In the laboratory, when Vaughan engineered mice to have only a 50% level of a protein associated with this mutation, their life spans increased by nearly fourfold. "This was a eureka moment," he says.

He tells his current medical students that in their careers they will prescribe interventions to slow down biological aging in their patients.

"I don't know exactly what that's going to be. It might be a drug. It might be a lifestyle intervention, for all I know it might be gene editing," Vaughan says. "But there are going to be ways that we are going to slow down this process and give people a longer health span."

People who live in the upscale Chicago neighborhood where the Human Longevity Lab is located can expect to live a much longer, healthier life compared to people who live just a few miles away. Vaughan wants to help close this gap.

"I'm worried about the poor soul in south Chicago who has a life expectancy of 55, compared to 92 in the neighborhood where we're standing right now," he says. A stunning difference of more than 30 years. (You can check out life expectancy in your ZIP code here.)

A lot of factors play into this life expectancy gap including poverty, housing, stress and crime, which can all work against health span.

Vaughan and his collaborators are enrolling people from a wide range of ages, ethnic groups, neighborhoods and socioeconomic status to see what works to slow biological aging for everybody.

"There are lots of people who've been dealt a bad hand with regard to aging," Vaughan says. Their goal is to find affordable, evidence-based interventions that can benefit everyone, regardless of socioeconomic status.

For example, there's interest in studying stress, which Vaughan says could be "part of the reason for the discrepancy in the life expectancy in different neighborhoods of Chicago." To study this, he could measure people's biological age at baseline, have them try a stress-reduction program, and test again to see if their results changed.

Vaughan is also interested in studying people with chronic HIV, who tend to age at an accelerated rate. A charitable gift from a Chicago family with a shared interest helped launch the institute. Vaughan's team is considering a range of interventions to test whether they can slow down aging in this population.

"It might be weight training, it might be intermittent fasting, it might be dietary manipulations, it might be drugs that are available now that might have anti-aging effects," Vaughan explains, citing the diabetes drug metformin.

Longevity and health span research is attracting lots of funding and attention, from places like the Hevolution Foundation, which provides grants and early stage investments, and Altos Labs, a biotechnology company, founded by Dr. Rick Klausner, which is investigating ways to reprogram or rejuvenate cells.

Dozens of groups have signaled their intent to compete in the $101 million X-PRIZE global competition focused on treatments that support healthy longevity everything from new drugs or supplements, to devices, to repurposing old drugs for new uses.

"Teams have to come to the starting line and we're going to set up the frameworks by which they prove their therapeutic works," says XPRIZE's Jamie Justice, who is also a researcher at Wake Forest University School of Medicine.

Fortunately, my GrimAge score came back younger than my actual age, though I did get some surprises. I learned that my body composition isn't optimal. Turns out, I need to build more lean muscle mass, which is pretty common as we age especially for women.

With muscle mass, if you don't use it, you lose it. After the age of 30 to 35, muscle starts to slowly decline. And after age 65 or so, this loss accelerates. So it's never too soon to start building a reserve. My goal for this year is to build muscle through resistance training and an optimal diet. And also, to reduce stress.

My experience in the longevity study has motivated me to get started on a new project: How To Thrive As You Age. We'll have more stories on healthy aging interventions coming soon.

As part of this project, we hope you'll share your healthy aging tips with us. What habits or lifestyle hacks have you've adopted to thrive as you age? Please use this form to share your thoughts or email us at Thrive@npr.org.

Series editors Jane Greenhalgh and Carmel Wroth

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The keys to longevity may start in the lab. How aging science is ... - NPR

Humans have searched for the secret to immortality for thousands of years. For some people today, that quest includes things like sleeping in a hyperbaric chamber, experimenting with cryotherapy or blasting oneself with infrared light.

Most aging experts are skeptical that these actions will meaningfully extend the upper limits of the human life span. What they do believe is that by practicing a few simple behaviors, many people can live healthier for longer, reaching 80, 90 and even 100 in good physical and mental shape. The interventions just arent as exotic as transfusing yourself with a young persons blood.

People are looking for the magic pill, said Dr. Luigi Ferrucci, the scientific director of the National Institute on Aging, and the magic pill is already here.

Below are seven tips from geriatricians on how to add more good years to your life.

The number one thing experts recommended was to keep your body active. Thats because study after study has shown that exercise reduces the risk of premature death.

Physical activity keeps the heart and circulatory system healthy and provides protection against numerous chronic diseases that affect the body and mind. It also strengthens muscles, which can reduce older peoples risk of falls.

If we spend some of our adult years building up our muscle mass, our strength, our balance, our cardiovascular endurance, then as the body ages, youre starting from a stronger place for whatever is to come, said Dr. Anna Chang, a professor of medicine specializing in geriatrics at the University of California, San Francisco.

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The 7 Keys to Living Longer and Healthier - The New York Times

Longevity is the achievement of a long life. We may hope for longevity so that we can experience many years of quality time with loved ones or have time to explore the world. But living to a ripe old age doesnt necessarily mean healthy or happy longevity if it is burdened by disability or disease. The population of people over age 65 has grown more quickly than other age groups due to longer life spans and declining birth rates, and yet people are living more years in poor health. [1] Therefore, we will explore not just ones lifespan but healthspan, which promotes more healthy years of life.

What you do today can transform your healthspan or how you age in the future. Although starting early is ideal, its never too late to reap benefits.

Researchers from Harvard University looked at factors that might increase the chances of a longer life. [2] Using data collected from men and women from the Nurses Health Study and Health Professionals Follow-up Study who were followed for up to 34 years, researchers identified five low-risk lifestyle factors: healthy diet, regular exercise (at least 30 minutes daily of moderate to vigorous activity), healthy weight (as defined by a body mass index of 18.5-24.9), no smoking, and moderate alcohol intake (up to 1 drink daily for women, and up to 2 daily for men). Compared with those who did not incorporate any of these lifestyle factors, those with all five factors lived up to 14 years longer.

In a follow-up study, the researchers found that those factors might contribute to not just a longer but also a healthier life. [2] They saw that women at age 50 who practiced four or five of the healthy habits listed above lived about 34 more years free of diabetes, cardiovascular diseases, and cancer, compared with 24 more disease-free years in women who practiced none of these healthy habits. Men practicing four or five healthy habits at age 50 lived about 31 years free of chronic disease, compared with 24 years among men who practiced none. Men who were current heavy smokers, and men and women with obesity, had the lowest disease-free life expectancy.

Beyond the five core lifestyle habits mentioned above, a growing body of research is identifying additional factors that may be key to increasing our healthspans:

These senses can decline over time for various reasons: normal aging, which causes a gradual decrease in taste and smell; prescription drugs that reduce taste sensitivity and promote dry mouth or lack of saliva; deficiencies in micronutrients such as zinc that reduce taste; and poor dentition with tooth loss or dentures leading to chewing problems. [19] Up to 60% of adults 70 years and older may lose their sense of taste. [20] With this loss may come heavier seasoning of food with sugar and salt. [21] They may prefer softer lower-fiber foods that dont require much chewing. Poor taste and smell in the elderly is associated with lower dietary quality and poorer appetite. [22]

Food aromas are important as they trigger the release of saliva, stomach acid, and enzymes in preparation for digestion. [23] The scent of food can trigger the release of dopamine and serotonin, causing a feeling of wellbeing to encourage eating. An impaired sense of smell in older adults is also associated with less variety in food choices and poorer nutrition, but can also lead to increased food intake and weight gain in some individuals. [23]

Seasoning food more liberally with sodium-free herbs, spices, and vinegars may help to compensate for sensory deficiencies. Using foods with a savory umami quality like mushrooms, tomatoes, some cheeses, and yeast can boost richness and flavor. Another sensory aspect of food called kokumi describes a full and rich mouthfeelsuch as that experienced from a minestrone soup, an aged cheese, or a seafood stew simmering for many hours. If poor appetite from sensory loss is a problem, providing variety through different textures, smells, and colors in the meal may stimulate an increased desire to eat. [21]

Eating and food preparation are also important activities offering socialization and mental stimulation such as when learning new cooking skills. Preparing meals helps to reduce sedentariness as there are several action steps involved: selecting and purchasing, washing and chopping, and cooking the ingredients.

Japanese women and men currently live five to six years longer than Americans, so their practices are of great interest. In Japanese families, elders are highly revered and households are intergenerational. Japanese elders are generally healthier than Western elders, but is this the chicken or the egg? Does better health from good lifestyle habits allow them to stay physically active and involved in society so they remain a valuable asset and reap psychosocial benefits, or is it the culture that reveres elders so they have better mental health, less loneliness, and better healthcare so that they stay healthier longer? Japan has also largely avoided the epidemic of obesity that the U.S. is experiencing; for example, the prevalence of obesity among U.S. women is about 37% but among Japanese women is less than 5%. [24] This difference is certainly an important contributor to differences in life expectancy, but raises questions about how the Japanese have been able to control their weight. In recent years, diets in Japan have become more similar to those in the U.S. but they still eat smaller portions, more fermented foods, less sweets, and less red meat.

Identifying additional factors that improve and extend our healthspans is an active area of scientific inquiry. In the meantime, current research findings are encouraging, and underscore the importance of following healthy lifestyle habits throughout ones life course. That said, sticking to these behaviors is easier said than done, and public policies must support and promote these habits by improving the food and physical environments that surround us.

Last reviewed December 2022

The contents of this website are for educational purposes and are not intended to offer personal medical advice. You should seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The Nutrition Source does not recommend or endorse any products.

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Healthy Longevity The Nutrition Source

The idea behind regenerative medicine is that we can use the bodys own reparative mechanisms to repair tissue without the need for surgery or drugs, says Dr. Zaslav. We may not be like salamanders who regrow their own tails, but we can repair our own tissue using mesenchymal stem cells. Our bodies do it every day.

With all the misinformation swirling around stem cells, Dr. Zaslav is quick to point out that mesenchymal stem cells are naturally occurring cells in our body and are not embryonic. What makes them special and so dynamic in the regenerative medicine field is that mesenchymal stem cells can direct healing cells to the site of inflammation or injury when introduced via injection. Part of the mission of researchers looking into regenerative medicine has been learning how to better concentrate these types of cells, or their secreted factors at the site of tissue damage, whether it be degenerating cartilage in a knee or a weak tendon in the elbow, thereby facilitating healing without invasive measures like surgery.

Cartilage, bone marrow, muscle, tendon this one cell which is found along blood vessels can become all of these, hence the term stem. All our organs have these types of progenitor cells, says Dr. Zaslav. [When used in regenerative medicine treatments], however, they do not grow into anything. Think of mesenchymal stem cells like little subcontractors telling your cells how to heal. Theyre medicinal signaling cells. They bring pro-growth, pro-healing proteins to the site of inflammation, injury, or infection.

Researchers like Dr. Zaslav believe the ability to teach the body to better heal itself could lead to wider applications in health care, from re-teaching the diabetic body to produce insulin, to repairing internal injuries that dont seem to heal themselves, to preventing cardiac issues. Regenerative medicine has the potential to completely revolutionize how we treat disease.

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What is regenerative medicine? | Northwell Health

Biotherapeutics

October 9, 2021

Regenerative medicine could slow the clock on degenerative diseases that often ravage the golden years, a Mayo Clinic study finds. Life span has nearly doubled since the 1950s, but health span the number of disease-free years has not kept pace. According to a paper published in NPJ Regenerative Medicine., people are generally living longer, but the last decade of life is often racked with chronic, age-related diseases that diminish quality of life. These final years come with a great cost burden to society.

Researchers contend that new solutions for increasing health span lie at the intersection of regenerative medicine research, anti-senescent investigation, clinical care and societal supports. A regenerative approach offers hope of extending the longevity of good health, so a person's final years can be lived to the fullest.

"Diverse aging populations, vulnerable to chronic disease, are at the cusp of a promising future. Indeed, growing regenerative options offer opportunities to boost innate healing, and address aging-associated decline. The outlook for an extended well-being strives to achieve health for all," says Andre Terzic, M.D., Ph.D., a Mayo Clinic cardiologist and the senior author. Dr. Terzic is the Marriott Family Director, Comprehensive Cardiac Regenerative Medicine for the Center for Regenerative Medicine and the Marriott Family Professor of Cardiovascular Research.

Regenerative medicine is a new field of research and practice that is shifting the emphasis from fighting disease to rebuilding health. Mayo Clinic's Center for Regenerative Medicine is at the forefront of this movement, supporting research into new ways of delaying, preventing or even curing disease.

Research advancing regenerative options

Research has increased understanding of technologies that target and remove so-called "zombie" cells that accumulate with age. Zombie cells, also known as senescent cells, secrete harmful proteins and chemicals that contribute to disease and failing health. When cells become senescent, they no longer divide and differentiate, and they lose their ability to repair diseased tissue.

"Advances in anti-senescent and regenerative technology give hope of extending life span and living the older years disease-free," says Armin Garmany, first author and an M.D./Ph.D. student in the Regenerative Sciences Track in Mayo Clinic Alix School of Medicine.New regenerative interventions on the horizon show promise for addressing chronic diseases such as cancer, heart disease and diabetes. For example, advances in regenerative immunotherapies, such as chimeric antigen receptor-T cell therapy unleash the body's ability to recognize and destroy some cancers.

"The clinical readiness of regenerative therapies is maturing in age-related disease," says Satsuki Yamada, M.D., Ph.D., a Mayo Clinic cardiologist and co-author of the study. "The evolving knowledge in regenerative sciences is offering tools to halt or reverse refractory disease progression, transforming the goals of disease management from care to cure."

Clinical care poised to deliver regenerative care

The rise in electronic health records and artificial intelligence provides new ways of sifting through vast datasets and pinpointing regenerative therapies matched to individual need. This could delay the onset of chronic diseases that surface later in life. Targeting regenerative procedures to a multiplicity of chronic age-related diseases could be a powerful way to close the gap between health span and life span.

"The regenerative model of care is poised to advance a perspective of disease-free longevity, transforming current practice in patient care," says Dr. Terzic. "Effective implementation of next-generation medical innovation will be accelerated by augmented decision-making."

Societal supports help extend a healthy life

Public health initiatives could contribute to health longevity. For example, banning public smoking, enforcing Nutrition Facts labels and promoting vaccinations could lead to healthier lives, and delay or prevent degenerative conditions that arise later in life.

In addition, addressing social determinants of heath conditions in the environment where people live could factor into preventing or delaying disease.

"Childhood adversity, social alienation, maladaptive socioeconomic status and compromised health care access are all associated with health inequality and reduced life span," says Garmany. "Addressing these issues is at the core of preventing disease."

Worldwide demographics place life expectancy at 73, but the average age of chronic disease onset is 64. That gap between health span and life spans could be closed with proper public policy initiatives and application of new regenerative and anti-senescence discoveries to clinical care. Breakthroughs that extend life expectancy could potentially be matched with more years of good health.

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Science Saturday: A regenerative reset for aging

New Graduates Leverage Genomics Education in Clinical and Research Settings  University of Colorado Anschutz Medical Campus

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New Graduates Leverage Genomics Education in Clinical and Research Settings - University of Colorado Anschutz Medical Campus

The Department of Ophthalmology and Visual Sciences at Montefiore Medical Center is dedicated to helping patients improve and maintain their vision. We apply the latest diagnostic and treatment techniques to all types of vision impairments and abnormalities, including glaucoma, age degeneration, diabetic eye damage, cataracts, pediatric eye problems, eyelid droop and wrinkles, uveitis, inflammation, dry eyes, infections, double vision, visual loss, tumors, glaucoma, and refractive errors.

Led by prominent refractive surgeon, stem cell and dry eye researcher Roy S. Chuck, MD, PhD, the Department is nationally recognized as one of the largest in the New York metropolitan region. Our team of ophthalmologists, optometrists, orthoptists, oculoplastic surgeons, neuro-ophthalmologists, glaucoma surgeons, cornea and LASIK surgeons, retina surgeons and pediatric surgeons provides comprehensive clinical services, including low vision and contact lens care.

Montefiore's specialists offer the most current and effective treatments for common ocular conditions and the most up-to-date procedures in all areas of ophthalmology. Nearly all of our surgeries are performed on a convenient outpatient basis, and more than 100,000 patient visits are conducted yearly at our outpatient clinics.

Montefiore uses sophisticated digital imaging and laser treatments to help identify and correct astigmatism, nearsightedness, farsightedness and a broad spectrum of eye disorders. Our state-of-the-art facilities enable staff members to use the latest technological advances in corneal and refractive surgery (LASIK), corneal transplant surgery, diabetic and glaucoma surgery and treatment, and cataract surgery.

The Department of Ophthalmology and Visual Sciences is particularly adept at handling the complications inherent in diabetic retinopathy. Our specialists have the proficiency and experience to expertly handle this intricate surgery, including repairing retinal detachments.

Fundamental to our approach to care is the department's clinical and scientific research aimed at further improving the field of ophthalmology. From our basic scientific research laboratories at Albert Einstein College of Medicine to our ophthalmic clinical trials units, we emphasize a "bench to bedside" approach to advanced medical care.

In partnership with Einstein, Montefiore is a major and longstanding educational institution in the field of ophthalmology, teaching and training many of the finest ophthalmologists in the New York area and across the country.

See why so many applicants choose Montefiore-Einstein

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Ophthalmology and Visual Sciences - Montefiore Medical Center

Dr. Jonathan Sheindlin, born and raised in New York, is a board-certified Ophthalmologist with a sub-specialty in diseases and surgery of the Retina and Vitreous. He graduated from New York Medical College and completed his residency in Ophthalmology at St. Lukes/Roosevelt Hospital Center in Manhattan. He continued his training at Harvard University Medical School with a fellowship in Vitreo-Retinal surgery. Dr. Sheindlin is an active member of many Ophthalmologic societies including the American Academy of Ophthalmology, American Society of Retinal Specialists, Bronx County Medical Society, NY State Ophthalmologic Society, and a founding member of the Bronx Ophthalmologic Surgical Society. He has been involved in numerous studies and publications. His research interests include posterior segment changes in the aging eye, complex diabetic retinal detachments, and long-term strategies to decrease the damaging effects of retinal vascular diseases. He is actively involved in education with residents and medical students at The Montefiore Einstein Ophthalmology and Visual Sciences Residency program. Dr. Sheindlin carries the distinction of being named an Honorary Police Surgeon for the NYPD. He is fluent in Spanish.

Dr. Sheindlin has been voted a Castle Connolly Top Doctor since 2021.

Dr. Sheindlin has been voted a New York Super Doctor since 2019.

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Jonathan A. Sheindlin, M.D. - The Bronx Eye Center

Blindness is usually due to age-related conditions such as macular degeneration, glaucoma, or cataracts. But other rare conditions can also cause blindness in people of all ages.

More than 4 million adults in the United States above the age of 40 years had low vision or were legally blind in 2022. Experts expect that number to double by 2050 as the population ages.

While vision loss is usually age-related, other factors can also play a role. Read on to learn about seven of the most common causes of blindness, their risk factors, and how to reduce your risk.

If youre older than 60 years, it helps to be aware of age-related macular degeneration (AMD). Its the most common cause of vision loss in people of this age group. While not painful, it can slowly damage your central vision.

AMD occurs when cells in the center of your retina (macula) get damaged over time. AMD has two types: wet and dry. Dry AMD is more common but less severe.

An early sign of wet AMD is straight lines appearing crooked. With dry AMD, you may first experience blurred or distorted central vision.

Risk factors for AMD include smoking or having a family history of the disease. White people may also be at a higher risk than other races.

Glaucoma is a group of diseases that can damage the optic nerve in the back of your eye. About half of all people with glaucoma dont know they have it because it can progress very slowly. It first damages your side (peripheral) vision and can eventually cause blindness.

Researchers arent sure what causes glaucoma. It may be related to high eye pressure, but even people with regular eye pressure can develop it. Regular eye exams every 12 years can help doctors detect it early.

Risk factors for glaucoma include:

A cataract is the clouding of the lenses because of the proteins in one or both of your eyes. These proteins form a dense area, making it hard for your lens to send clear images to other parts of your eye.

Cataracts are a common, vision threatening eye conditions. The National Eye Institute estimates that by the age of 80 years, half of all adults in the United States will have cataract or cataract surgery in one or both eyes.

Risk factors for cataracts include:

People with diabetes are at risk of developing diabetic retinopathy, including those with type 1 and type 2 or who are pregnant (gestational diabetes).

Frequent high blood sugar levels can damage blood vessels all over your body. It includes the tiny vessels in your retina, the area in the back of your eye thats sensitive to light. The blood vessels can leak or grow unusually, causing vision loss and eventually blindness.

Retinitis pigmentosa (RP) is a rare group of inherited eye diseases. Genetic mutations that affect your retina can cause its cells to break down slowly.

While RP typically gets passed from parent to child at birth, injuries, infections, and some medications can cause damage to the retina that resembles RP.

Most people with RP eventually lose most of their sight.

Risk factors for RP include a family history of the condition or having other genetic disorders like Usher syndrome.

More commonly known as lazy eye, amblyopia typically affects just one eye. It usually starts in childhood, when your brain has trouble interpreting information from one of your eyes. Over time, the eye with better sight becomes stronger, while the eye affected by amblyopia becomes weaker.

Many parents dont know their children have the condition until a doctor diagnoses it.

Risk factors for amblyopia include:

Ambylopia can often occur with strabismus or crossed eyes. Strabismus can also occur without amblyopia.

Muscles surround your eyes, allowing them to move and focus. When they dont team together well, the sight in both eyes doesnt align correctly. That can cause your brain to rely on one eye more than the other. It takes treatment to help them see together.

Researchers arent sure what causes strabismus, but risk factors include:

Less common causes of blindness include:

Regular dilated eye exams are one of the best ways to prevent vision loss. They can also help you catch a condition early when the treatment can be more effective.

You can also protect your vision by:

Here are some answers to common questions about the causes of blindness.

Cataracts are the top cause of blindness worldwide and vision loss in the United States.

The leading causes of vision loss in U.S. adults under age 40 are refractive errors, accidental eye injuries, and diabetes.

Children make up to 3% of people with blindness worldwide. The most common causes of blindness in children in the United States are:

Legal blindness is when you cannot correct your vision above 20/200 in your better eye. That means you need to stand 20 feet away to see an object most people can see from 200 feet away. The Social Security Administration considers legal blindness a disability.

You have low vision when its less than 20/40 in the better-seeing eye, even when you have corrected vision.

Vision loss is becoming more common in the United States as the population ages. Age plays a significant role in the most common causes of vision loss, such as AMD, glaucoma, cataracts, and diabetic retinopathy.

But vision loss can happen to anyone at any age. Checking your sight with regular eye exams, healthy habits, and a knowledge of possible risk factors is essential for prevention and early diagnosis.

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What Are the 7 Causes of Blindness? - Healthline

Since its inception, the American Foundation for the Blind (AFB) has served as the leading source of information and research encompassing blindness and low vision in the United States. This information not only educates those experiencing blindness or difficulty seeing, but it also informs thought leaders, policymakers, and practitioners who work each day to expand opportunity and inclusion for people who are blind or have low vision everywhere.

While many may think of blindness as a complete loss of sight, the reality is that it exists across a wide spectrum, with most people still retaining some vision. Traditionally, those with significant sight loss have been referred to as being visually impaired. However, many factors result in a persons difficulty seeing, and not all are directly related to the eyes. For this reason, AFB, along with others in the field, considers sight loss to fall within this spectrum, ranging from total blindness to low vision resulting from a wide range of conditions. While there are many similarities, every individuals situation is unique, and the pathway to independence can differ for each person.

The degree by which an individuals loss of sight occurs can significantly impact their ability to function independently when performing daily routines. Just because a person may experience blindness or low vision does not mean that they cannot live a fulfilling and independent life. Through appropriate support, such as training and rehabilitation, people who are blind or have low vision can live just as freely as anyone else. Thanks to advancements in assistive technology, the hurdles of losing one of the bodys major sense perceptions can be supplemented. From traditional aids like tactile reading with braille to advanced artificially intelligent (AI) devices that help navigate streets, the barriers often resulting from blindness continue to be broken down by those innovating solutions for independence.

Misconceptions and stereotypes are often the biggest obstacles to equal opportunity and full inclusion for individuals with blindness or low vision. The more we know and understand, the more we can dismantle this significant social barrier, fostering a more inclusive and understanding society.

The following resources provide additional details on all things encompassing blindness and low vision. We have also included links to additional resources through our partner organizations. Questions and comments can be sent to communications@afb.org.

Your one-stop source for statistical facts, figures, and resources about Americans with vision loss.

A brief overview of conditions that are the cause of blindness or visual impairment.

VisionAware, now stewarded by the American Printing House for the Blind, is a comprehensive resource for basic information about adjusting to vision loss, including tips for adapting your home and daily living. There's also extensive information and support for senior citizens who are losing vision, as well as their family members and caregivers.

Originally created by AFB and the National Association for Parents of Children with Visual Impairments, FamilyConnect offers information and an interactive community for parents of children with visual impairments, with resources to help navigate infancy to the teenage years.

A round-up of issues related to technology for visually impaired and blind people, including AFB's acclaimed online technology magazine AccessWorld, which offers objective reviews of mainstream and assistive technology products for people who are living with vision loss.

CareerConnect is your guide to the working world as a blind or visually impaired person. Learn from the experts about exploring careers, conducting a job search, getting hired, and succeeding in the workplace.

An overview of braille and literacy, resources for finding braille publications, and the Braille Bug, an interactive website for kids.

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Blindness and Low Vision | American Foundation for the Blind

Genetics Definition

Genetics is the study of genes and inheritance in living organisms. This branch of science has a fascinating history, stretching from the 19th century when scientists began to study how organisms inherited traits from their parents, to the present day when we can read the source code of living things letter-by-letter.

Genetics started out with curiosity about why things are the way things are why do children resemble one parent more than another? Why do some species resemble each other more closely than others?

It has evolved into an almost universal answer handbook for biology. By reading the source code or blueprint for an organism, scientists today are often able to pinpoint exactly where an organism came from, how it has changed over time, what diseases it might develop, and how its life processes are similar to or different from those of other organisms.

In the 19th century, it was known that offspring resemble their parents but almost nothing was known about why this happened. Why did some children take after one parent, but not the other. Why could plants and animals have offspring that had traits seen in neither parent? Why did some species resemble each other more closely than others?

In the 19th century, Gregor Mendel began examining inheritance in a systematic way by breeding pea plants. He tracked several traits of pea plants across several generations, recording what kinds of parents had what kinds off offspring. He successfully derived the mathematics behind dominant and recessive genes the first empirical evidence that traits really were passed down in some measurable way from parent to offspring.

The image below shows a Punnett square of Mendels pea plants. The Punnett square was developed by English geneticist Reginald Punnett to visually represent how dominant and recessive traits were passed to offspring. The math yielded by the Punnett square matched the results Mendel found in his hands-on studies of pea plants.

Around the same time, Charles Darwin was writing The Origin of Species, after examining changes in the traits if island finches during times of drought and plenty. Darwin concluded that finches which had the traits best-suited for survival were most likely to survive to pass those traits on, yielding changes in the traits of the overall population over time.

His work, when taken together with Mendels, began to suggest that all species on Earth might be related to each other, and might have gradually drifted apart by inheriting different traits through natural selection.

From there, the field of genetics advanced slowly. By the early 20th century, scientists using light microscopes powerful enough to see into a cells nucleus suspected that chromosomes were the seat of genetic information. They were able to connect chromosomal inheritance to trait inheritance, proving that the instructions for inherited traits were carried on chromosomes within the nucleus of eukaryotic cells.

The next great break in genetics started in the late 20th century, when the technology to read the nucleotide source code of the genome began to become available. Since then, the technology has gotten faster, more affordable, and more accurate allowing scientists to sequence the whole genomes of many organisms and compare them.

The ability to read the source code of life has led to a revolution in the way we think about and classify organisms.

Prior to the advent of gene sequencing, scientists guessed at organisms relationships to each other by studying their physical characteristics. Organisms with similar characteristics were often assumed to be related even though many examples were known of convergent evolution, where two unrelated organisms evolve the same traits separately.

With the advent of gene sequencing and molecular genetics- referring to the ability to read the DNA molecule at the molecular level- it became possible to trace descent lineages directly. Scientists can now read a cells source code and determine at where, and roughly when, an organisms genome changed.

As a result, a great deal of material that was taught in schools as recently as ten years ago is now known to be incomplete. Archaea and bacteria once classified in the same kingdom are now known to be genetically quite different from each other. Fungi are now known to be more closely related to animals than plants. Many other fantastically weird and fascinating discoveries have come out of the genome revolution each one bringing us a step closer to understanding what makes us who we are, and how we are interconnected.

Gene sequencing has also led to a revolution in the way we think about, diagnose, and treat disease. In many cases, its now possible to know how likely a person is to get a given disease based on looking at their genome.

Scientists hope that this will lead to great revolutions in medicine in the centuries to come as medicine catches up to genetics, it may someday be possible to determine what medications will work best on a disease, or what lifestyle changes will keep a person healthy, simply by reading their DNA.

This has also led to new ethical and economic challenges.

Some women whose genes have certain mutation of the BRCA1/2 gene, for example, opt to have their breasts and ovaries removed even if they are healthy because they know there is a high chance that they will develop cancer in these organs.

In 2013, Angelina Jolie made headlines by going public with her choice to have her own breasts removed after finding out through a genetic test that she had an 87% chance of some day acquiring breast cancer.

In other cases, geneticists can tell people that they will develop a serious disease but do not yet have the tools to stop it from happening. People in families with Huntingtons disease, for example, can find out if they have the gene for this devastating and inevitably fatal dementia. But what can they do with this information?

An unexpected economic challenge has come from health insurance companies. Insurance companies have always made their money by gambling on who was likely to get sick and who wasnt. Now that the tools exist for companies to find out who is more likely to get sick at a very fine level of detail, concerns have been raised that people with unhealthy genes might be charged much more for health insurance than people with healthy genes.

1. Which of the following was NOT known when Gregor Mendel began his studies?A. That offspring tended to resemble their parentsB. That parents sometimes had offspring who didnt look like either of themC. That some traits are dominant and some are recessiveD. None of the above

Answer to Question #1

C is correct. Mendel developed the theory of dominant and recessive genes after carefully studying the pattern of inheritance of traits among pea plants over several generations.

2. Which of the following was NOT a reason for misclassifying many organisms prior to the advent of molecular genetics?A. The organisms looked similar under the microscopeB. The organisms had evolved similar traitsC. Scientists were unable to read the organisms source codes and had to work off of superficial characteristicsD. Scientists of the past were less intelligent than scientists of today

Answer to Question #2

D is correct. Scientists of the past were incredibly innovative, designing experiments that yielded brilliant insights with very limited tools. But without the ability to read an organisms genetic code, they were restricted to making guesses about how to classify organisms based on their superficial characteristics.

3. Which of the following is NOT a possibility as genetic science advances?A. It may become possible to replace unhealthy genes with healthy genes, if a safe genetic engineering vector for humans is developed.B. It may become possible to choose the best medication for a disease right away based on the diseases genetic profile.C. Laws may need to be passed ensuring that people with genes for certain illnesses are protected from discrimination and have access to healthcare.D. None of the above.

Answer to Question #3

D is correct. All of these are possibilities for the next century, as scientists continue to learn more about genes and how to work with them!

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Genetics - Definition, History and Impact | Biology Dictionary

gene, unit of hereditary information that occupies a fixed position (locus) on a chromosome. Genes achieve their effects by directing the synthesis of proteins.

In eukaryotes (such as animals, plants, and fungi), genes are contained within the cell nucleus. The mitochondria (in animals) and the chloroplasts (in plants) also contain small subsets of genes distinct from the genes found in the nucleus. In prokaryotes (organisms lacking a distinct nucleus, such as bacteria), genes are contained in a single chromosome that is free-floating in the cell cytoplasm. Many bacteria also contain plasmidsextrachromosomal genetic elements with a small number of genes.

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The number of genes in an organisms genome (the entire set of chromosomes) varies significantly between species. For example, whereas the human genome contains an estimated 20,000 to 25,000 genes, the genome of the bacterium Escherichia coli O157:H7 houses precisely 5,416 genes. Arabidopsis thalianathe first plant for which a complete genomic sequence was recoveredhas roughly 25,500 genes; its genome is one of the smallest known to plants. Among extant independently replicating organisms, the bacterium Mycoplasma genitalium has the fewest number of genes, just 517.

A brief treatment of genes follows. For full treatment, see heredity.

Genes are composed of deoxyribonucleic acid (DNA), except in some viruses, which have genes consisting of a closely related compound called ribonucleic acid (RNA). A DNA molecule is composed of two chains of nucleotides that wind about each other to resemble a twisted ladder. The sides of the ladder are made up of sugars and phosphates, and the rungs are formed by bonded pairs of nitrogenous bases. These bases are adenine (A), guanine (G), cytosine (C), and thymine (T). An A on one chain bonds to a T on the other (thus forming an AT ladder rung); similarly, a C on one chain bonds to a G on the other. If the bonds between the bases are broken, the two chains unwind, and free nucleotides within the cell attach themselves to the exposed bases of the now-separated chains. The free nucleotides line up along each chain according to the base-pairing ruleA bonds to T, C bonds to G. This process results in the creation of two identical DNA molecules from one original and is the method by which hereditary information is passed from one generation of cells to the next.

The sequence of bases along a strand of DNA determines the genetic code. When the product of a particular gene is needed, the portion of the DNA molecule that contains that gene will split. Through the process of transcription, a strand of RNA with bases complementary to those of the gene is created from the free nucleotides in the cell. (RNA has the base uracil [U] instead of thymine, so A and U form base pairs during RNA synthesis.) This single chain of RNA, called messenger RNA (mRNA), then passes to the organelles called ribosomes, where the process of translation, or protein synthesis, takes place. During translation, a second type of RNA, transfer RNA (tRNA), matches up the nucleotides on mRNA with specific amino acids. Each set of three nucleotides codes for one amino acid. The series of amino acids built according to the sequence of nucleotides forms a polypeptide chain; all proteins are made from one or more linked polypeptide chains.

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Experiments conducted in the 1940s indicated one gene being responsible for the assembly of one enzyme, or one polypeptide chain. This is known as the one geneone enzyme hypothesis. However, since this discovery, it has been realized that not all genes encode an enzyme and that some enzymes are made up of several short polypeptides encoded by two or more genes.

Experiments have shown that many of the genes within the cells of organisms are inactive much or even all of the time. Thus, at any time, in both eukaryotes and prokaryotes, it seems that a gene can be switched on or off. The regulation of genes between eukaryotes and prokaryotes differs in important ways.

The process by which genes are activated and deactivated in bacteria is well characterized. Bacteria have three types of genes: structural, operator, and regulator. Structural genes code for the synthesis of specific polypeptides. Operator genes contain the code necessary to begin the process of transcribing the DNA message of one or more structural genes into mRNA. Thus, structural genes are linked to an operator gene in a functional unit called an operon. Ultimately, the activity of the operon is controlled by a regulator gene, which produces a small protein molecule called a repressor. The repressor binds to the operator gene and prevents it from initiating the synthesis of the protein called for by the operon. The presence or absence of certain repressor molecules determines whether the operon is off or on. As mentioned, this model applies to bacteria.

The genes of eukaryotes, which do not have operons, are regulated independently. The series of events associated with gene expression in higher organisms involves multiple levels of regulation and is often influenced by the presence or absence of molecules called transcription factors. These factors influence the fundamental level of gene control, which is the rate of transcription, and may function as activators or enhancers. Specific transcription factors regulate the production of RNA from genes at certain times and in certain types of cells. Transcription factors often bind to the promoter, or regulatory region, found in the genes of higher organisms. Following transcription, introns (noncoding nucleotide sequences) are excised from the primary transcript through processes known as editing and splicing. The result of these processes is a functional strand of mRNA. For most genes this is a routine step in the production of mRNA, but in some genes there are multiple ways to splice the primary transcript, resulting in different mRNAs, which in turn result in different proteins. Some genes also are controlled at the translational and posttranslational levels.

Mutations occur when the number or order of bases in a gene is disrupted. Nucleotides can be deleted, doubled, rearranged, or replaced, each alteration having a particular effect. Mutation generally has little or no effect, but, when it does alter an organism, the change may be lethal or cause disease. A beneficial mutation will rise in frequency within a population until it becomes the norm.

For more information on the influence of genetic mutations in humans and other organisms, see human genetic disease and evolution.

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Gene | Definition, Structure, Expression, & Facts | Britannica

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PARIS and CAMBRIDGE, Mass., May 23, 2024 (GLOBE NEWSWIRE) -- NANOBIOTIX (Euronext: NANO –– NASDAQ: NBTX – the ‘‘Company’’), a late-clinical stage biotechnology company pioneering physics-based approaches to expand treatment possibilities for patients with cancer, announced today that Company management will participate in a fireside chat at the upcoming Jefferies Global Healthcare Conference. Please see below for details of the event.

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