Now a University of Florida team and researchers from University of Wisconsin and three other institutions have identified a protein that is central to processes that cause oxidative damage to cells and lead to age-related hearing loss.

The findings help point the way toward a new target for antioxidant therapies and will be published online this week in the Proceedings of the National Academy of Sciences.

One theory of aging holds that free radicals damage components of mitochondria, the energy center of cells. Such damage accumulates over time, leading to a destabilization of the mitochondria, which leads to release of certain proteins.

“Within the mitochondria these proteins cause life, but when they’re out they’re deadly,” professor Christiaan Leeuwenburgh, chief of the biology of aging division at UF’s College of Medicine and a member of the Institute on Aging.

The cell death triggered by the escaped proteins lead to physical effects we associate with aging, such as hearing loss.

More than 40 percent of people in the United States older than 65 suffer from age-related hearing loss, according to data from the National Health Survey. It is estimated that the condition will affect more than 28 million Americans by 2030.

“Because of the high prevalence of this disorder, AHL is a major social and health problem,” said Shinichi Someya, first author of the paper and a postdoctoral fellow in the group of Tomas Prolla of University of Wisconsin.

Age-related hearing loss involves the death of certain sensory hair, nerve and membrane cells in the inner ear. Since the hair and nerve cells do not regenerate in humans, their death leads to permanent hearing loss.

One protein called Bak is known to play a role in the weakening of the mitochondrial membrane. The more of the protein present, the leakier the mitochondrial membrane becomes, allowing harmful proteins to travel out into the rest of the cell.

Bak is typically induced by oxidative stress and its levels increase as people age. The researchers wanted to see whether its absence would prevent the age-related hearing loss that is associated with the death of certain sensory hair, nerve and membrane cells in the inner ear.

Hearing tests showed that Bak-deficient middle-aged mice were found to have hearing levels comparable to that of young mice. In addition, fewer of the critical hearing cells died, compared with so-called wild type mice that did not have the protein deficiency.

To examine how resistant the inner ear cells of the Bak-deficient mice were, the researchers exposed cells to a chemical that causes oxidative stress. Such stress generally induces Bak expression in inner ear cells.

There was only minor loss of cochlear cells at all doses of the stressor chemical, in contrast with the level observed in wild-type animals. The researchers concluded that Bak promotes cochlear cell death in response to oxidative stress.

“This paper clearly shows us that oxidative stress causes hearing loss,” said Jinze Xu, a postdoctoral fellow in Leeuwenburgh’s group, and second author of the paper.

So if oxidative stress triggers damage and death of hearing-related cells, enhancing the antioxidant defenses of the mitochondria should reduce such damage.

The researchers found that both in animals that had excess amounts of an enzyme that scavenges reactive oxygen species, as well as in those who were fed certain antioxidants orally, onset of age-related hearing loss was delayed.

“It looks like a viable biological target that may be applicable to drug use,” Leeuwenburgh said. “The issue is always timing — when to start antioxidant interventions at what combination and what dose.”

Caloric restriction, another way to reduce oxidative damage, has previously been shown to extend life and prevent age-related hearing loss in the type of mice used in the study. With the new findings, the investigators propose that one of the ways that restriction of calories acts is by reducing the level of cell death that is induced by the protein Bak.

“This extends research into life extension by caloric restriction into a whole new area that hasn’t been looked at before,” said Huber Warner, associate dean for research a University of Minnesota College of Biological Sciences and former director of the biology of aging program at the National Institute on Aging, who was not involved in the study. “The work shows that rather than caloric restriction just having an overall effect on metabolism of nutrients, bak modulation can have segmental effects on particular physical systems that have age-related problems in humans.”

“The economic benefits of an advancement like this in a health care field are tremendous, particularly in a state like Florida where there are so many elderly and people with hearing impairments,” said Alice Holmes, a professor in UF’s Department of Communicative Disorders at the College of Public Health and Health Professions. “If you develop a hearing loss, you may end up having to retire early or go on disability. By keeping people functioning in society, it has all sort of positive outcomes.”

At the suggestion of one of Holmes’ patients at UF’s hearing clinic, who was severely hearing impaired, she and other UF researchers pioneered a way to program digital hearing aid devices and cochlear or inner ear implants, based on speech sounds such as “aba,” “ata” and “asha” instead of tonal beeps. People with hearing loss can now hear spoken words much more clearly and their hearing aid devices can be adjusted in a fraction of the time, Holmes said.

“I really think we have the possibility of revolutionizing how digital hearing devices can be programmed,” said Holmes, who collaborated with Rahul Shrivastav, another UF professor in communicative disorders, and Purvis Bedenbaugh, a former UF neuroscience professor. “Our next step is looking into the possibility of accomplishing the same thing with cell phones.”

After UF researchers received a patent, Lee Krause, Holmes’ patient whose training in computer engineering led him to propose the idea of using speech sounds, started the company Audigence Inc. in Melbourne to develop and market the software.

Audigence, which now has 12 employees, is licensing the technology to a hearing aid company in Orlando, Holmes said. “We’re hoping to have the product launched in October at the national meeting of the Academy of Dispensing Audiology in Clearwater,” she said.

In addition, a major clinical trial is now under way with an international hearing aid company that could result in another licensing agreement within the next year, she said.

The arrival of these products on the market will offer economic benefits to audiology clinics as well as improving the lives of their patients, Holmes said. By being able to program hearing aids quicker with better results, audiologists can see greater numbers of patients in a shorter period of time, she said.

An estimated 31 million Americans have hearing loss that could be helped by some form of amplification, yet only about 20 percent of them use hearing aids, Holmes said. Besides the stigma attached to hearing aids, many people who should wear them give up because they are adjusted incorrectly, she said.

“Hearing loss, particularly in the older population, is second only to arthritis as a permanent disability,” she said.

The problem with the traditional method for programming hearing aid devices is it relies on standardized formulas developed for the average patient, while the UF technology customizes the tuning to a patient’s individual hearing deficiencies, Holmes said. Hearing loss occurs at different pitches, which vary from one person to the next, she said.

Krause, chief executive officer and president of Audigence, had lost so much hearing that he needed a cochlear implant, an electrical device that is attached in one’s head and stimulates auditory nerves. Krause continued to have difficulty understanding human speech, especially on the phone, but that changed when it was programmed by speech sounds, Holmes said.

“We do conference calls probably every other day and he leads the calls,” she said. “I almost think he hears better than I do at times.”

When completed, funding for the project is expected to total more than $60 million from the NIA, including the $29.5 million through the American Recovery and Reinvestment Act of 2009. The total will amount to the largest federal award to UF, as well as fund the largest study to prevent mobility disability in seniors.

Many studies have shown that regular exercise improves physical performance. And the U.S. Department of Health and Human Services recommends that adults engage in at least 150 minutes of moderate-intensity or 75 minutes of vigorous-intensity aerobic activity each week, as well as muscle-strengthening activities.

Still, little is known about whether exercise can actually help prevent major mobility disability, defined as the inability to walk a quarter of a mile, or four blocks.

For older adults, staving off disability could help them maintain their physical independence and enhance the quality of their later years.

“We all know that physical activity is good for our health, but the definitive evidence whether it can prevent disability in older people — whether you can prevent them from being unable to walk — is lacking,” said principal investigator Dr. Marco Pahor, director of the UF Institute on Aging.

The new study, called the Lifestyle Interventions and Independence for Elders, or LIFE study, seeks to fill that gap in scientific knowledge. This phase 3 randomized controlled trial of 1,600 sedentary adults ages 70 to 89 who are at risk of mobility disability will be conducted at eight institutions around the country.

It expands on the results of a pilot study that found the rate of onset of mobility disability was lower among a group of older adults who engaged in a structured exercise program for a year, compared with a group of seniors who took part in a health education program for a year.

“This grant reflects NIH’s recognition of the excellence of Dr. Pahor’s work in this area over the past 10 years,” said Dr. David S. Guzick, UF’s senior vice president for health affairs and president of the UF&Shands Health System. “It represents the kind of translational research that UF will increasingly be in a position to conduct.”

UF is the coordinating center and a field site for the LIFE study, with other field sites at Northwestern University, Pennington Biomedical Research Center — a campus of the Louisiana State University system, Stanford University, Tufts University, the University of Pittsburgh, Wake Forest University Health Sciences and Yale University.

Recruitment will begin in early 2010. Eligible participants will be randomly assigned either to take part in a program of moderate-intensity physical activity or a health education program on successful aging. Individuals will be followed for up to three-and-a-half years.

It will be the largest randomized controlled trial ever conducted on physical activity in older adults, and the size of the study will allow scientists to examine the effect of physical activity on a large number of outcomes in ways that have not been possible before.

Primarily, the study seeks to gauge whether there are long-term effects of physical activity interventions on major mobility disability. Investigators will also examine the effects of physical activity on a number of factors, including cognitive function, serious fall injuries, disability in basic activities of daily living, cardiovascular events and hospitalization and nursing home admission. They will also examine quality-of-life measures such as depression symptoms, sleep quality, stress and satisfaction with life.

In addition, the project will allow an assessment of the cost effectiveness of walking programs for the elderly, and whether the money spent on such programs can help reduce medical expenses for injuries and illness that might otherwise result from lack of adequate physical activity.

As life expectancy increases in the United States, the care of older adults has become a major issue for clinical practice as well as public health policy. Average life expectancy today is 77.7 years — almost seven years more than in 1970, according to CDC data.

As adults age, many lose vitality and the inclination or ability to engage in physical activities as simple as walking. Older adults ages 60 to 85 spend almost 60 percent of their time — more than eight of their waking hours — in sedentary behaviors, according to data from the National Health and Nutrition Examination Survey.

The length of time spent in sedentary behaviors has been associated with increased risk of weight gain and various diseases, including diabetes and heart disease. And people who lose their mobility have higher rates of sickness, hospitalization and death than others who do not have disabilities.

“Limitations in walking ability compromise independence, and contribute to the need for assistive care,” said Dr. Evan C. Hadley, director of NIA’s Division of Geriatrics and Clinical Gerontology, whose program is overseeing the trial. “Older people with impaired walking are less likely to remain in the community, have higher rates of certain diseases and death, and experience a poorer quality of life. A successful intervention might help prevent these bad outcomes.”

The discovery in rats answers an important question — how can new, therapeutic genes that have been irrevocably delivered to the human brain to treat Parkinson’s be controlled if the genes unexpectedly start causing problems?

Meanwhile, in a review of Parkinson treatments, the researchers say that prior experimental attempts using growth factors — naturally occurring substances that cause cells to grow and divide — to rescue dying brain cells may have failed because they occurred too late in the course of the disease.

Together, the findings suggest that gene therapy to enable the brain to retain its ability to produce dopamine, a neurotransmitter that falls in critically short supply in Parkinson’s patients, could be safely attempted during earlier stages of the disease with an added likelihood of success.

Parkinson’s disease affects more than 1 million Americans, causing patients to gradually develop movement problems, including tremors, stiffness and slowness. It is caused by degeneration and death of nerve connections that produce dopamine, a substance necessary for communication between cells that coordinate movement.

“We have worked every day for 10 years to design a construct to the gene delivery vector that enhances the safety profile of gene transfer for Parkinson’s disease,” said Ronald Mandel, a professor of neuroscience at UF’s McKnight Brain Institute and the Powell Gene Therapy Center. “With that added measure of safety, we believe we can intervene with gene transfer in patients at earlier stages of the disease. We strongly believe that trials to save dopamine-producing connections in patients with Parkinson’s disease have failed because the therapy went into patients who were in the late stages of the disease and who had too few remaining dopamine-producing connections.”

Often patients are given prescriptions for levodopa, or L-dopa, which is converted into dopamine by enzymes in the brain. But the treatment loses its effectiveness over time and does nothing to slow the disease’s progression.

Meanwhile, trials in the United States to treat Parkinson’s involving direct infusion of growth factors or the transplantation of genes that produce growth factors have had limited success, with some side effects.

Mandel’s research group has concentrated on using an adeno-associated virus to engineer brain cells in animal models with genes that can protect dopamine-producing cells, which then do the vital work of producing GDNF, short for glial cell line-derived neurotrophic factor. The naturally occurring protein is important for the survival of dopamine-producing neurons during brain development, and a survival factor when given to adults.

In this case, scientists engineered the virus with two genes that must act in concert to produce the protein. But this precise interaction can be inhibited with dietary doxycycline, an antibiotic that is often prescribed in low doses to treat bacterial growth related to acne.

Depending on the amount of the antibiotic, protein production can be reduced or stopped, which would for the first time give medical investigators the ability to regulate gene therapy after the treatment was delivered.

“With this technique, you could adjust the therapy in the patient,” said Fredric P. Manfredsson, a postdoctoral associate in UF’s department of neuroscience. “That would be extremely helpful because no one is really certain yet what dosage is required for a protective effect in humans. The process is also much more sensitive than we had imagined it would be. GDNF production can be shut down completely with a dose of doxycycline that is much smaller than what is commonly prescribed.”

Mandel said that adding the safety construct to the gene vector and proving its effectiveness were arduous tasks in which Manfredsson played an essential role.

A variety of methods were used to gauge GDNF production, but one was uncommon and involved the novel observation of the rats’ weight. In prior research, the scientists had found delivering the protein to certain regions of the brain would hinder weight gain in younger rats and can cause weight loss in older rats. In the recent experiments, scientists found they could control the rate of weight gain in the rats with dietary doxycycline, which essentially verified they were controlling the GDNF therapy.

“The ability to control gene regulation is important for the future development of gene therapy, and optimizing its safe application to humans,” said Dr. Mark Tuszynski, a professor of neurosciences and director of the Center for Neural Repair at the University of California, San Diego, who did not participate in the research. “The work of Dr. Mandel and colleagues brings us an important step closer to this goal.”

The work was supported by the National Institute of Neurological Disorders and Stroke.

Researchers with the McKnight Brain Institute of the University of Florida, in collaboration with scientists at the University of Frankfurt, Germany, discovered that inflammation of microglia — an abundant cell type that plays an important supporting role in the brain — does not appear to be associated with dementia in Alzheimer’s disease.

The finding supports recent clinical trial results that indicate anti-inflammatory drugs are not effective at fighting dementia in patients with Alzheimer’s disease, which affects about 5.3 million Americans.

“For almost 20 years now, it’s been claimed that brain inflammation contributes to the development of Alzheimer’s disease dementia, and based on that claim, numerous clinical trials with anti-inflammatory drugs have been conducted. They have been unsuccessful,” said Wolfgang Streit, a professor of neuroscience at the College of Medicine. “In the current paper we have shown that the brain’s immune system, made up of microglia, is not activated in the brains of Alzheimer’s patients, as would be the case if there were inflammation. Instead, microglia are degenerating. We claim that a loss of microglial cells contributes to the loss of neurons, and thus to the development of dementia.”

Microglial cells are a subset of a very large population of brain cells known as glial cells. Neurons are the workhorse cells of the brain, enabling thought and movement, but glia are their faithful sidekicks, providing physical and nutritional support.

Glial cells, which outnumber neurons 10-to-1, are at the heart of a popular explanation for Alzheimer’s disease that suggests protein fragments called beta amyloid — Abeta for short — clump together in the spaces between brain cells, causing memory loss and dementia. Inflammation theories suggest that microglia become “activated” and mount an immune response to these protein clumps, and instead of being helpful, a toxic release of chemicals occurs, worsening the disease effects.

However, Streit’s high-resolution observations did not find evidence that Abeta activates, or inflames, human microglia cells. Nor did researchers find evidence that inflammation is to blame for brain cell death.

“This paper potentially represents a paradigm shift in the way we look at Alzheimer’s disease,” said Mark A. Smith, a professor of pathology at Case Western Reserve University and editor-in-chief of the Journal of Alzheimer’s Disease. “The study goes against the very popular idea of neuro-inflammation; instead, the idea that microglia are senescent is consistent with a number of features of the disease.

“The research makes a very good case that these cells are subject to aging,” said Smith, who did not participate in the study. “These cells were thought to be activated (against Alzheimer’s), but this paper makes a strong case that they are not. The study has taken a novel approach that has led to a novel insight.”

Using a commercially available antibody, Streit for the first time created a marker for microglial cells in human brain specimens that had been in chemical storage. The specimens were from 19 people with varying degrees of Alzheimer’s, ranging from severe to none at all. Two of the samples were from Down syndrome patients, who are known to develop Alzheimer’s pathology in middle age.

When researchers examined these cells alongside neurons under a high-resolution microscope, they found that — unless an infection had occurred elsewhere in the body — microglial cells from Alzheimer’s patients were not distinctly larger or unusually shaped, which would have been the case had they been inflamed.

“What I expected to see is activated microglia right next to dying neurons,” Streit said. “That is what I did not find. What I propose is glia are dying, and the neurons lose support. We now need to find out what caused glia to degenerate. Rather than trying to find ways to inhibit microglia with anti-inflammatory drugs, we need to find ways to keep them alive and strong. It’s a whole new field.”

The microglial cells had a tangled, fragmented appearance, similar to neurons in the throes of Alzheimer’s disease or — old age.

“These cells are breaking into pieces,” said Streit, who collaborated with Alzheimer’s researcher Dr. Heiko Braak, of the Institute for Clinical Neuroanatomy in Frankfurt. “They are on their way out. For the first time, we are proving that microglial cells are subject to aging and may undergo degeneration, and that the loss of these cells precedes the loss of neurons. Research has been so focused on finding activated microglia, no one considered that these cells were degenerating and neurons lost support.”

The work was supported by the National Institutes of Health, the German Research Council and the Evelyn F. and William L. McKnight Brain Institute.

Alzheimer’s disease is the sixth leading cause of death in the United States and the fifth leading cause of death for Americans 65 and older, according to the Alzheimer’s Association. The association estimates Alzheimer’s and other dementias cost Medicare, Medicaid and businesses a total of $148 billion annually.

Although people 50 or older in the study metabolized alcohol similar to how younger people did, they performed worse on special tests after having moderate amounts of alcohol and did not always realize when they were impaired. Soon after having alcohol, older adults also took on average five seconds longer to complete a test than their counterparts who did not have a drink.

“That doesn’t sound like much, but five seconds is a big difference if you’re in a car and need to apply the brakes,” said lead author Sara Jo Nixon, a psychiatry professor at UF’s McKnight Brain Institute. “It can mean the difference between a wreck, and not-a-wreck.”

In 2007, an estimated 12,998 people were killed in crashes involving alcohol-impaired drivers, according to the National Highway Traffic Safety Administration.

“We still have a tremendous overhead in the United States of terrible tragedy with drinking and driving,” said Edith Vioni Sullivan, a professor of psychiatry and behavioral sciences at the Stanford University School of Medicine. “We usually hear about the deaths; we seldom hear about the serious accidents that put people into nursing homes and hospitals for the rest of their lives.”

More than half of adults older than 55 drink socially, according to a 2008 report from the Substance Abuse and Mental Health Services Administration. But few studies have focused on the short-term effects of social drinking among older adults. Previous research mainly investigated consumption of large amounts of alcohol at one time, and generally in young people. But results from studies of younger adults might not be applicable to older people because of age-related declines in cognitive skills, as well as changes in how alcohol is metabolized and removed from the body.

Nixon’s group aimed to expand understanding of the effects over time of moderate levels of alcohol consumption in healthy, active older adults.

“You want to know how long does it take for them to become sober enough to engage in potentially dangerous activity such as driving,” Sullivan said.

The study involved 68 nonsmokers — one group aged 50 to 74 and a comparison group aged 25 to 35 — who had at least one drink a month. Within each group, some individuals were given alcohol while others were given a placebo beverage that did not elevate their breath alcohol levels. The groups were carefully matched by gender, body mass index, history of alcohol consumption and other demographic characteristics.

When a person consumes alcohol, concentration in the blood builds to a peak, then dissipates. During the first phase of the metabolic process, alcohol has a stimulating effect. During the second phase, there is a sedative or depressive effect.

During each phase — at 25 minutes and 75 minutes after alcohol consumption, respectively — participants were given tests that required them to draw lines connecting numbered and lettered dots on a paper, in chronological order, without lifting the pen from the paper. They were timed and evaluated for how many errors they made. The first test involved numbers, while the second involved alternating between numbers and letters. Those tests give clues about a person’s mental processing related to movement, and about the ability to mentally shift from one problem-solving strategy to another. The researchers also asked participants to rate on 10-point scales how intoxicated they felt, and how much they thought the alcohol impaired their performance.

Older adults who had alcohol took longer to complete the tasks than younger adults who had alcohol. But there was no such age difference between the older and younger groups that had not had alcohol. The researchers found that even though blood alcohol levels for participants in both groups rose at a similar rate right after drinking and reached the same peak, the older adults did worse on tests. That suggested the performance gap seen after moderate amounts of alcohol was not because of age-related differences in how the body processes the substance, but because of other factors influencing how alcohol affected the individuals.

In the test portion during the “stimulating” alcohol phase, older adults who had alcohol were slower than those who had not had any. In contrast, alcohol seemed to give the younger group a performance boost during that phase.

“People shouldn’t take it to mean that younger people can drink with impunity,” Sullivan said.

During that same post-drinking phase, when the older adults were impaired, they didn’t think they were. And in the second phase — an hour and 15 minutes after having alcohol — older adults thought their performance was impaired, even when it wasn’t.

“An older person might say ‘Really, I feel all right, I’m sure I can drive,’” Sullivan said. “But the study shows that you can’t always take someone at their word.”

So what advice would Nixon give to active, older adults?

“If you have a couple of drinks at dinner, sit around, have dessert — don’t drive for a while.”

The researchers didn’t evaluate the role of interactions between alcohol and prescription and other medicines.

They hope to conduct studies with larger numbers of people, more age groups and a wider range of alcohol intake levels. Future studies in which subjects take multiple, more difficult tests; the same individual is observed under different circumstances; and differences between the sexes are evaluated might shed more light on alcohol effects in older active adults.

GAINESVILLE, Fla. — Chemical concoctions can smooth over wrinkles and hide those pesky grays, but what about the signs of aging that aren’t so easy to fix, such as losing muscle mass? Cutting calories early could help, say University of Florida researchers who studied the phenomenon in rats.

A restricted-calorie diet, when started in early adulthood, seems to stymie a mitochondrial mishap that may contribute to muscle loss in aging adults, the researchers reported recently in the journal PLoS One.

In rats, the scientists found pockets of excess iron in muscle cell mitochondria, the tiny power plants found in every cell. The excess iron affects the chemistry inside the mitochondria, sparking the formation of harmful free radicals that can lead a mitochondrion straight to the emergency exit, said Christiaan Leeuwenburgh, a UF professor of aging in the UF College of Medicine and the Institute on Aging. Leeuwenburgh was the senior author of the study and of a related report published online this month in Aging Cell that details the damage done by excess iron in mitochondria.

“We become less efficient at an old age and we need to understand why this is,” Leeuwenburgh said. “One thing, maybe, is the accumulation of redox-active metals in cells. If the mitochondria become unhappy or are ready to kick the bucket, they have proteins in the inner and outer membranes that they can open up and commit suicide. They’re tricky beasts.”

The suicidal mitochondria can damage the rest of the muscle cell, leading to cell death and perhaps to muscle wasting, a big problem for adults as they reach their mid-70s, Leeuwenburgh added.

“Muscle is critical for your overall well-being,” Leeuwenburgh said. “As you walk, muscle functions partly as a pump to keep your blood going. Muscle is an incredible source of reserves.”

The researchers found increasing amounts of iron in the muscle cells of aging rats fed a typical unrestricted diet. The older the rats got, the more iron accumulated in the mitochondria and the more damage was done to its RNA and DNA. Rats of the same ages that were kept on a calorie-restricted diet — about 60 percent of the food typically ingested — seemed to maintain more normal iron levels in mitochondria, the researchers reported.

“The novel thing here is that iron is accumulating in places it does not normally accumulate,” said Mitch Knutson, a UF assistant professor of food science and human nutrition and a study co-author. “Such iron accumulation in muscle was quite unexpected. This may be of concern because more people are genetically predisposed to developing iron overload than we originally thought.”

The problem occurs when metals such as iron accumulate in the mitochondria and react with oxygen. Iron can change the chemical structure of oxygen, triggering its metamorphosis into a free radical, an unstable atom that can upset the delicate balance inside the mitochondria. The result? Leeuwenburgh describes it sort of like internal rust.

“Not all free radicals are harmful,” Leeuwenburgh said. “To just use antioxidants to neutralize all free radicals is a huge misconception because some radicals are helpful. You just need to try and target very specific free radicals that form in specific parts of the body.”

Researchers don’t know exactly what causes iron to accumulate in mitochondria in aging animals, but a breakdown in how iron is transported through cells could be one reason why, Leeuwenburgh said. Understanding how caloric restriction limits the problem in rats could help researchers better understand how to combat it, he added.

Russell T. Hepple, an associate professor of kinesiology and medicine at the University of Calgary in Canada, said the findings are another step forward in linking iron to muscle cell death, but there are more questions researchers must answer.

“They’ve shown that apoptosis (cell death) goes up in aging muscle but where does that happen?” Hepple asked. “There are more than muscle cells in muscle. (For example) in older adults there are inflammatory cells.”

GAINESVILLE, Fla. — Estrogen treatments may sharpen mental performance in women with certain medical conditions, but University of Florida researchers suggest that recharging a naturally occurring estrogen receptor in the brain may also clear cognitive cobwebs.

The discovery suggests that drugs can be developed to offset “senior moments” related to low estrogen levels, as well as to protect against neurological diseases, all while avoiding the problems associated with adding estrogen to the body.

Writing online in Molecular Therapy in July, scientists with UF’s McKnight Brain Institute describe how they improved thought processes in female mice bred with the inability to produce estrogen receptor-alpha, a protein apparently necessary for healthy learning and memory.

“We were able to restore function in these animals, not by dosing them with estrogen, but by enabling them to use the estrogen that was naturally present in their bodies,” said Tom Foster, the Evelyn F. McKnight chair for brain research in memory loss at the UF College of Medicine. “We discovered that you can affect the estrogen receptor directly in the hippocampus, right where it’s needed to address memory and spatial learning.”

Changes in the estrogen receptor have been associated with age-related memory deficits and an increased incidence of Alzheimer’s disease among women. In addition, previous studies have shown estrogen replacement may improve cognition in postmenopausal women and younger women with low estrogen levels. Estrogen also appears to protect against Alzheimer’s disease and dementia.

The downside is that estrogen is a powerful hormone that has far-reaching effects throughout the body. It has been associated with a slight increase in women’s risk for breast cancer, heart disease in patients with existing cardiovascular problems, and stroke.

“Estrogen may act as a growth agent for cancer, but in the brain, it appears to maintain health and counteract stress,” Foster said. “We wanted to come back and enhance the signaling pathway that makes estrogen functional. We used a gene therapy technique that enables us to target the brain, but ultimately there could be a pharmaceutical that enhances the signaling pathway solely in the brain.”

The mice had unusually low levels of estrogen because their ovaries were removed at an early age. However, scientists were still able to rescue learning ability by delivering the correct gene to produce estrogen receptor-alpha directly to the hippocampus.

Mice that lacked the estrogen receptor showed poor ability to locate a platform hidden in a small swimming tank over a training period of several days. After receiving the gene, the mice learned to locate the platform in two days of training.

“This research shows that when the estrogen receptor-alpha is restored to adult mice that have been missing it their entire lives, it is still possible to enhance memory and learning,” said John H. Morrison, dean of basic sciences and the Graduate School of Biological Sciences at Mount Sinai School of Medicine, who did not participate in the research. “This is good news for moving forward to develop clinical interventions and therapeutics because it appears critical damage was not done to brain circuitry during early development. There has also been debate about which of at least two estrogen receptors is key to synaptic health. Clearly estrogen receptor-alpha plays a critically important role in hippocampal organization and function.”

Recordings made from the brain tissue of treated mice showed signals were strongly communicated across the gaps, or synapses, between hippocampal cells, similar to what would happen with estrogen replacement.

“Investigating the impact of genetically replacing the estrogen receptor at the cellular, synaptic and behavioral levels is a scientific tour de force which provides a strong foundation for the role of estrogen receptor alpha in mediating estrogen action in the hippocampus to restore select types of memory function,” said Roberta Diaz Brinton, a professor of pharmacology and pharmaceutical sciences and biomedical engineering at the University of Southern California, who was not involved in the study. “From a technology perspective, their technique to transfect the estrogen receptor is an exciting advance for researching steroid receptors in the brain.”

Studying the effects of increasing the estrogen receptor in other brain regions may shed additional light on memory processes.

“The research brings up the idea that local activation of non-nuclear estrogen receptor-alpha is important for regulating memory processes in the hippocampus,” said Teresa A. Milner, a professor of neuroscience at Weill Cornell Medical College, who also was also not involved in the research.

UF neuroscience associate Asha Rani and UF scientists Ashok Kumar, Li Cui and Susan L. Semple-Rowland participated in the study, which was supported by the National Institutes of Health and the Evelyn F. McKnight Brain Research Foundation.

With that in mind, faculty at the University of Florida’s Institute of Food and Agricultural Sciences adapted the federal government’s MyPyramid poster for older Americans in February 2007.

Researchers then tested the poster’s effectiveness in increasing nutrition knowledge at six lower-income senior centers in North Central Florida.

Karla Shelnutt, coordinator of UF’s Elder Nutrition and Food Safety program, will present an overview of the research project at the Society for Nutrition Education’s annual conference in Atlanta today. Faculty members Linda Bobroff and David Diehl also worked on the study.

The participants were tested before and after a review of the poster. Those who correctly identified beverages low in added sugars increased from 56 to 77 percent. Those who could identify vitamins that should be obtained from fortified foods or supplements (vitamin D and vitamin B12) increased from 70 to 93 percent. And those who identified the two sources of fiber among four possible answers went from 79 to 83 percent.

In addition, 96 percent of the participants said they planned to make at least one behavior change, including drinking more water or other low-sugar beverages (79 percent); eating more fiber-rich foods (75 percent); eating foods from all five food groups each day (63 percent), and eating more fortified foods (61 percent).

The MyPyramid for Older Adults poster is aimed at those 60 and older, but is especially critical for persons over 70, Shelnutt said, because for this age group, getting good nutrition is trickier, especially for those on fixed incomes.

“As we get older, it gets harder to meet our nutritional needs. You don’t need as many calories, but the need for specific nutrients either stays the same or increases,” she said.

Two critical nutrients for older adults are vitamins D and B12, which should be obtained from fortified foods or supplements to ensure adequate absorption, Shelnutt said.

Despite those needs, older adults often do not take the trouble to cook meals, she said.

Instead, they’ll often buy convenience foods that aren’t as nutritious, or graze throughout the day — making snack choices especially important, she said.

Pinellas County Extension agent Nan Jensen, who has used the MyPyramid for Older Adults poster to help coach older adults about nutrition and exercise, said she likes that it shows people of different shapes and sizes engaged in activities such as gardening and tossing a ball with a child.

“It’s just very appropriate for that audience,” she said.

Versions of the MyPyramid for Older Adults poster can be downloaded at http://enafs.ifas.ufl.edu or glossy paper versions can be purchased in packs of 50 from the University of Florida IFAS Extension bookstore at 1-800-226-1764 or online at http://www.ifasbooks.ufl.edu (“Education – Posters” section)

GAINESVILLE, Fla. — The continued decline of the nursing home — once the mainstay care for the frail elderly — and an upsurge in popularity of assisted living will lead to many dramatic changes in long-term care, according to a University of Florida expert and editor of a new book on the subject.

“The American public has expressed a strong distaste for going to a nursing home because it smacks of a hospital-like, institutional way of living and receiving care,” said Stephen Golant, a UF geography professor and expert on elderly housing. “Assisted living has emerged as a highly attractive option for older persons who have experienced some physical or cognitive decline and feel less secure about receiving care in their own home.”

Yet there are few certainties about either the future of assisted living for the elderly or the huge number of baby boomers who stand to be its recipients, Golant said.

“Although baby boomers will constitute a large market, it is unclear what share will have impairments and chronic health problems that make them candidates for assisted living,” he said. “The emergence of an unexpected new medical or rehabilitation breakthrough, such as a cure or the discovery of a disease-controlling drug for Alzheimer’s disease – could result in a substantial decline in the number of elderly Americans who need such care.”

Golant and Joan Hyde, an assisted living provider and a senior fellow at the Gerontology Institute at the University of Massachusetts in Boston, are editors of the new book “The Assisted Living Residence: A Vision for the Future,” published this month by The Johns Hopkins University, which examines elderly housing and possible care trends over the next 20 to 30 years.

The biggest competitors to assisted living are daughters and daughters-in-law who provide most elderly caregiving and determine whether their loved ones can remain in their own homes, Golant said. But the availability and attitudes of the current generation of female offspring who must juggle work and family responsibilities are unclear, he said.

“We know that women have succeeded in being comfortable in going back to work even when they have a baby less than a year old and assigning that care to somebody else,” he said. “Now the question is how will they react when they confront the possibility of leaving their older parents?”

New technology may make that transition easier, Golant said. The development of sophisticated monitoring and surveillance devices that would allow grown children to track their parents’ daily movements on a computer screen from home or work, for example, would revolutionize attitudes about nursing home and assisted living facilities, he said.

“Suddenly some of the downsides of not living at home would be minimized because sons and daughters could feel very much involved with the caregiving experience of their mothers and fathers even without physically being there,” he said. “They could see parents in their rooms, walk with them to the dining hall and even communicate with them in real time.”

Businesses and social service agencies are preparing for the surge of aging baby boomers, an estimated seven out of 10 of whom are expected to require long-term care at some point after they reach the age of 65, Golant said. Many will also face the issue of a parent needing long-term care before reaching that stage themselves, he said.

Nursing homes are increasingly gearing their business toward acute episodes, such as strokes, which call for short rehabilitative recovery periods, Golant said. When they offer long-term care, nursing homes increasingly serve poorer people and are funded through the Medicaid program, while assisted living caters to private paying individuals with higher incomes or salable assets such as an expensive home or stock portfolio.

To be competitive, nursing homes are trying to transform themselves into becoming more home-like and less like an institution; in short, more like assisted living facilities, he said.

Low savings rates and falling home equity raise the question of whether fewer baby boomers will be able to afford assisted living compared with their parents’ generation, Golant said. The average one-year base price is close to $36,000, not including the additional supervision required with Alzheimer’s disease and more serious medical conditions, he said.

“Assisted living is here to stay – and is now very much part of the ordinary consumer’s lexicon,” he said. “But its rate of growth and the number and share of older boomers who will choose this long-term care option in the future is very uncertain.”

Frank Caro, senior fellow in the Gerontology Institute at the University of Massachusetts in Boston and editor of the Journal of Aging and Social Policy, praised the book as “essential reading for everyone with a stake in the future of assisted living in the United States.”

GAINESVILLE, Fla. — “Build it and they will stay” would be wise policy with today’s growing number of elderly and disabled people who want to remain in their own homes, a new University of Florida study finds.

By planning ahead, homes built now with features that meet the needs of people who have difficulty getting around will prevent more costly retrofitting in the future and perhaps avoid the trauma of moving to a retirement home, said Stan Smith, director of UF’s Bureau of Economic and Business Research and the study’s lead author.

“With the aging of the baby boomers, it’s pretty clear that the number of people who absolutely need these features to continue living in their own homes will rise substantially over the next several decades,” he said. “Unfortunately, there are relatively few single-family houses that will be able to accommodate them.”

Fewer than 10 percent of new homes have features that make them accessible to people who have trouble getting around, despite the large and growing need for those accommodations, said Smith, whose study is published in the latest issue of the Journal of the American Planning Association.
“When accessibility features are designed and built into the initial construction, they are very inexpensive in most cases,” he said. “It’s far more costly once a house is built to widen doorways, remove steps or add bathrooms on the ground floor of a two-story unit.”

Without such features, the elderly and disabled not only face greater risk of injury but have more difficulty entering and leaving their house, adding to feelings of social isolation and loneliness, Smith said.

“If people can no longer live comfortably and safely in their homes, they may be forced to enter an assisted living facility or nursing home, which can be extremely expensive,” he said. “People can very quickly go through their life savings in a nursing home, and once their assets are depleted they may have to go on Medicaid, with the tab being picked up by the public.”

Working with Stefan Rayer, a research analyst at UF’s Bureau, and Eleanor Smith, executive director of Concrete Change, Smith applied a technique he developed to estimate the probability that a single-family dwelling built in 2000 will house at least one disabled resident during its expected life span. “To our knowledge, this is the first study to project the future number of households that will have a disabled resident and the first to estimate the likelihood that a new house will have at least one disabled resident during its lifetime,” said Smith, whose team prepared low, medium and high estimates and projections.

The mid-range projection predicts that by 2050 more than one in five households – 21 percent – will have a resident with a physical disability that makes walking and climbing stairs difficult, and 7 percent will have someone unable to get around without help, he said.

Furthermore, over a dwelling’s lifetime, as people move in and out with changes in ownership, the odds leap to 60 percent that it will house at least one resident who has difficult moving around and 25 percent that it will shelter someone who cannot get around without help, according to the researchers’ analysis. And when the odds of having disabled visitors — such as elderly parents — are taken into account, these numbers rise to 91 percent for those with mobility problems and 53 percent for those requiring help, they found.

Already, nearly one-third of Americans over age 65 – 31 percent – have some sort of mobility impairment, and with aging and population growth the proportion is expected to go up, Smith said. “The number of people with disabilities is expected to rise faster than the population as a whole, more than doubling between 2000 and 2050.”

The most important accessibility features are at least one entrance with no steps, a full or half bathroom on the first floor and 32-inch interior door widths instead of the standard 28-inch widths, Smith said. Additional features include electrical outlets within easy reach, accessible showers and bathroom grab bars, he said.

Although the study did not include short-term disabilities, someone who breaks a leg skiing and is temporarily on crutches or in a wheelchair also would benefit, along with people whose elderly parents move in for brief stays, Smith said.

Some legislation has been passed requiring that certain design features be incorporated into new homes to make them accessible to people with mobility limitations, but it has largely been limited to large apartment buildings and single-family housing built with public funds, he said.

Simply traveling to a region in the coastal Southeast raises the odds of a visitor succumbing to a stroke, while residents who leave the area reduce their chances of suffering the same fate, said Ilan Shrira, a University of Florida psychologist. His study is published in the current issue of the journal Neuroepidemiology.

“For decades the coastal plains of North Carolina, South Carolina and Georgia have had a high incidence of stroke deaths compared to the rest of the country,” he said. “Our research shows for the first time that even short-term exposure to this ‘stroke buckle’ is associated with higher-than-expected mortality rates.”

The “stroke buckle” is so named because it is located within the larger and more commonly known “stroke belt,” eight states in the southeastern United States that have a stroke death rate nearly one and a half times that of the rest of the country, Shrira said. The smaller buckle region has an even higher concentration of stroke deaths, he said.

Using all U.S. death certificates from 1979 to 1988, the researchers examined deaths inside and outside the stroke buckle, which comprises 153 counties in the eastern halves of Georgia, North Carolina and South Carolina. They also distinguished residents and nonresidents of the region.

They found that visitors to the region were 11 percent more likely to die of a stroke than were visitors to any other part of the U.S. Additionally, stroke buckle residents who temporarily left the area reduced their chances of stroke death by 10 percent.

Among the many explanations proposed for the existence of the stroke belt and stroke buckle are poorer health care, infectious agents, genetic predispositions and environmental toxins in the water or soil, Shrira said.
But, according to Shrira, none of the explanations has been able to account for the excess deaths, leaving the cause a mystery.

Identifying the cause has been challenging because some of the explanations are difficult to test, and the ones that are testable have not produced any convincing answers, he said.

Nor do the results resolve why short-term exposure to the ‘stroke buckle’ is related to stroke death, he said.

“The fact that it also affects visitors suggests that the effects are partially due to some factor inherent to the region itself, rather than the region’s residents,” Shrira said. “For instance, because the stroke buckle is situated in the coastal plain, and the land to the west is mountainous, the region’s distinct geography may play a role.”

Or the high death rate may be the result of some undetermined infectious agents in the region that lead to strokes, Shrira said. A number of studies have found that up to one third of all stroke victims have some kind of infection prior to the onset of an attack, he said.

“Most investigations into disease and death look at individual-level factors such as genes, diet, exercise and the like,” Shrira said. “But research like this has shown that it is not just who you are and what you do, but also where you live and where you travel to that can influence how you die.”

Shrira collaborated on the research with Nicholas Christenfeld, a psychologist at the University of California at San Diego, and George Howard, a biostatistician at the University of Alabama School of Public Health. Howard is the lead investigator of the Reasons for Geographic and Racial Differences in Stroke project, the country’s largest study investigating regional differences in stroke affliction.

Writing this week in the online, open-access journal Public Library of Science (PLoS) ONE, researchers from industry and academia, including the University of Wisconsin-Madison and the University of Florida, report that low doses of resveratrol — a natural constituent of grapes, pomegranates, red wine and other foods — can potentially boost the quality of life by improving heart health in old age.

The scientists included small amounts of resveratrol in the diets of middle-aged mice and found that the compound has a widespread influence on the genetic causes of aging. Specifically, the researchers found that low doses of resveratrol mimic the heart-healthy effects of what is known as caloric restriction, diets with 20 to 30 percent fewer calories than a typical diet. The new study is important because it suggests that resveratrol and caloric restriction, which has been widely studied in animals from spiders to humans, may govern the same master genetic pathways related to aging.

“Caloric restriction is highly effective in extending life in many species. If you provide species with less food, the regulated cellular stress response of this healthy habit actually makes them live longer,” says study author Christiaan Leeuwenburgh, chief of the division of biology of aging at UF’s Institute on Aging. “In this study, the effects of low doses of resveratrol (on genes) were comparable to caloric restriction, the hallmark for life extension.”

Previous research has shown that high doses of resveratrol extend life in invertebrates and prevent early death in mice given a high-fat diet. The new study extends those findings, showing that resveratrol in low doses, beginning in middle age, can elicit many of the same benefits as a reduced-calorie diet.

“Resveratrol is active in much lower doses than previously thought,” said Tomas Prolla, a UW professor of genetics and a senior author of the new report.

The group explored the agent’s influence on the heart, muscle and brain by looking to see which genes were switched on and off during the aging process.

In the new study — which compared the genetic responses of animals to either restricted diets or normal diets including small doses of resveratrol — the similarities were remarkable, explains lead author Jamie Barger of Madison, Wis.-based LifeGen Technologies, who spearheaded the research.

In the heart, for example, there are at least 1,029 genes whose functions change with age. In animals on restricted diets, 90 percent of those heart genes experienced alterations in gene expression, while low doses of resveratrol thwarted age-related change in 92 percent. The new findings, say the study’s authors, reveal how red wine’s special ingredient helps keep the heart young.

In short, the authors note that a glass of wine or food or supplements containing even small doses of resveratrol are likely to help stave off cardiac aging.

That finding, may also explain the remarkable heart health of people who live in some regions of France where diets are soaked in saturated fats but the incidence of heart disease, a major cause of mortality in the United States, is low. In France, meals are traditionally complemented with a glass of red wine.

“There must be a few master biochemical pathways activated in response to caloric restriction, which in turn activate many other pathways,” explained Prolla. “And resveratrol seems to activate some of these master pathways as well.”

Resveratrol is currently sold over-the-counter as a nutritional supplement with supposed anti-cancer, anti-viral, anti-inflammatory and anti-aging benefits, although few scientific studies have verified these claims in humans. That may soon change: Researchers at the University of Florida hope to explore the effects of resveratrol on older people in a phase 1 clinical trial, set to begin this summer.

The study will assess the supplement’s effects on memory, physical performance, inflammation and oxidative damage, according to Steve Anton, a principal investigator of the upcoming trial and an assistant professor of aging and geriatrics in the UF College of Medicine.

Mitochondria, the tiny power plants that keep a cell functioning, are especially vulnerable to the oxidative damage that accumulates during the aging process.

“In animal studies, (resveratrol) seems to promote mitochondrial health,” said Todd Manini, also a principal investigator of the upcoming trial and an assistant professor of aging and geriatrics in the UF College of Medicine. “Mitochondria are everywhere: They’re in the brain, in the muscle, the liver. So it could have kind of a global impact on many different organ systems.”

“Searching for the presence of this gene may be one way to better identify patients who are at an increased risk for the phenomenon,” said Dr. David S. Sheps, a professor and associate chairman of cardiovascular medicine at UF’s College of Medicine and the Malcom Randall Veterans Affairs Medical Center.

Those with the gene variation are three times more likely to experience dangerous decreases in blood flow to the heart — a condition doctors call ischemia — than heart disease patients without it. Ischemia increases the chance these patients will suffer a heart attack, heart rhythm abnormalities or sudden death, UF researchers report in the April 14 issue of Archives of Internal Medicine.

“There’s no question that in certain populations it is associated with worse prognosis than in patients who do not have mental stress-induced ischemia in terms of overall adverse events and also mortality,” Sheps said. “And it has become apparent that it is far more prevalent than we initially thought. Most of the studies that have been published to date have involved populations of patients who had coronary disease and positive exercise stress tests. But recently we and other investigators have shown that a much broader category of patients also are prone to mental stress ischemia.”

Past studies have shown that as many as two-thirds of patients with coronary artery disease who experience exercise-related reductions in blood flow to the heart respond similarly to mental stress. These bouts often produce no symptoms of chest pain and are rarely detectable on a standard electrocardiogram. Yet previous UF research has shown that these patients have a threefold greater risk of dying — as large a risk factor as cigarette smoking or high cholesterol. Other studies have linked stress experienced after mass disasters or natural catastrophes with a rise in heart attacks and sudden death.

Psychological stress can leave the heart more prone to developing arrhythmias or electrical instability and the blood more prone to clotting. Stress appears to raise heart rate and rapidly hike blood pressure, increasing the heart’s need for oxygen-rich blood, Sheps said. Yet less oxygen is supplied, in part because coronary arteries constrict, impeding blood flow. Doctors are concerned that this reaction to stress in the laboratory is simply a snapshot of how patients respond to the stress of life on a daily basis.

An estimated 10 percent of all patients with coronary disease experience detectable mental stress-induced reductions in blood flow to the heart. In some subsets of patients the phenomenon may be even more prevalent, involving up to 40 percent of these patients.

UF researchers studied 148 patients with coronary artery disease who were on average about 65 years old. Participants were asked to perform a public speaking test designed to induce stress. Images were taken of blood flow to the heart at rest and during the speech task. Blood samples also were collected and analyzed for five common gene variations.

About a fourth of the patients experienced mental stress-induced reduced blood flow to the heart, and about two-thirds of them harbored a particular variation of the adrenergic beta-1 receptor genotype that was associated with a three-fold increased risk of this phenomenon, said Dr. Mustafa Hassan, the study’s lead author and a research fellow in UF’s division of cardiovascular medicine. This receptor typically helps the body respond to stress by regulating blood pressure and heart rate, but a common variability in its gene may make certain patients more vulnerable to the effects of psychological stress.

The study was funded by the National Heart, Lung and Blood Institute and also was supported by the Malcom Randall Veterans Affairs Medical Center and the UF colleges of Pharmacy and Dentistry.

Why does mental stress restrict blood flow in some patients even when exercise fails to have the same effect? The effects of mental stress could predominantly affect the heart’s smaller vessels, causing them to spasm and temporarily limiting blood flow, Sheps speculated. In contrast, exercise tends to affect the heart’s blood supply through different mechanisms.

“We should focus our research on two areas,” he said. “One is better identification of patients who are prone to have this problem and two is looking for effective treatments once we know they have it. We need to know whether we can reverse this phenomenon. We are embarking on other treatment studies fairly soon.”

UF researchers are hunting for other genetic subtypes that could identify other patients at increased risk, he added.

“One of the advantages of detecting these sorts of things is that we may be able to in the future be more specific about what kind of treatment might work better in certain patients depending on their genetic makeup,” Sheps said. “That is one of the important things happening in many fields of medicine. There are many diseases that already have been shown to respond differently to different types of treatment based on genetic differences.”

AAA and the University of Florida National Older Driver Research and Training Center are making these and other recommendations for addressing the physical, visual and cognitive changes that affect senior drivers as part of the Smart Features for Mature Drivers program. AAA and UF announced the smart features today (March 21) at the New York International Auto Show.

Reduced range of motion, arthritic joints, diminished fine motor skills and trouble with night vision and recovery from glare are all common age-related physical changes that can affect driving ability. A recent AAA survey found that 43 percent of drivers over 55 suffered from at least one of nine driving-related difficulties commonly caused by aging.

“There are ways to counteract the difficulties brought on by age-related changes so that seniors can maintain their safe driving abilities,” said Dennis McCarthy, co-director of the National Older Driver Research and Training Center and a research assistant professor in the UF College of Public Health and Health Professions’ department of occupational therapy. “One of these is through proper use of particular vehicle features.”

In 2003 about one in seven licensed drivers was 65 or older. By 2029, that proportion is expected to rise to one in four drivers, according to the AARP Public Policy Institute.

“The goal of Smart Features for Mature Drivers is to ensure that mature drivers are comfortable in their vehicles and to keep them driving safely as long as possible,” said Desiree Lanford, a UF driving rehabilitation specialist.

Smart Features for Mature Drivers recommends particular vehicle features based on the driver’s needs. For example, thick steering wheels, keyless entry and ignition, power mirrors and larger dashboard controls can make driving easier for seniors with arthritic hands or diminished fine motor skills. The doors on four-door models require less strength to open and close than two-door vehicles. Those with limited range of motion in the back, neck, shoulder or arm should consider large, wide-angle mirrors, tilt steering wheels and comfortable, six-way adjustable seats with lumbar support when choosing a vehicle. Seniors with vision issues may benefit from extendable sun visors and larger dashboard controls with contrasting text.

“The best vehicle features are those that fit the individual person and his or her limitations or needs,” Lanford said.

AAA and UF experts also suggest all mature drivers consider proven crashworthiness, antilock brakes, head restraints to reduce the risk of neck injuries, dynamic stability control to help prevent loss of control in a turn, and side and dual-stage or dual-threshold air bags that inflate based on the severity of the crash, lowering the risk of injury if airbags deploy with too much force.

“Safe driving is a function of person, environment and vehicle factors,” said Sherrilene Classen, a UF older driver injury prevention researcher and project team member. “The Smart Features for Mature Drivers project recognizes normal age-related changes and provides beneficial vehicle features to accommodate such changes — a critical step in injury prevention.”

To learn more about the Smart Features for Mature Drivers program, visit the Web site www.AAA.com/seniors.

“By providing public services such as Smart Features for Mature Drivers, AAA aims to keep our growing senior population safe behind the wheel,” said AAA President and Chief Executive Officer Robert L. Darbelnet. “We encourage older drivers and their families to use this as a guide in the selection of their next vehicle or evaluating their current one.”