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.”

Scientists studying rats induced to display a form of Parkinson’s disease discovered that a protein commonly found in brain cells can be toxic if — at one pinpoint location in its amino acid structure — it lacks a chemical compound called a phosphate.

When scientists used gene therapy to simulate a phosphate at this critical position, the rats’ brain cells didn’t develop the Parkinson-like pathology that would normally occur.

The finding provides new insight into the fundamentals of Parkinson’s disease and the role of an abundant yet mysterious brain protein known as alpha-synuclein, which is believed to help brain cells communicate but may have a more sinister role in the development of neurological diseases.

“We have another potential target for therapy, but there is a great deal left to discover,” said Nicholas Muzyczka, a professor of molecular genetics and microbiology in the College of Medicine and an eminent scholar with the UF Genetics Institute. “This is one more piece of information about what might be causing the toxicity in Parkinson’s disease, and it gives us a little more to go on about what alpha-synuclein does in the brain.”

Generally located at the synapses of nerve cells, alpha-synuclein is believed to aid in brain function, possibly by helping cells communicate with one another by controlling the release of neurotransmitters such as dopamine.

Mutations of alpha-synuclein may cause a rare, inherited form of Parkinson’s, and the protein has been found to be the major component of Lewy bodies, which are abnormal clusters of protein in the brain cells of patients with Parkinson’s disease.

The National Parkinson Foundation estimates 1.5 million Americans currently have Parkinson’s disease and about 60,000 new cases are diagnosed each year. It is caused by the death or impairment of certain nerve cells in a part of the brain called the substantia nigra. When these cells die, the body is deprived of dopamine, a neurotransmitter vital for movement.

“We know of several enzymes that can cause phosphorylation in the proper position of the alpha-synuclein protein,” said Oleg Gorbatyuk, an assistant professor of molecular genetics and microbiology. “Increasing their expression in brains afflicted with Parkinson’s disease could possibly provide a gene therapy approach to the disease.”

In experiments described in the Jan. 15 issue of PNAS, UF researchers used gene transfer to enhance the production of three versions of alpha-synuclein in the substantia nigra region on one side of the rats’ brains. The other side was not treated, for comparison purposes.

Of the types of alpha-synuclein, the one that simulated phosphorylation at position 129 of the protein was nontoxic. But the other versions of the protein all caused significant loss of dopamine neurons in the substantia nigra.

“Adding a phosphate group is about the smallest thing that can possibly happen in biology,” said Mark R. Cookson, an investigator in the Cell Biology and Gene Expression Unit of the National Institute on Aging who was not involved in the research. “But this relatively minor, innocuous change can switch everything around from being a big problem to being no problem. This research really gives us an idea of some things going on in inherited cases of Parkinson’s disease, and if we use that genetic information as a handle to get into the common disease, it is possible to take this from genetics to a drug discovery program.”

The study findings, published in a recent issue of Urologic Nursing, underscore the need for health-care practitioners to educate their patients about the physical and psychological effects the surgery will have on their everyday lives.

“The effects of this treatment are quite immediate and can lead to depression and frustration,” said Bryan Weber, an assistant professor in the UF College of Nursing and the study’s lead author. “After an initial diagnosis of prostate cancer, men may be so focused on eradicating the disease that they don’t realize the effects the treatment will have on their quality of life, both for them and their families.”

Prostate cancer is the No. 1 cancer among men, excluding skin cancer, and with more baby boomers reaching their 50s and 60s, it’s expected to grow even more prevalent, with more than 200,000 cases diagnosed in 2007. Given the various treatment options for prostate cancer, men who undergo radical prostatectomy may initially decide that the risk of physical dysfunction is worth the benefit of improved likelihood of survival. But many don’t know what to expect in the months after surgery, Weber said.

Physical side effects of prostate cancer treatment limit daily activities and may interfere with a man’s sense of masculinity and self-confidence. Urinary incontinence, for example, requires the use of pads that add considerable bulkiness to clothing and create concern about leakage and odor. Sexual dysfunction interferes with a man’s sense of self and may limit the relationship he has with his significant other, Weber said.

In the study, UF researchers evaluated 72 men six weeks after they underwent prostatectomy. In addition to measuring participants’ physical function and assessing whether they had urinary and bowel symptoms and sexual dysfunction, the researchers also evaluated measures of self-confidence, social support and uncertainty about the disease and treatment. Most participants were white, married and employed full-time or retired, and most had some college education.

Fifty-seven percent of the men reported low to moderate social support, indicating that many of the topics proved embarrassing for them to discuss with others, Weber said. The level of social support was significantly related to urinary problems, revealing that men with urinary incontinence may need more support than those with more control.

“Within the first 100 days of diagnosis, men may be so distressed and so focused on curing their cancer that they don’t focus on these side effects, which is what makes it imperative for health-care professionals to educate them on ways that their lives will change and how they can cope,” Weber said. “Almost immediately after treatment, men may experience depression, awkwardness and emasculation, which will have a great effect on their quality of life.”

Weber suggests that clinicians assess men and their support systems, identify changes in physical function that may occur as a result of treatment, and direct them to products and services designed to help them cope with the immediate effects of sexual dysfunction and urinary and bowel incontinence.

For example, Weber said numerous medications aim to ease sexual dysfunction, but many men may not realize the great expense associated with these drugs or be aware of their potential side effects. Similarly, a number of options for urinary incontinence exist, such as boxer shorts that are designed to hold urinary pads, lessening the embarrassment of having to wear such items.

“Education and counseling should be provided to these men to better inform and prepare patients for the physical side effects they are likely to experience postoperatively,” Weber said. “Since we know that men are less likely to rely on support groups or be more embarrassed to discuss these items with family and friends, it’s even more vital for health-care professionals to stress these issues and include options for patients. Men need to be introduced to different options, make choices and regain control over their lives.”

Health practitioners need to remember to thoroughly discuss the consequences of treatment with patients, and information should be tailored to each individual’s needs, said Joyce Davison, an assistant professor at the University of British Columbia Department of Urologic Sciences.

“Once diagnosed with prostate cancer, men vary with regard to the type and amount of information they wish to access and the degree of decision control they wish to have,” Davison said. “It is up to health-care professionals to assess and provide information and support accordingly.”

The procedure was performed last month to test the safety and effectiveness of a synthetic peptide — a small protein fragment — in procedures involving the human eye.

“All patients with macular degeneration have good peripheral, or side, vision, but it’s their central vision that’s affected in both the dry and the wet forms of the disease,” said Dr. Shalesh Kaushal, an assistant professor of ophthalmology and director of the vitreoretinal service in the UF department of ophthalmology.

Macular degeneration affects about 9 million Americans, according to the National Eye Institute. About 15 percent of those people have the wet form of the disease, in which leaky blood vessels crop up like weeds beneath the macula, a part of the retina responsible for central vision.

Doctors can inject the eyes with drugs to stem the abnormal growth of blood vessels, but that approach benefits only the 15 percent of patients afflicted with the wet version, leaving the vast majority of people with macular degeneration in the dark.

These therapies only manage the symptoms, according to Dr. Cedric Francois, the president and CEO of Potentia Pharmaceuticals Inc., the company that designed the anti-inflammatory compound and is funding the safety trial at UF.

“In about 15 percent of people with macular degeneration, you get bleeding in the back of the eye. The drugs that are on the market can stop that bleeding from occurring but they don’t treat the cause of the disease,” said Francois. “The problem was that until recently, no one knew how the illness worked.”

That changed two years ago, when a series of reports in the journal Science shed light on the underlying mechanisms of macular degeneration. The reports revealed a link between the chronic inflammation and tissue damage that accompany both forms of the disease and a genetic defect in the complement system, a series of enzymes that defend the body against pathogens by stimulating a potent inflammatory response.

“Complement is a set of proteins that are often triggered in inflammatory diseases, including the eye in particular,” Kaushal said. “There are now multiple reports that these complement proteins may be overstimulated in wet macular degeneration.”

Those reports allowed scientists to begin tackling the disease from the roots up.

“What’s become clear in the biology of this disease is that there are multiple facets to the disease process. The inflammatory component may be central to the development of age-related macular degeneration because it affects the survival of visual cells and also promotes new blood vessel growth,” Kaushal said.

With that in mind, researchers from Potentia Pharmaceuticals set out to develop an existing family of complement inhibitors called Compstatin for use in the human eye. In animal studies, complement inhibitors have been shown to prevent the inappropriate inflammatory response that accompanies both the wet and dry forms of macular degeneration.

Compstatin and its derivative, POT-4, are the first molecules of their kind to prevent overactivation of the complement pathway.

“Compstatin is a unique complement inhibitor,” said John Lambris, the University of Pennsylvania professor of pathology and laboratory medicine who initially discovered the peptide over 12 years ago. “POT-4 is a much more active version of the original compound.”

Now, teams from Florida, New Hampshire, Minnesota and Arizona are evaluating the safety of POT-4 in humans with the wet form of macular degeneration. The first and third subjects received injections of the peptide at UF in November and December. The second subject was treated in New Hampshire in November.

The UF scientists continue to monitor the subjects closely to gather important information about the safety profile of POT-4. After a safety committee reviews data from the first round of participants, an additional 12 subjects will participate in the study.

“Any peptide or protein that you inject into the eye has the potential for kicking up inflammation,” Kaushal said, noting that because POT-4 is injected locally into the eye in the same method used to deliver existing treatments for macular degeneration, the possibilities for widespread side effects are limited.

Scientists are beginning to explore the role of complement in rheumatoid arthritis, psoriasis, asthma and Alzheimer’s disease.

“There are many human diseases related to complement,” Kaushal said. “That whole area of research has just blossomed over the last four or five years.”

“Caloric restriction is a way to extend life in animals. If you give them less food, the stress of this healthy habit actually makes them live longer,” said Christiaan Leeuwenburgh, chief of the division of biology of aging in UF’s Institute on Aging. Understanding how the process works at the cellular level in rodents could help scientists develop drugs that mimic the process in humans, Leeuwenburgh added.
How does it work? During the aging process, free radicals – highly reactive byproducts of our cells’ respiration – wreak havoc on our cellular machinery. Mitochondria, the tiny power plants that keep a cell functioning, are especially vulnerable to this type of damage. The effects can be disastrous – if malfunctioning mitochondria aren’t removed, they begin to spew out suicidal proteins that prompt the entire cell to die. Cell death, on a whole-body scale, is what aging is all about.

Fortunately, younger cells are adept at reducing, recycling and rebuilding. In this process, damaged mitochondria are quickly swallowed up and degraded. The broken down pieces are then recycled and used to build new mitochondria. However, older cells are less adept at this process, so damaged mitochondria tend to accumulate and contribute to aging.

“Cell survival is dependent upon the ability of the cell to reduce and recycle by a mechanism called autophagy,” said William Dunn Jr., a professor of anatomy and cell biology in UF’s College of Medicine and senior author of the study, which was published online this month in the journal Rejuvenation Research. “When a cell is under stress, autophagy is turned on to clean up the cell by removing damaged cellular components, while recycling building blocks necessary to rebuild the cell. It’s there to protect the cell. But in aged cells, they’re basically not able to adjust to stress as well.”

UF scientists studied 22 young and old rats, comparing those allowed to eat freely with those fed a low-calorie, nutritious diet. The stress of a low-calorie diet was enough to boost cellular cleaning in the hearts of older rats by 120 percent over levels seen in rats that were allowed to eat what they wanted. The diet had little or no effect on younger rats.

“Autophagy is a housekeeping mechanism that keeps cells free of damaged and thereby detrimental mitochondria and other toxic materials while recycling their building blocks - nutrients needed by the cell,” said Stephanie Wohlgemuth, a lecturer in UF’s department of aging and geriatrics and the study’s lead author. “So if that process is maintained with age — or even increased — that can only be beneficial.”

To determine how dietary restriction boosted cells’ ability to reduce the toxic trash, the scientists studied how the amount of certain proteins changed with the rats’ age and diet. They found that some proteins responsible for degrading the damaged parts of the cell by autophagy were more abundant in older, calorie-restricted rats.

Boosting autophagy is especially important in the heart, a vital organ packed with mitochondria, Wohlgemuth said. Swift disposal of damaged cellular components is essential to maintaining an abundance of healthy heart cells as we age.

“Cardiac cells have lost the capability to divide readily to replace dying cells. So the maintenance of the cells’ survival mechanisms is crucial for the heart,” Wohlgemuth said.

Now that some of these proteins have been identified, UF researchers say the next step is to figure out how the proteins can be activated without inflicting dietary stress.

“What if we bypass the caloric restriction and find a way of increasing autophagy?” asked Dunn. “That is, instead of starving yourself you can find another way of enhancing autophagy that will allow the enhanced removal of various damaged organelles that accumulate in aged cells.”

Dr. Ulf Brunk, a professor emeritus of experimental pathology at Linköping University in Sweden, said the study builds on past research showing that removal of toxic mitochondria may extend life in a variety of mammals.

“The paper is a further step in the direction of showing that the stimulation of autophagy may be beneficial,” Brunk said.