For the study, published in the journal Neurology, researchers at the University of Edinburgh in Scotland enlisted 638 men and women, starting at age 70. Over the next three years, the participants completed detailed questionnaires about their daily activities, including how often they exercised or engaged in intellectual leisure time activities like reading. They were also given MRI scans that measured the brain’s white matter, a part of the brain critical for thinking and memory.

Three years later, at age 73, those participants who were the most physically active had less shrinkage of their white matter and other areas of the brain critical for thought than those who got little or no exercise. The researchers controlled for factors like I.Q., other medical problems and social class, which may have affected white matter volume and brain health, but still the correlation held.

The brain tends to shrink with age, a process that has been linked to declines in cognitive skills. And brain shrinkage has been linked to Alzheimer’s disease in other studies.

But as this study showed, “people in their 70s who participated in more physical exercise, including walking several times a week, had less brain shrinkage and other signs of aging in the brain than those who were less physically active,” said study author Alan J. Gow. “Our results show that regularly exercising in old age is potentially important to protecting the brain as we age.”

Participating in mentally stimulating activities like reading or doing crossword puzzles, which have been linked to better brain function and a decreased risk of Alzheimer’s disease in other research, did not have an effect on brain volume in this study. However, the study only lasted three years, which may have been too short a time for effects to become apparent. Engaging in such activities earlier in life or over longer periods may have benefits, the authors note.

Other research has shown that social interaction and mental challenges have other benefits, including living longer and a better quality of life, so everyone should strive to stay mentally and socially engaged regardless of age.

By ALZinfo.org, The Alzheimer's Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer's Research Foundation at The Rockefeller University.

Source: Alan J. Gow, Mark E. Bastin, Susana Munoz Maniega, et al: “Neuroprotective lifestyles and the aging brain: Activity, atrophy, and white matter integrity.” Neurology, October 23, 2012 Vol. 79: pages 1802-1808.

Two groups of scientists independently identified mutations in the gene, called TREM2. Their findings were reported online in the New England Journal of Medicine.

The newly identified gene mutation occurs in about one in 50 people with Alzheimer’s disease. It is far less common than the better known APOE-E4 gene, which scientists discovered in 1993 likewise increases the risk of developing Alzheimer’s. While having either gene mutation increases the likelihood of developing Alzheimer’s, it does not mean you will get the disease. Most cases of Alzheimer’s are likely caused by a complex blend of environmental and genetic factors.

Scientists previously identified several genes that are linked to Alzheimer’s onset. Variants in genes known as APP, presenilin-1 and presenilin-2, for example, cause the early-onset form of Alzheimer’s, which strikes people before age 60. Unlike the TREM2 and APOE-E4 variants, carrying one of these genes invariably leads to Alzheimer’s.

A handful of other rare genes have also been linked to an increased risk of late-onset Alzheimer’s, which typically becomes apparent after age 70. But the effects of the TREM2 gene are more pronounced, rivaling or exceeding the impact of APOE-E4.

"The risk associated with this new variant is the largest seen to date and heralds the start of a new era in Alzheimer’s disease genetic research,” said Kevin Morgan, Professor of Human Genomics and Molecular Genetics at The University of Nottingham in the U.K., where some of the research was carried out. “At long last we are beginning to witness major breakthroughs that will hopefully result in therapeutic developments to help alleviate this devastating condition."

The TREM2 variant is rare, occurring in just 0.3 percent of people. By contrast, APOE-E4 is present in up to 25 percent of the population.

TREM2 is known to play a role in the immune system’s ability to fight off infection and illness. When the mutation in TREM2 is present, immune system cells in the brain become less able to repair damage or control inflammation. Inflammation in the brain is a well-recognized feature of Alzheimer’s and may occur early in the course of the disease.

The TREM2 defect may make it difficult for brain cells to clear beta-amyloid, the toxic protein that builds up in the brains of those with Alzheimer’s, the research suggests. As beta-amyloid accumulates, it forms hard barnacle-like plaques and brain cells are killed, leading to the hallmark loss of memory and thinking skills that characterize the dementia of Alzheimer’s.

While much more study is needed to delineate the role of TREM2 in brain health and Alzheimer’s, scientists are hopeful that the new findings may lead to new and more effective strategies for treating the disease. Finding new drugs that boost the beneficial effects of TREM2 on the immune system, for example, could help to delay the onset of Alzheimer’s symptoms.

By ALZinfo.org, The Alzheimer's Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer's Research Foundation at The Rockefeller University.

Source: Thorlakur Jonsson, Ph.D., Hreinn Stefansson, Ph.D., Stacy Steinberg Ph.D., et al: “Variant of TREM2 Associated with the Risk of Alzheimer's Disease.” Rita Guerreiro, Ph.D., Aleksandra Wojtas, M.S., Jose Bras, Ph.D., et al: “TREM2 Variants in Alzheimer's Disease.” Harald Neumann, M.D., and Mark J. Daly, Ph.D.: “Variant TREM2 as Risk Factor for Alzheimer's Disease” (editorial). New England Journal of Medicine, published online, Nov. 14, 2012.

UK Prime Minister David Cameron, RU President Marc Tessier-Lavigne, and Professor Paul Greengard, head of the Fisher Center for Alzheimer’s Disease Research

On Wednesday, May 15, 2013, British Prime Minister David Cameron visited The Rockefeller University where he met with President Marc Tessier-Lavigne, Nobel laureate Paul Greengard, and other scientists working on Alzheimer’s disease and related neurodegenerative conditions. The Prime Minister was accompanied by George Freeman, Member of Parliament and Adviser to the UK Government on Life Sciences; Tim Luke, a Senior Adviser on Business, Trade and Innovation; and Danny Lopez, the British Consul General in New York.

The visit grew out of the Prime Minister’s deep interest in research on dementia. Last year, he launched the Prime Minister’s Challenge on Dementia, his Government’s commitment to dramatically speed up how dementia diagnosis and therapy are approached and how research is conducted. On the same day as Mr. Cameron’s visit to Rockefeller University, the UK Government announced that it will use its Presidency of the G8 this year to identify and agree on an international approach to dementia research, in recognition that the condition is fast becoming the biggest pressure on health care systems around the world.

“We are deeply grateful to the Prime Minister for including a visit to Rockefeller University on his trip, and more importantly, for championing the cause of research on dementia,” said President Tessier-Lavigne. “It is enormously encouraging to scientists when government leaders take a strong and active role in advancing our work.”

Mr. Cameron’s visit to Rockefeller began with a private meeting in Welch Hall with New York-area biotechnology and pharmaceutical executives, after which President Tessier-Lavigne escorted the Prime Minister to his neuroscience lab, the Laboratory of Brain Development and Repair. Mr. Cameron met three young members of the lab—Drs. Cynthia Duggan, Olav Olsen, and Dominik Paquet—who are studying the molecular mechanisms that underlie the degeneration of axons, the slender fibers projecting from nerve cells that link one neuron to another.

During his visit to the Tessier-Lavigne laboratory, Mr. Cameron also had the opportunity to meet Dr. Paul Greengard, the University’s Vincent Astor Professor and Director of the Fisher Center for Alzheimer’s Disease Research. “Paul and the Prime Minister discussed some of the biology of Alzheimer’s,” said Dr. Tessier-Lavigne after the visit. “Thanks to the clarity of Paul’s explanations, Mr. Cameron left with a better understanding of some of the mechanisms that go awry in the disease.”

Earlier in the day, UK Life Sciences Adviser George Freeman discussed possible collaborative ventures with Dr. Barry S. Coller, Physician in Chief of The Rockefeller University Hospital, David Rockefeller Professor, and head of the Allen and Frances Adler Laboratory of Blood and Vascular Biology.

The Rockefeller University has many connections with the UK. President Tessier-Lavigne, a former Rhodes Scholar who conducted postdoctoral research at University College London, is one of seven Rockefeller scientists who are Fellows of the Royal Society. Sir Paul Nurse, President of the Royal Society and Director of London’s new Francis Crick Institute, is a Rockefeller professor and the University’s immediate past president.

Source: The Rockefeller University, Press Release, May 17, 2013.

These tests are still undergoing study, although they are increasingly being offered at various medical centers. And it's unlikely that most people with serious memory problems would undergo all three costly tests. But the findings highlight the difficulty involved in determining who will go on to develop Alzheimer's disease.

Currently, Alzheimer's can be diagnosed definitively only after death, when an autopsy reveals the telltale plaques and tangles that litter the brains of those affected by the disease. But scientists are getting closer to developing tests that can diagnose Alzheimer's in its earlier stages, before damage to the brain becomes extensive. Doctors hope that early diagnosis will offer the possibility of early, and more effective, treatment that may slow, or even stop, the progression of the disease.

For the study, which appeared in the journal Radiology, the researchers studied two different types of brain scans -- magnetic resonance imaging (MRI) and positron emission tomography (PET) -- as well as analysis of cerebrospinal fluid, the fluid that bathes the brain and spinal cord.

Participants also received routine medical exams, including testing of memory and thinking skills. The researchers found that getting both types of scans as well as a spinal fluid analysis proved more effective than any test alone in diagnosing mild cognitive impairment.

"This study marks the first time these diagnostic tests have been used together to help predict the progression of Alzheimer's," said study author Dr. Jeffrey Petrella of Duke University. "Each of these tests adds new information by looking at Alzheimer's from a different angle." Although brain scans using MRI and PET are often used together to diagnose probable Alzheimer’s, the use of these scans together with analysis of cerebrospinal fluid for specific biomarkers is not yet part of routine medical practice.

The Duke team collected data from 97 older adults with mild cognitive impairment who were part of the Alzheimer's Disease Neuroimaging Initiative, a national study that collects data in hundreds of elderly patients with varying levels of memory and cognitive problems. All the participants got regular memory tests, as well as MRI and PET brain scans and spinal fluid tests, for up to four years. The combination of all three tests was able to reduce the current uncertainty of who potentially was at high risk of developing Alzheimer's within the next few years from over 40 percent to under 30 percent. In other words, the tests aimed at identifying MCI patients who were most likely to go on to develop Alzheimer’s.

The uncertainty highlights the difficulty involved in diagnosing early Alzheimer's. The researchers noted that while the tests clearly provided the most diagnostic information in combination, additional studies are needed to better understand their role in a clinical setting. "Additional studies, including those looking at the cost effectiveness of these tests, are also needed," they said.

"Given that the definitive gold standard for diagnosing Alzheimer's is autopsy, we need a better way to look into the brain," added P. Murali Doraiswamy of Duke, another study author. "In people with mild memory complaints, our accuracy is barely better than chance."

By ALZinfo.org, The Alzheimer's Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer's Research Foundation at The Rockefeller University.

Source: Duke University Medical Center. Shaffer JL, Petrella JR, Sheldon FC, et al: "Predicting Cognitive Decline in Subjects at Risk for Alzheimer' Disease by Using Combined Cerebrospinal Fluid, MR Imaging and PET biomarkers." Radiology, Dec. 11, 2012

It is common for someone with Alzheimer’s to become lost while driving. Quickly finding the missing person is critical, since it is estimated that half of those who are not found in the first 24 hours will suffer serious injury or death.

In recent years, Silver Alert programs have been adopted by many states to locate missing seniors. The programs, modeled on the Amber Alert system to find lost or abducted children, involve alerts sent out to local law enforcement and media outlets that provide a detailed description of the missing person as well as the kind of car they may be driving and the license plate number. Billboards on highways and TV and radio spots alert the public to those details.

Silver Alerts help local law enforcement find elders with Alzheimer’s or other cognitive impairment and return them home safely. For families and caregivers of loved ones assisted by the Silver Alert, it also increases awareness of the possibility of future problems or the need for additional assistance.

For the study, that was published online in the Journal of the American Geriatrics Society, researchers analyzed 156 records from the Florida Silver Alert program from October 2008 through May 2010. They looked at how people with dementia become lost while driving, how missing drivers are found, and the role of public notification systems like Silver Alert in these discoveries.

The researchers found that most missing drivers were men, ages 58 to 94, who were cared for by a spouse. Most got lost on routine, caregiver-sanctioned trips to usual locations. Only 15 percent were found while driving, with most discovered in or near a parked car. Law enforcement officers recovered the large majority of drivers with dementia.

In addition, only 40 percent were found in the county where they were reported missing and 10 percent were found in a different state. Another 15 percent were found in dangerous situations, such as stopped on railroad tracks. Five percent of those who got lost died, with those living alone more likely to be found dead than alive.

The researchers concluded that rapid and direct notification of law enforcement agencies was critical in a successful lost person response. They also noted that it is important that officers be trained to quickly assess whether a driver might have Alzheimer’s or other cognitive problems. In addition, a detailed physical description of the missing person, and not just the car, was critical for finding lost pedestrians, since many drive will leave their cars.

The only way to prevent these lost driving incidents is to get someone with dementia to give up the car keys, which is not always easy to do. But since dementia disrupts the ability to remain oriented and to drive safely, retirement from driving may be critical for safety.

"While some persons with dementia may continue to drive safely, it is imperative that we identify individuals who will get lost and establish policies that will improve location of those individuals who get lost," said Dr. James E. Galvin, Professor of Neurology and Psychiatry at New York University Langone Medical Center and a study co-author.

“Strategies commonly recommended, such as hiding the car keys, are potentially protective only in a small number of cases," said study leader Meredeth A. Rowe, a professor at the University of South Florida College of Nursing. “It will be critical to identify other means of transportation for people with dementia to facilitate driving retirement. This strategy will be the most effective intervention to reduce and prevent incidents of missing persons with dementia.”

"Important aspects of successful driving retirement include a partnership between the healthcare practitioner and caregiver to support the decision for driving retirement, the identification of local and state programs, and assistance in finding alternative forms of transportation in the community," the researchers concluded.

By www.ALZinfo.org, The Alzheimer's Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer's Research Foundation at The Rockefeller University.

Source: Meredeth A. Rowe, Catherine A. Greenblum, Marie Boltz and James E. Galvin: “Missing Drivers with Dementia: Antecedents and Recovery.” Journal of the American Geriatrics Society, Volume 60, Issue 11, Nov. 2012.

Secondhand smoke, or passing smoking, is known to cause heart disease, lung cancer and respiratory ailments. It has also been linked to thinking and memory problems, but it was unknown if secondhand smoke might be linked to dementia.

This latest study, published in the journal Occupational and Environmental Medicine, found that people exposed to smoky air were at greatly increased risk of “severe dementia,” which would include Alzheimer’s disease and other types of dementia. The study followed 5,921 men and women over 60 living in rural and urban areas of China.

About 10 percent of the study participants had dementia. Being a current or former smoker was linked to an increased risk of having dementia. But so was living with someone who smoked, even if someone has never been a smoker. The longer that someone had been exposed to environmental tobacco smoke, the greater the likelihood of developing dementia.

Dr. Ruoling Chen, a visiting professor at Anhui Medical University and one of the study authors, said, “Passive smoking should be considered an important risk factor for severe dementia syndromes, as this study in China shows. Avoiding exposure to environmental tobacco smoke may reduce the risk of severe dementia syndromes.”

“The increased risk of severe dementia syndromes in those exposed to passive smoking is similar to increased risk of coronary heart disease,” Dr. Chen added.

Other studies have confirmed a link between smoking and Alzheimer’s disease. A study from 2011, for example, found that people who are heavy smokers in middle age have nearly double the risk of developing Alzheimer’s disease in old age. [See the ALZinfo.org story, “Heavy Smoking Increases Alzheimer’s Risk”.] A more recent study found that men who smoke tend to have faster declines in memory as they age than their nonsmoking peers. [See “Smoking Linked to Memory Loss in Men”.]

The current study found that those exposed to secondhand smoke had a 29 percent greater likelihood of developing severe dementia in old age than those who had not been exposed to smoky air. The link is correlational – other factors besides smoke exposure could have contributed to the increased dementia risk. But it does raise troubling questions about passive smoking and Alzheimer’s disease. Given that other studies have found that even living in the same apartment building as someone who smokes may increase health risks, experts agree that it’s a good idea for yourself, and those around you, to stop smoking.

By ALZinfo.org, The Alzheimer's Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer's Research Foundation at The Rockefeller University.

Source: Chen R, Wilson K, Chen Y, et al. Association between environmental tobacco smoke exposure and dementia syndromes. Occupational and Environmental Medicine. Published online October 26, 2012.

The findings provide some hope for new drugs aimed at beta-amyloid, a toxic protein that builds up in the brains of those with Alzheimer’s. Earlier this year, drug makers halted testing of a related drug called bapineuzumab, which had shown promise in early trials.

Current Alzheimer’s drugs may ease symptoms for a time, but they do nothing to stop the relentless downward progression of disease. New drugs like solanezumab are designed to halt disease progression, though so far results of most such drugs have been discouraging.

Scientists aren’t sure if beta-amyloid is a cause of Alzheimer’s or whether the toxic protein builds up as a side effect of the disease. In the current study, solanezumab provided hints of benefit in those in the earliest stages of Alzheimer’s, suggesting that the drug may be effective only before buildup of beta-amyloid becomes extensive.

In those with moderate disease, in which damage to the brain is more established, the drug did not appear to provide benefit.

The studies of solanezumab involved more than 2,000 men and women with mild or moderate Alzheimer’s disease who were enrolled in one of two clinical trials. Some received solanezumab for 18 months, while others got a placebo.

At the end of the study period, those treated with the drug fared no better than those getting the placebo in terms of memory or thinking skills or day-to-day functioning. However, when the results of the two trials were combined, creating a larger sample size, those with mild disease who were getting the drug showed a slowing in cognitive decline.

Further testing will be needed to determine whether the drug is truly effective for combating early Alzheimer’s. Many drugs show promise in early testing, only to prove ineffective in late-stage trials in large numbers of patients.

New trials of this and other experimental drugs are being planned to try to arrest the development of Alzheimer’s disease.

By www.ALZinfo.org, The Alzheimer's Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer's Research Foundation at The Rockefeller University.

Source: Eli Lilly drug company.

For the study, researchers analyzed death reports among 3,439 National Football League players who completed at least five seasons from 1959 to 1988. Only 10 percent of the players had died at the time of the analysis, a lower overall death rate than those of similar age in the general population.

Though the overall death rate was low, the researchers, from the National Institute for Occupational Safety and Health in Cincinnati, found that the football players were four times more likely to have died from Alzheimer’s disease. They were also at increased risk of dying from amyotrophic lateral sclerosis, a paralytic brain disease also called ALS or Lou Gehrig’s disease. Of the 334 retired football players who died, seven had Alzheimer’s disease and seven had ALS.

The researchers also looked at the risk of dying from Parkinson’s disease, though the risk of that disease was not significantly different than that of the general population. The findings appeared in Neurology, a journal from the American Academy of Neurology.

Doctors increasingly recognize the dangers of contact sports like football, which can lead to serious concussions and subsequent memory problems decades later. Better understanding of the links between head injuries, Alzheimer’s and other neurologic conditions, they say should help doctors better understand how Alzheimer’s develops and could lead to new ways to prevent or treat the disease.

Other studies have shown that among retired professional football players, those who experienced three or more concussions are at increased risk of memory and thinking problems compared to those who had fewer or no concussions. An increased risk of neurologic problems have also been reported in athletes in other sports like boxing, soccer, horse racing and hockey, all of which can involve head injuries. Neurologic problems have also been reported in high school and college players who suffer from head injuries.

In the current study, players most likely to suffer hard blows to the head were at the greatest risk of dying from Alzheimer’s. So-called speed players, who build considerable momentum before tackling or being tackled by other players, were at particular risk. Speed positions include quarterbacks, running backs, halfbacks, fullbacks, wide receivers, tight ends, defensive backs, safeties and linebackers.

The authors note that repeated head injuries have also been linked to a condition called chronic traumatic encephalopathy, a form of lasting brain injury that can lead to personality changes, depression and other symptoms resembling Alzheimer’s disease. It is possible that some of the athletes who were reported as having died from Alzheimer’s in the current study actually had chronic traumatic encephalopathy, which is not usually listed as a cause of death.

By ALZinfo.org, The Alzheimer's Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer's Research Foundation at The Rockefeller University.

Source: Everett J. Lehman, Misty J. Hein, Sherry L. Baron, Christine M. Gersic: “Neurodegenerative Causes of Death Among Retired National Football League Players.” Neurology, Vol. 79, Sept. 3, 2012, page 1.

The study was a randomized, double-blinded study, the gold standard of medical testing. Neither doctors nor the nearly 3,000 study volunteers, aged 70 and older and living in France, knew who was getting a standardized extract of the ginkgo biloba plant, and who was getting a dummy pill.

All had complained about “senior moments” and minor memory problems at the start of the study, though none had full-blown Alzheimer’s disease. Ginkgo was administered in a dose of 120 milligrams of EGb761, a standardized extract of the plant, twice a day. Participants were given regular medical checkups and memory tests during the two-year study period.

By the end of the study, 61 of the 1,406 seniors getting ginkgo, or about 4 percent, had been diagnosed with probable Alzheimer’s disease, compared to 73 of the 1,414, or about 5 percent, who were getting a placebo. The differences between the two groups were not considered statistically significant, and therefore do not indicate that ginkgo provided any memory-preserving benefits or stopped the progression to Alzheimer’s disease.

The findings, published in the journal Lancet Neurology, are consistent with some earlier research showing that ginkgo may do little to prevent the onset of Alzheimer’s. A rigorous study from 2008 involving thousands of seniors across the United States, for example, found that supplements containing the herb did nothing to ward off the onset of the memory-robbing ailment. Some earlier reports, though, suggested the herb may have some benefits and ease agitation and other psychiatric aspects of the disease.

Ginkgo is a potent antioxidant that, in laboratory studies, helps to protect cells grown in a dish against damage from reactive oxygen molecules. It is thought that antioxidant protection of the cells in the brain may help protect against Alzheimer's and other forms of dementia. Some research has suggested that ginkgo may have protective activity against beta-amyloid, a toxic protein that builds up in the brains of those with Alzheimer's.

Physicians in Europe often prescribe ginkgo biloba to help ward off memory loss. And while current Alzheimer’s drugs may ease symptoms temporarily, there are no proven ways to prevent the disease or halt its progression.

Experts also caution that anyone taking ginkgo or products containing the herb should let their doctors know. It may interact with prescription or over-the-counter medications, including aspirin and warfarin, raising the risk of dangerous bleeding. In the current study, there were no differences in side effects among those taking ginkgo versus a placebo.

By ALZinfo.org, The Alzheimer's Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer's Research Foundation at The Rockefeller University.

Source: Bruno Vellas, Nicola Coley, Pierre-Jean Ousset, et al: Long-term use of standardised ginkgo biloba extract for the prevention of Alzheimer's disease (GuidAge): a randomised placebo-controlled trial. Lancet Neurology, Sept. 6, 2012

In addition to treating high blood pressure, the drugs, also known as “sartans,” are sometimes prescribed to help manage heart failure associated with diabetes-related kidney disease. They include such drugs as valsartan (brand name Angiotan or Diovan), losartan (Cozaar), irbesartan (Avapro), telmisartan (Micardis), candesartan (Atacand), olmesartan (Benicar) and eprosartan (Teveten).

In the study, published online in the Archives of Neurology, doctors examined the brains of 890 people who were being treated with various high blood pressure drugs, including sartans. Most were in their 70s or 80s when they died. Only some had Alzheimer’s disease.

The researchers found that on autopsy, those who were taking sartans had less plaque in their brains than those who were taking other high blood pressure drugs, regardless of whether they had Alzheimer’s disease or not. Buildup of plaque, composed of the toxic protein beta-amyloid, is a hallmark of Alzheimer’s, though some people with plaque buildup do not show signs of the disease. And whether the diminution of plaque buildup observed in this study in those taking sartans translates to fewer memory problems remains to be determined.

“It would have to be proved in a clinical trial if these effects observed in a study with autopsies are expressed in a clinic realm,” said the lead researcher, Dr. Ihab Hajjar of the University of Southern California’s Keck School of Medicine.

He noted that high blood pressure has been linked to an increase risk of Alzheimer’s and other forms of dementia. And other studies have suggested that angiotensin receptor blockers may have benefits for brain health.

A large study of American veterans with high blood pressure, for example, found that those taking the drugs had a lower risk of developing Alzheimer’s and other forms of dementia than those taking other high blood pressure drugs, including ACE inhibitors, another class of antihypertensives. Studies in animals also suggest that angiotensin receptor blockers may have effects that hinder the production of beta-amyloid.

Still, scientists do not know a lot about the effects of high blood pressure drugs on Alzheimer’s disease in people.

These autopsy findings offer some intriguing clues. Some earlier research has shown that high blood pressure drugs were associated with less plaque buildup, even compared to those who did not have high blood pressure. And this study showed that angiotensin receptor blockers, or sartans, may have more potency against beta-amyloid than other classes of hypertension drugs.

When treating high blood pressure, doctors have a wide range of drugs to choose from. Each class of drugs has unique benefits, and drawbacks. In the current study, for example, patients taking sartans were more likely to have had a stroke than those getting other types of drugs, which may have affected results. More study will be needed to confirm the findings and determine who might most benefit from taking sartans.

By ALZinfo.org, The Alzheimer's Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer's Research Foundation at The Rockefeller University.

Source: Ihab Hajjar, MD, MS; Lauren Brown, BS, MPH; Wendy J. Mack, PhD; Helena Chui, MD: “Impact of Angiotensin Receptor Blockers on Alzheimer Disease Neuropathology in a Large Brain Autopsy Series .” Archives of Neurology Online, Sept. 2012.