Why More Education Lowers Dementia Risk

July 26, 2010

Adapted from the University of Cambridge

A team of researchers from the United Kingdom and Finland has discovered why people who stay in education longer have a lower risk of developing dementia—a question that has puzzled scientists for the past decade.

Examining the brains of 872 people who had been part of three large ageing studies, and who before their deaths had completed questionnaires about their education, the researchers found that more education makes people better able to cope with changes in the brain associated with dementia.

Over the past decade, studies on dementia have consistently showed that the more time you spend in education, the lower your risk of dementia. For each additional year of education there is an 11% decrease in risk of developing dementia, this study reports.

However, these studies have been unable to determine whether or not education—which is linked to higher socioeconomic status and healthier lifestyles—protects the brain against dementia.

This is not the case, the new study lead by Professor Carol Brayne of the University of Cambridge has found. Instead, the study shows people with different levels of education have similar brain pathology but that those with more education are better able to compensate for the effects of dementia.

According to co-author Dr Hannah Keage of the University of Cambridge: "Previous research has shown that there is not a one-to-one relationship between being diagnosed with dementia during life and changes seen in the brain at death. One person may show lots of pathology in their brain while another shows very little, yet both may have had dementia. Our study shows education in early life appears to enable some people to cope with a lot of changes in their brain before showing dementia symptoms."

Compared with previous research, this study was able to answer the question because of its large size and statistical power.

The studies have assessed participants for up to 20 years and are three of only six such studies in the world.

The results have important implications for public health at a time when populations in many countries are ageing.

"Education is known to be good for population health and equity. This study provides strong support for investment in early life factors which should have an impact on society and the whole lifespan. This is hugely relevant to policy decisions about the importance of resource allocation between health and education," says Professor Brayne.

The results of this study are published in the journal Brain.

View all news updates for Alzheimer's disease

Early Stages Of Age-Related Macular Degeneration Associated With Smoking, Cholesterol Levels

June 15, 2010

Adapted from the JAMA and Archives Journals

Early-stage age-related macular degeneration appears to be related to modifiable risk factors, including smoking and low levels of high-density lipoprotein (HDL or "good" cholesterol), according to a report in the June issue of Archives of Ophthalmology, one of the JAMA/Archives journals. The condition appears uncommon before age 55 but the risk increases with age thereafter.

Most studies assessing the prevalence of age-related macular degeneration (AMD) have focused on middle- and older-age adults, according to background information in the article. "To our knowledge, accurate estimates of prevalence of AMD among adults younger than 40 years are lacking," the authors write. "Such information is important for understanding the relationships of risk factors to AMD across the age spectrum and for identifying factors that might affect this disease earlier in life."

Ronald Klein, M.D., M.P.H., of the University of Wisconsin, Madison, and colleagues assessed 2,810 individuals age 21 to 84 participating in the Beaver Dam Offspring Study. The presence and severity of drusen—yellow or white deposits in the retina, an early sign of AMD—was determined, along with that of other characteristics of AMD.

Early AMD was present in 3.4 percent of the participants, with rates varying from 2.4 percent in those age 21 to 34 to 9.8 percent in those age 65 years and older. Besides age, other factors associated with increased risk for AMD included being male, smoking more heavily for a longer period of time, and being hearing impaired, whereas having higher levels of HDL cholesterol was associated with reduced risk.

Factors not associated with early AMD included blood pressure, body mass index, physical activity level, history of heavy drinking, white blood cell count or total cholesterol level.

Drusen were present in the macula—the area in the retina responsible for sharp vision—in 63.3 percent of the participants, and the frequency of drusen increased with age. When age was considered, men and women had approximately the same number of drusen.

"In summary, the Beaver Dam Offspring Study data provide precise estimates of the prevalence of various signs of AMD (soft drusen, pigmentary abnormalities) over a wide spectrum of ages from the third to the ninth decade of life," the authors write. "They demonstrate that early AMD onset may occur in midlife. Some modifiable factors (smoking status and serum HDL cholesterol level) associated with AMD in older cohorts were associated with early AMD in this cohort of middle-aged adults."

"The higher frequency of AMD in people aged 65 or older in an aging population makes this an important public health problem," they conclude. "Further information regarding the natural history of AMD and its risk factors, especially early in life, is important for developing preventive approaches to it."

Mayo Clinic Researchers Find Dementia In Diabetics Differs From Dementia In Non-Diabetics

July 15, 2010

On behalf of its donors, Alzheimer's Disease Research (ADR), a program of the American Health Assistance Foundation (AHAF), is very proud to have funded Dr. Mary Haan for this very important study.

Adapted from the Mayo Clinic

Researchers from Mayo Clinic's Florida campus say that dementia in some diabetics appears to be caused often by vascular disease in the brain, and the dementia that develops in people without diabetes is more likely associated with deposition of the plaque seen in people with Alzheimer's disease.

The findings will be presented at the Alzheimer's Association International Conference on Alzheimer's Disease 2010 meeting in Honolulu. They resulted from a study conducted among persons with Mexican ancestry but may have relevance to other populations, say the researchers. Also involved in the study were investigators from the University of California, San Francisco.

"This helps in understanding diabetes and dementia," says Mayo neurologist Neill Graff-Radford, M.D., who is presenting the findings. "It suggests that the vascular dementia seen in diabetics, which appears to be related to small blood vessel disease and strokes, can potentially be averted if development of diabetes is prevented."

The results agree with a number of autopsy studies conducted on patients with dementia and diabetes, in which vascular abnormalities were found to be related to the dementia but the Alzheimer's pathology of plaque and tangles was not, he says.

The findings also suggest that an experimental blood test to predict development of Alzheimer's disease may be more accurate than some studies of people with dementia have suggested, because those studies included participants with diabetes, says Dr. Graff-Radford. "We now propose that future studies of this test should take into account diabetic status," he says.

The test is based on discoveries made by Mayo neuroscientists, which measure the ratio of two different kinds of amyloid beta proteins in blood. Plaque found in the brains of Alzheimer's disease patients at autopsy started when the toxic form of amyloid beta, known as Aß42, began to be deposited.

Dr. Graff-Radford and his colleagues earlier discovered that if the Aß42 to Aß40 ratio in blood was low, Aß42 was likely being deposited in the brain and that Alzheimer's disease was developing. Five independent studies have confirmed that hypothesis. One found that the risk of Alzheimer's disease was up to 10 times greater in people with a low Aß42/Aß40 ratio. Three additional studies did not find this, and Dr. Graff-Radford suggests those studies may have included enough diabetic patients to skew the results.

The findings also make sense biologically, Dr. Graff-Radford says. Both the insulin hormone and amyloid beta proteins are degraded by the insulin-degrading enzyme (IDE). He adds that if the blood contains excess insulin, as is the case in diabetics, then IDE preferentially degrades insulin instead of amyloid. "That means there would be higher levels of both Aß42 and Aß40 in the blood of diabetics," he says.

This research comes from a sub-study of an ongoing National Institutes of Health-funded study, the Sacramento Area Latino Study on Aging (SALSA), which includes 1,789 people, primarily Mexican-American. In this study, the researchers analyzed Aß42/Aß40 ratios in 211 participants who developed dementia and 403 "controls"—participants matched in age and gender who remained cognitively normal. Researchers found that among non-diabetics, only the Aß42/Aß40 low ratio was associated with dementia. In diabetics, the ratio of Aß42 to Aß40 was not decreased.

This study was supported by the National Institutes of Health, the American Health Assistance Foundation, the Robert and Clarice Smith and Abigail Van Buren Alzheimer's Disease Research Program.

View all news updates for Alzheimer's disease

Hallmark Alzheimer's Disease Changes Found In Retinas Of Humans And Imaged In Live Animals

July 6, 2010

Adapted from Cedars-Sinai Medical Center

The nerve cell-damaging plaque that builds up in the brain with Alzheimer’s disease also builds up in the retinas of the eyes—and it shows up there earlier, leading to the prospect that noninvasive optical imaging of the eyes could lead to earlier diagnosis, intervention and monitoring of the disease, according to new research.

Scientists discovered characteristic amyloid plaques in retinas from deceased Alzheimer’s disease patients and used a noninvasive optical imaging technique to detect retinal plaques in live laboratory mice genetically modified to model the human disease. The combined results suggest the possibility that noninvasive retinal imaging may be helpful in early diagnosis of the disease.

The research was conducted by a team of scientists at Cedars-Sinai Medical Center in collaboration with colleagues from the Weizmann Institute of Science in Israel and the University of Southern California. Results were published online June 13 in the journal NeuroImage. Alzheimer’s disease is a devastating condition that is becoming more prevalent worldwide as the baby boom generation advances into its senior years, but there is no conclusive, noninvasive way to diagnose it. Previous studies have suggested that changes in the brain may begin years or even decades before symptoms occur—emphasizing the need for earlier, reliable detection for early therapeutic intervention to achieve effective remedy. The new study suggests the possibility of monitoring Alzheimer’s disease through a simple retinal imaging approach.

Abnormal deposits in the brain called beta-amyloid plaques, which damage cells and interrupt cell-to-cell communications, are recognized as a hallmark sign of the disease. However, because existing noninvasive brain-imaging technologies cannot provide sufficient detail about these changes, the most definitive diagnosis of Alzheimer’s disease comes after an autopsy.

The research team considered the retina a better target for noninvasive imaging of Alzheimer’s disease because it is readily accessible and, unlike other components of the eye, it is part of the central nervous system, having a direct connection and thus many similarities with the brain. Previous studies have documented non-specific visual disturbances, eye disorders and certain types of retinal abnormalities occurring with Alzheimer’s disease and other neurodegenerative conditions, but this is the first to identify human retinal plaque deposits that could provide a specific diagnostic marker of Alzheimer’s disease.

Among the new findings:

• In lab tests, plaques in the retinas of mice genetically modified to model Alzheimer’s disease could be detected at a very early, pre-symptomatic stage – before the plaque appeared in the brain.


• A high-resolution, noninvasive optical imaging approach was developed to monitor individual beta amyloid plaques in the retinas of live mice. The system is based on a harmless specific marker and the adaptation of an existing optical system used to examine rodent eyes.


• The research team used a fluorescent compound called curcumin to label and detect retinal plaques. This is believed to be the first use of curcumin as an imaging agent to detect Alzheimer’s disease-related plaques in the retinas of live animals. Curcumin, a natural component of the spice turmeric, binds to beta-amyloid plaques and makes them visible when viewed microscopically. In the Cedars-Sinai research, curcumin injected into the bloodstream of live mice crossed the blood-retinal barrier and specifically bound to the retinal plaques, allowing them to be viewed in high resolution with a noninvasive procedure.


• Observations from multiple genetically engineered mouse models of Alzheimer’s disease demonstrated a correlation between retinal plaques and brain plaques as disease progressed.


• In the laboratory mice, a unique immune system-based therapy that reduces the amount of plaques in the brain also reduced plaque load in the retina to the same extent, suggesting that the retina could faithfully represent the brain in assessing response to therapy.


• Beta-amyloid plaques were identified in retinal samples from human patients who had died from Alzheimer’s disease, and their features correlated with the diagnosed stage of the disease. Importantly, plaques were clearly detected not only in patients who definitely had the disease, but also in the retinas of some people who were suspected of having early-stage Alzheimer’s disease based on clinical diagnosis and microscopic examination of brain tissue after death.

Together, the results offer the first evidence for the existence of Alzheimer’s-specific plaques in the retina of human patients and the ability to detect individual plaques in live mouse models, creating a strong basis for future research building on these findings. According to the authors, these studies establish the potential of direct retinal beta-amyloid plaque imaging in live subjects as a tool for early Alzheimer’s disease diagnosis and prognosis, as well as assessment of therapies.

View all news updates for Alzheimer's disease