Alzheimer’s Disease: Working to Solve the Mystery
Alzheimer’s disease (AD) affects 5.1 million Americans, and there is currently no cure. However, neurologist Sam Gandy, MD, PhD, director of Mount Sinai’s Center for Cognitive health and NFL Cognitive Care says that there are some hopeful developments in AD research—along with potentially promising data you may have seen reported in the news that needs further investigation before its clinical significance can be clarified. Here, Dr. Gandy offers his verdict on some recent studies.
Downward Trend in Dementia A large study published in JAMA Internal Medicine, Nov. 12, 2016, suggests that between 2000 and 2012, the prevalence of dementia decreased by about 25 percent in people age 65 and older, even though the population has continued to age. Those with the most years of education had the lowest chances of developing dementia.
Dr. Gandy’s verdict: Cardiovascular risk factors such as high blood pressure, cholesterol, and blood sugar may play a role in AD. During the last decade, progress has been made in addressing these risk factors, and more people are taking medications to treat them. These data reflect that progress.
Cholesterol Fluctuations a Factor? The connection between heart and brain health is underlined by a study associating greater fluctuations in LDL (“bad” cholesterol) levels with worse cognitive function in seniors. The study (Circulation, July 19, 2016) included 4,428 older adults who underwent standard memory tests. Compared to people with the lowest variability in LDL, those with the highest LDL variability took 2.7 seconds longer, on average, to name the real colors of color names written in different ink (for example, the word blue written in red ink). Greater LDL fluctuations also were associated with lower brain blood flow, and a greater number of white matter hyperintensities (tiny lesions that have been associated with a greater risk for AD).
Dr. Gandy’s verdict: High cholesterol is associated with a build-up of an abnormal protein called beta-amyloid in the brain. It is believed that beta-amyloid deposits contribute to AD by destroying the brain cells’ ability to communicate with each other. In mouse studies, lowering cholesterol works like magic: beta-amyloid melts away—but no human trial has come close to achieving the same result. Further studies are needed to examine whether these data could be useful in clinical practice, but right now they support expert advice to follow healthy lifestyle measures that can help maintain normal cholesterol levels.
The Role of Tau Of the two abnormal proteins that characterize AD, beta amyloid has been more thoroughly studied than tau, which builds up and forms tangles in the brains of people with AD. This is largely due to the development of new brain scanning techniques that allow researchers to visualize beta-amyloid—and similar techniques can now visualize tau. A recent small study (Science Translational Medicine, May 11, 2016) included 10 people with mild AD and 36 healthy older adults. Participants underwent imaging scans for beta-amyloid and tau, and completed standard tests of memory and cognition. People with AD had an accumulation of beta-amyloid and tau tangles. The location in the brain of the tau tangles correlated to the specific problems with memory and thinking experienced by the participants with AD, but this was less true for beta-amyloid.
Dr. Gandy’s verdict: These findings suggest that tau tangles more closely track the symptoms of AD. The failure of drugs that are designed to target beta-amyloid means scientists are now investigating tau-lowering therapies. The first tau drugs are in trials—in fact, trials will be going on at Mount Sinai during 2017. However, the key will still be early intervention, before the damage caused by AD has been set in motion.
Vitamin D Connection In addition to its essential role in building healthy bones, vitamin D has effects on other organs in the body, including the brain. Studies suggest that people with AD have low vitamin D levels. For a 15-year study published in the Journal of Alzheimer’s Disease, Feb. 6, 2016, researchers measured vitamin D levels in more than 3,400 people age 60 and older. Those with a vitamin D deficiency performed worse on tests of cognitive function, and also tended to have a smaller hippocampus. This brain structure, which is involved in short term memory, is one of the first affected by AD.
Dr. Gandy’s verdict: There is lots of new research into vitamin D, which appears to activate the immune system’s “garbage disposal” cells in the brain. These cells may help clear beta-amyloid. Vitamin D should be checked routinely and treated if low, but it is important to keep in mind that there currently is no evidence that supplementing with vitamin D slows cognitive decline.
Low Weight and AD Risk Researchers writing in the Journal of Alzheimer’s Disease, Aug. 3 2016, suggest that low weight may increase the risk for AD. The 280 study participants, ages 62 to 90, all had normal brain function, and were in good general health. Physical exams and brain scans suggested a link between lower body mass index (BMI, a relation of height to weight) and having more beta-amyloid in the brain.
Dr. Gandy’s verdict: This study did not find a cause-and-effect relationship—moreover, any association between weight and AD may work in reverse, since it is possible that AD pathology in the hypothalamus, an area of the brain that controls hunger, may interfere with appetite. Being underweight also is a red flag for frailty, an age-related syndrome characterized by diminished strength that is known to be associated with a greater risk for AD.
Could a Simple Smell Test Help Predict AD Risk? Finding a way to pinpoint who may be at risk for AD well before memory problems develop is a crucial step towards devising treatments that slow or even prevent the progression of the disease. Previous research has revealed that people with AD exhibit diminished ability to identify odors. A recent study tested older adults’ ability to recognize and remember 40 different odors, including menthol, clove, strawberry, lemon, lilac, and garlic. Brain imaging tests revealed that those who were less able to identify the odors had greater thinning in two brain regions associated with AD risk.
Dr. Gandy’s verdict: The researchers are planning a larger-scale study to confirm these data. If the results are validated, olfactory testing could provide an inexpensive, noninvasive method of screening candidates for new therapies. However, it is important to note that normal aging can affect an individual’s sense of smell, as can Lewy body disease, Parkinson’s disease, and even smoking.
Examining the Eyes for Early Signs A simple eye test may spot changes that are an early sign of AD, according to a study presented at the Alzheimer’s Association International Conference in July 2016. Researchers used eye scans to measure the thickness of a layer of nerves at the back of the eye. The thickness of this layer of nerves decreases with age in everyone, but it is especially thin in people with AD. In a study of more than 33,000 people who had eye scans and cognitive testing, the nerve fiber layer was thinner among those who did poorly on cognition tests.
Dr. Gandy’s verdict: Several studies have suggested the early signs of AD might be discernible in the retina or pupil. However, as yet there is no compelling data, and what there is would need to be reproduced in larger numbers of people, with an appropriate control group.
Progress is Slow, But Promising We haven’t yet pinpointed what causes AD, but Dr. Gandy feels that we are moving in that direction. “Better imaging techniques are enabling us to study living brains to better detect the earliest stages of AD,” he notes. “This is a key development, since numerous studies have suggested that the neurodegeneration underpinning AD starts at least a decade before memory symptoms start to become noticeable, and identifying people with the disease early is key to treating them before symptoms take hold. New drugs continue to be studied, and evidence is emerging about the social and lifestyle approaches that may protect brain health and function as we age. Progress is being made, albeit slowly.”
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