A new report from the University of Washington links long-term use of anticholinergic medications and dementia. Anticholinergic drugs block the action of acetylcholine. This substance transmits messages in the nervous system. In the brain, acetylcholine is involved in learning and memory. In the rest of the body, it stimulates muscle contractions. Anticholinergic drugs include some antihistamines, tricyclic antidepressants, medications to control overactive bladder, and drugs to relieve the symptoms of Parkinson’s disease. The study found that people who used anticholinergic drugs were more likely to have developed dementia as those who didn’t use them. Dementia risk increased with the cumulative dose. Taking an anticholinergic for the equivalent of three years or more was associated with a 54% higher dementia risk than taking the same dose for three months or less. Safer alternatives to anticholinergic drugs exist.
Drugs in the benzodiazepine family have long been used to treat anxiety and sleep problems. They can cause a bit of a brain hangover the next day. Experts have long assumed that people’s heads would clear once they stopped taking the drug. That may not be the case. In a study published last night by the journal BMJ, a team of researchers from France and Canada linked benzodiazepine use to an increased risk of being diagnosed with Alzheimer’s disease. In the study, the greater a person’s cumulative dose of benzodiazepines, the higher his or her risk of Alzheimer’s. Taking a benzodiazepine for less than three months had no effect on Alzheimer’s risk. Taking the drug for three to six months raised the risk of developing Alzheimer’s by 32%, and taking it for more than six months boosted the risk by 84%. People taking a long-acting benzodiazepine were at greater risk than those on a short-acting one.
A new report in JAMA Neurology offers yet another reminder why keeping your blood pressure in the healthy range for as long as you can is a good life strategy. Researchers with the long-term Atherosclerosis Risk in Communities (ARIC) Neurocognitive Study found that memory and thinking skills declined significantly more over the course of a 20-year study in middle-aged people with high blood pressure than it did in those with healthy blood pressure. Interestingly, those who had normal blood pressure in midlife but who developed high blood pressure in their late 60s, 70s, and 80s didn’t have similar declines as those who developed high blood pressure earlier. The main take-home lesson from this study? The longer you live with normal blood pressure, the less likely you are to have memory and reasoning problems when you’re older.
There are plenty of good reasons to be physically active. Big ones include reducing the odds of developing heart disease, stroke, and diabetes. Maybe you want to lose weight, lower your blood pressure, prevent depression, or just look better. Here’s another one, which especially applies to anyone experiencing the brain fog that comes with age: exercise changes the brain in ways that protect memory and thinking skills. In a study done at the University of British Columbia, researchers found that regular aerobic exercise, the kind that gets your heart and your sweat glands pumping, appears to boost the size of the hippocampus, the brain area involved in verbal memory and learning.
A new report from the Alzheimer’s Association says that as many as 5 million Americans have Alzheimer’s disease or some other form of dementia. Every 67 seconds someone in the United States develops Alzheimer’s disease or dementia. That’s 470,000 Americans this year alone. Given that these thieves of memory and personality are so common and so feared, should all older Americans be tested for them? In proposed guidelines released yesterday, the U.S. Preventive Services Task Force said “no.” Why not? Even after conducting a thorough review of the evidence, the panel said that there isn’t enough solid evidence to recommend screening, especially since not enough is known about the benefits and the harms. In part, the recommendation is based on the sad fact that so far there aren’t any truly effective approaches to stop the forward progress of dementia.
What’s bad for the heart is often bad for the brain. High cholesterol, high blood pressure, diabetes, and unhealthy “hardening” of the arteries increase the risk of mental decline or dementia later in life. A study published online today in Neurology shows that older people with the stiffest arteries are more likely to show the kinds of damage to brain tissue often seen in people with dementia. The study adds support to the “two hit” theory of dementia. It suggests that the accumulation of Alzheimer’s-linked amyloid protein in the brain may not pose problems until damage to small blood vessels that nourish the brain nudges them over into dementia. There may be a silver lining to this line of research: Efforts to improve cardiovascular health can also protect the brain.
There are many reasons to keep your blood sugar under control: protecting your arteries and nerves are two of them. Here’s another biggie: preventing dementia, the loss of memory and thinking skills that afflicts millions of older Americans. A study published today in the New England Journal of Medicine shows that even in people without diabetes, above normal blood sugar is associated with an increased risk of developing dementia. The study does not prove that high blood sugar causes dementia, only that there is an association between the two. For that reason, don’t start trying to lower your blood sugar simply to preserve your thinking skills, cautions Dr. Nathan. There’s no evidence that strategy will work, although he says it should be studied. But it is still worth keeping an eye on your blood sugar. Excess blood sugar can lead to diabetes and a variety of other health problems, including heart, eye, kidney, and nerve disease.
How’s this for a mind-bender: Lou Gehrig may not have had Lou Gehrig’s disease. Instead, the disease that ended his life may have been chronic traumatic encephalopathy (CTE). This brain disease is caused by repeated concussions—Gehrig sustained at least four during his baseball career—or other head injuries. It can cause symptoms very similar to those of amyotrophic lateral sclerosis (ALS), now commonly called Lou Gehrig’s disease. More evidence of a connection between CTE and ALS comes from a new study of almost 3,500 retired professional football players, all of whom had played for at least five years in the National Football League. Among the 334 who died during the course of the study, the risk of death from Alzheimer’s disease or ALS was nearly four times higher than expected. Players who manned a “speed” position (such as quarterbacks or receivers) had a risk of dying from Alzheimer’s disease or ALS that was more than three times higher than those playing “non-speed” positions (such as linemen).
Is there a spring in your step—or a wobble in your walk? The speed and stability of your stride could offer important clues about the state of your brain’s health. According to new research, an unsteady gait is one early warning sign that you might be headed for memory problems down the road. A group of studies reported last week at the Alzheimer’s Association International Conference in Vancouver, Canada, revealed a strong link between walking ability and mental function. What’s behind this connection? Walking is a complex task that requires more than just moving the leg muscles. Walking requires scanning the environment for obstacles and safely navigating around them, all while talking and carrying out various other tasks. The studies found that walking rhythm was related to information processing speed; walking variations and speed were associated with executive function (the mental processes we use to plan and organize); and walking speed became significantly slower as mental decline grew more severe.
Some encouraging Alzheimer’s news from Sweden: a vaccine called CAD106 appears to be safe and ramps up the body’s immune system against a protein likely involved in Alzheimer’s. The hope is that this vaccine will slow the progression of Alzheimer’s disease, and possibly even stop it. The vaccine is designed to activate the body’s immune system against beta amyloid, a protein fragment that forms deposits called amyloid plaques between nerve cells in the brain. Three-quarters of those who received CAD106 developed antibodies against beta amyloid protein. Virtually all of them—including those getting the placebo—reported one or more side effects, ranging from inflammation of the nose and throat to headache, muscle pain, and fatigue. None, though, developed meningoencephalitis, an inflammation of brain tissue that derailed work on an earlier version of the vaccine. The next step in the development of CAD106 is a larger clinical trial to confirm the vaccine’s safety and to see if it is effective at slowing the relentless progression of Alzheimer’s disease.