Common Eye Conditions Tied to Higher Risk for Dementia

Ernie Mundell and Steven Reinberg wrote . . . . . . . . .

Diseases that can rob you of vision as you age also appear to be tied to an increased risk for dementia, a new study finds.

Specifically, age-related macular degeneration, cataracts and diabetes-related eye disease were linked with a higher likelihood of dementia, researchers in China said. However, one other common eye ailment, glaucoma, was not linked to dementia risk.

The new study can’t prove that vision problems cause dementia, only that the two appear to be associated, the researchers stressed. Risks for dementia rose even higher if other chronic ills were added in.

“Newly developed hypertension, diabetes, stroke, heart disease and depression mediated [affected] the association between cataract/ diabetes-related eye disease and dementia,” noted the researchers led by Dr. Xianwen Shang, an ophthalmologist at Guangdong Academy of Medical Sciences in Guangzhou. His team published the findings Sept. 13 in the British Journal of Ophthalmology.

One expert in the United States agreed that the findings don’t mean that eye trouble causes dementia.

“The exact mechanism or reason that the eye disease could increase someone’s risk of dementia was not fully discussed in the study,” said Dr. Matthew Gorski, an ophthalmologist at Northwell Health in Great Neck, N.Y.

For example, he said, “since cataracts are a treatable, reversible condition, I would be curious what effect cataract surgery has on one’s risk of developing dementia. It is also interesting that glaucoma, another potentially blinding eye condition, was not associated with an increased risk of dementia and raises further questions as to how these diseases are related to dementia.”

In the new study, Shang’s group collected data on more than 12,300 British adults, ages 55-73, who took part in the UK Biobank study. The participants were assessed between 2006 and 2010 and followed up until early 2021.

Over that time more than 2,300 people developed dementia.

The researchers found that compared with people who did not have vision conditions at the start of the study, the risk of dementia was 26% higher among those with age-related macular degeneration, 11% higher in those with cataracts, and 61% higher in those with diabetes-related eye disease. Glaucoma was not tied with an increased risk of Alzheimer’s disease, but it was linked with a higher risk of vascular dementia, such as can happen after a stroke.

Participants who had diabetes, heart disease, stroke and depression along with vision problems had an even greater risk of dementia as were those with more than one vision problem, the researchers noted.

Dr. Mark Fromer is an ophthalmologist at Lenox Hill Hospital in New York City. Reading over the findings, he said they suggest that older people with illnesses affecting multiple organs — including the eyes — have higher odds for dementia.

“There may be an additive effect of ophthalmic and systemic diseases” on dementia risk, Fromer said.

For his part, Gorski said “patients should use the results of this study as a reminder of the importance of having regular eye exams with your eye doctor, especially as you get older.”

Source: HealthDay

Time Until Dementia Symptoms Appear Can be Estimated Via Brain Scan

Tamara Bhandari wrote . . . . . . . . .

Researchers at Washington University School of Medicine in St. Louis have developed an approach to estimating when a person with no cognitive symptoms will start showing signs of Alzheimer’s dementia based on data from brain scans and the person’s age.

Researchers at Washington University School of Medicine in St. Louis have developed an approach to estimating when a person who is likely to develop Alzheimer’s disease, but has no cognitive symptoms, will start showing signs of Alzheimer’s dementia.

The algorithm, available online in the journal Neurology, uses data from a kind of brain scan known as amyloid positron emission tomography (PET) to gauge brain levels of the key Alzheimer’s protein amyloid beta.

In those who eventually develop Alzheimer’s dementia, amyloid silently builds up in the brain for up to two decades before the first signs of confusion and forgetfulness appear. Amyloid PET scans already are used widely in Alzheimer’s research, and this algorithm represents a new way of analyzing such scans to approximate when symptoms will arise. Using a person’s age and data from a single amyloid PET scan, the algorithm yields an estimate of how far a person has progressed toward dementia — and how much time is left before cognitive impairment sets in.

“I perform amyloid PET scans for research studies, and when I tell cognitively normal individuals about positive results, the first question is always, ‘How long do I have until I get dementia?’,” said senior author Suzanne Schindler, MD, PhD, an assistant professor of neurology. “Until now, the answer I’d have to give was something like, ‘You have an increased risk of developing dementia in the next five years.’ But what does that mean? Individuals want to know when they are likely to develop symptoms, not just whether they are at higher risk.”

Schindler and colleagues analyzed amyloid PET scans from 236 people participating in Alzheimer’s research studies through Washington University’s Charles F. and Joanne Knight Alzheimer Disease Research Center. The participants were an average of 67 years old at the beginning of the study. All participants underwent at least two brain scans an average of 4½ years apart. The researchers applied a widely used metric known as the standard uptake value ratio (SUVR) to the scans to estimate the amount of amyloid in each participant’s brain at each time point.

The researchers also accessed over 1,300 clinical assessments on 180 of the participants. The assessments typically were performed every one to three years. Most participants were cognitively normal at the start of data collection, so the repeated assessments allowed the researchers to pinpoint when each participant’s cognitive skills began to slip.

Schindler spent years trying to figure out how to use the data in amyloid PET scans to estimate the age at which symptoms would appear. The breakthrough came when she realized that amyloid accumulation has a tipping point and that each individual hits that tipping point at a different age. After this tipping point, amyloid accumulation follows a reliable trajectory.

“You may hit the tipping point when you’re 50; it may happen when you’re 80; it may never happen,” Schindler said. “But once you pass the tipping point, you’re going to accumulate high levels of amyloid that are likely to cause dementia. If we know how much amyloid someone has right now, we can calculate how long ago they hit the tipping point and estimate how much longer it will be until they are likely to develop symptoms.”

People in the study who reached the tipping point at younger ages took longer to develop cognitive symptoms than those who reached it later in life. Participants who hit the tipping point at age 50 typically took nearly 20 years to develop symptoms; those who hit it at age 80 took less than 10 years.

“When we look at the brains of relatively young people who have died with Alzheimer’s, they typically look pretty healthy, other than Alzheimer’s,” Schindler said. “But older people more frequently have damage to the brain from other causes, so their cognitive reserves are lower, and it takes less amyloid to cause impairment.”

The power of this new technique is that it requires just one brain scan, plus the person’s age. With that data, the model can estimate the time to symptom onset, plus or minus several years. In this study, the correlation between the expected age of symptom onset and the true age at diagnosis was better than 0.9 on a scale of 0 (no correlation) to 1 (perfect correlation).

After age, the genetic variant APOE4 is the strongest risk factor for Alzheimer’s dementia. People who carry one copy of the variant are two to three times more likely to develop Alzheimer’s dementia than the general population, and people who carry two copies are 10 times more likely. In this study, people with the high-risk variant hit the tipping point younger, but once that point was passed, they followed the same trajectory as everyone else.

“APOE4 seems to have a seeding effect,” Schindler said. “At very low levels, below the tipping point, you see amyloid rising in people with APOE4 while it’s not changing in people without APOE4. That means APOE4 carriers are going to hit the tipping point sooner. People with two copies of APOE4 hit the tipping point about 10 years earlier than people with no copies. But after that point, we see no difference between the APOE4 carriers and noncarriers.”

With an out-of-pocket cost of around $6,000, amyloid PET brain scans may be financially out of reach for many people. However, this algorithm could help accelerate the pace of drug development by streamlining clinical trials.

“Most participants in clinical trials designed to prevent or slow Alzheimer’s symptoms do not develop symptoms during the trials,” Schindler said. “That’s a lot of time and effort — for the participants as well as the researchers — that doesn’t yield useful data. If we could do trials only on people who are likely to develop symptoms in the next few years, that would make the process of finding therapies much more efficient.”

Source: Washington University School of Medicine

Could Traffic Noise Raise Your Odds for Dementia?

It’s more than just an annoyance: Long-term exposure to traffic and train noise may increase the risk of dementia and Alzheimer’s disease, Danish researchers report.

The study authors said that more than 1,200 of Denmark’s nearly 8,500 cases of dementia in 2017 may have resulted from exposure to noise, which means that reducing traffic noise might help prevent the thinking, memory and behavior problems associated with this condition.

The study, published online in The BMJ, doesn’t prove noise causes dementia or Alzheimer’s, only that there appears to be a link.

“Expanding our knowledge on the harmful effects of noise on health is essential for setting priorities and implementing effective policies and public health strategies focused on the prevention and control of diseases, including dementia,” the researchers said in a journal news release.

Prior studies have linked transportation noise to coronary heart disease, obesity and diabetes, said study author Manuella Lech Cantuaria, assistant professor at The Maersk McKinney Moller Institute, University of Southern Denmark, Odense, Denmark, and colleagues.

If the new findings are confirmed in future studies, the researchers said they could have a large effect on estimation of the burden of disease and health care costs attributed to transportation noise.

For this study, the investigators compared long-term residential exposure to road traffic and train noise with dementia risk among 2 million Danes over 60 years of age.

The team combed national health registers to find cases of dementia and Alzheimer’s disease, vascular dementia and Parkinson’s disease-related dementia over an average of nearly nine years. Between 2004 and 2017, more than 103,000 new cases of dementia were identified.

After taking into account other factors related to residents and their neighborhoods, the researchers found that a 10-year average exposure to road and railway noise increased the odds of dementia. There was a general pattern of higher risk with higher noise exposure.

The study authors reported that road and railway noise were linked with a 27% higher risk of Alzheimer’s disease. Only road noise, however, was tied with an increased risk of vascular dementia.

The researchers said these associations might owe to the release of stress hormones and sleep disturbance, leading to coronary artery disease, and changes in the immune system and inflammation, which are seen at the start of dementia and Alzheimer’s disease.

Source: HealthDay

Postponing Retirement Might Help Keep Dementia at Bay

Amy Norton wrote . . . . . . . . .

Early retirement may sound appealing, but a recent study hints that putting it off a few years might help older adults retain more of their mental sharpness.

Using data on more than 20,000 older Americans, researchers estimated that if all of those people waited until age 67 to retire, their collective cognitive health would benefit.

“Cognition” refers to a person’s ability to think, reason, plan and remember, among other vital brain functions. Research suggests that various factors over a lifetime — from education level to exercise habits to heart health — can affect a person’s rate of cognitive decline, and risk of dementia, later in life.

For the new study, researchers wanted to estimate the possible impact of later retirement on people’s cognitive functioning.

In theory, spending more years on the job would be protective — in a “use it or lose it” kind of way, explained lead researcher Jo Mhairi Hale of the University of St. Andrews, in Scotland.

“Those who keep working are ‘forced,’ let’s say, to stay cognitively engaged, while those who retire may choose to be involved in cognitively engaging activities, but not necessarily,” Hale said.

Her team started with data on more than 20,000 Americans aged 55 to 75 who took part in a long-running health survey called the Health and Retirement Study. It included standard questions that gauge memory and other brain functions.

Many respondents were still working, at least part-time, while about 45% were retired.

The researchers used statistical methods to estimate what would happen if all study participants were “forced” to delay retirement until at least age 67.

In real life, there is a whole host of factors that could sway both a person’s cognitive health and retirement age. And some people might retire earlier because their mental acuity is declining.

Hale said the Health and Retirement Study examined a “plethora of life-course factors,” so that allowed her team to account for some of that complexity.

The investigators weighed factors like people’s education levels; childhood family income and current wealth; health conditions such as diabetes and heart disease; depression symptoms; and whether their longest-held job was professional or “non-professional” (such as manual labor).

In the end, the researchers calculated that delaying retirement until age 67 or older would help people retain some mental sharpness. On average, the group lost about 1 point on their cognitive scores between the ages of 61 and 67; delaying retirement, the researchers estimated, could reduce that by one-third.

The team also found that the benefit could persist for at least five years beyond retirement.

That was not because the extra work years offered bonus brain power. It was because earlier retirement was linked to a faster cognitive decline, the researchers said.

So should older adults keep punching the clock in order to protect their brain health?

The study does not answer that question, according to Claire Sexton, director of scientific programs and outreach for the Alzheimer’s Association.

“It’s definitely a tricky thing to examine the effect of just one event, like retirement age,” said Sexton, who was not involved in the study.

For one, she noted, many factors affect people’s retirement decisions — including whether they enjoy their work and find it stimulating, and whether their job is stressful or physically taxing.

Similarly, Sexton said, a range of factors sway dementia risk, from genes to health conditions like high blood pressure, diabetes and heart disease to obesity and lack of exercise.

That caveat made, Sexton agreed that staying on the job might be beneficial — if it provides people with mental stimulation and social interaction. A body of research suggests those things may help protect the aging brain.

Of course, jobs are not the only way to stay mentally and socially engaged.

Retirement could be used as a “springboard,” Sexton said, freeing up time to take a class, start a new exercise routine, or join a club or volunteer group.

Hale agreed that retirees “would be well-served to regularly participate in cognitively engaging activities.”

A next research step, she said, “would be to explore the extent to which alternative activities that promote cognitive engagement — such as grandparenting or volunteering — are protective against cognitive decline.”

The findings were recently published online in the journal SSM Population Health.

Source: HealthDay

What Are Researchers Doing to Stop Dementia?

Laura Williamson wrote . . . . . . . . .

They are words nobody wants to hear: Alzheimer’s disease and dementia. As the population ages, a growing number of older adults gradually lose cherished memories and the ability to think and, ultimately, to perform even the most basic functions of daily living.

Researchers say dementias are so varied and complex, there remain more questions than answers when it comes to how to thwart them.

“This is a condition with multiple pathologies,” said Cynthia Lemere, immediate past chair of the medical and scientific advisory group of the Alzheimer’s Association. “There’s a lot of research going on right now.”

While there are many causes of dementias, much of the research revolves around Alzheimer’s, which accounts for 60%-70% of all cases. According to the Alzheimer’s Association, more than 6.2 million people are living with Alzheimer’s disease, a number expected to double by 2050.

The federal government spends about $3.1 billion annually on Alzheimer’s research. Another $250 million comes from the Alzheimer’s Association, and last year the American Heart Association announced a joint brain health research project with Bill Gates, as well as support for a global networking effort among research centers to accelerate early detection and treatment of Alzheimer’s and related dementias.

Many drugs are being tested. Some work by going after what is considered one of the hallmarks of the disease – beta-amyloid protein. When this protein builds up in the brain, it clumps together to form plaques that stick in between nerve cells, interfering with the cells’ ability to communicate.

Lemere, an associate professor of neurology in the Ann Romney Center for Neurologic Diseases at Brigham and Women’s Hospital and Harvard Medical School in Boston, has spent the past two decades working on an Alzheimer’s vaccine and antibodies that would attack amyloid plaques.

While trials have shown some potential, it has been difficult to get sufficient amounts of antibodies to cross the blood-brain barrier, she said. Nonetheless, “there are three or four drugs in this class coming down the pipeline that look promising.” A drug that targets amyloid plaque received conditional approval from the Food and Drug Administration this summer and requires further testing to verify its benefits.

A newer area of investigation focuses on drugs to stop the spread of a protein called tau, needed to stabilize the structure of nerve cells. In the brains of people with Alzheimer’s disease, tau changes its structure and aggregates inside the cells, causing tangles to form. The tangles block nutrients and any communication from moving through the cells, which eventually die. That’s when symptoms appear.

“Alzheimer’s disease doesn’t start when you begin to see memory loss. It starts 15-25 years earlier, when these plaques and tangles are forming,” Lemere said. “When you have them both for a long period of time, neurodegeneration starts.”

So far, researchers have seen the best results with patients who are in the earliest stages of Alzheimer’s, Lemere said. “Previous clinical trials have shown that these drugs do not work well for people with moderate to severe Alzheimer’s disease. If someone has already lost 40% of their hippocampal neurons, clearing plaque won’t bring those back. That’s why we still need to continue to find ways to help those in later stages of the disease.”

What’s causing beta-amyloid to accumulate in the first place remains unclear. Some believe it may be an immune system response to viral infections, such as herpes, and may even be linked to the bacteria in gum disease.

“It turns out that amyloid plays a role in protecting the brain from infection,” said Dr. Mitchell Elkind, immediate past president of the American Heart Association. He is a professor of neurology and epidemiology at Columbia University Irving Medical Center in New York City.

When an infection attacks the brain, beta-amyloid may be overproduced as part of an immune response, he said. One avenue of investigation hypothesizes that anti-viral agents could therefore prevent Alzheimer’s or slow progression of the disease based on the theory that “if we eliminate the inciting insult of the infection, perhaps we can decrease the amount of amyloid. That’s an exciting possibility.”

Studying COVID-19 may help, Elkind said. “For those of us interested in the concept that infections may worsen dementia, COVID provides a great model because there is so much of it around. It can help us answer the question of whether a virus can cause long-term cognitive decline. We don’t know yet.”

When viruses and bacteria activate the immune system, they also produce inflammation, which researchers believe contributes to plaque development.

“Inflammation is a hot button now for Alzheimer’s disease research,” Elkind said. Investigators are exploring whether anti-inflammatory agents can be used to ward off symptoms.

Lemere said she believes the most promising approach may be combinations of drugs that help the immune cells in the brain do their job while tamping down inflammation.

“That is going to be the wave of the future,” she said. “Maybe an anti-inflammatory agent with a tau antibody to prevent the downstream neurodegeneration.”

But even if researchers succeed in developing drugs that clear the brain of amyloid plaques and tau tangles, it won’t stop other forms of dementia, said Dr. Mary Sano, director of the Alzheimer’s Disease Research Center at Mount Sinai Health System in New York City.

About 10% of dementias are vascular – they’re linked to strokes or issues with poor blood flow to the brain. Others have mixed dementia, which can be a combination of Alzheimer’s, vascular and other less common types of dementia.

Sano’s center works with people who often develop dementias related to Type 2 diabetes and heart disease risk factors, such as high blood pressure, and these “have a very different profile of cognitive deficits.” For example, people with diabetes begin with greater problems with executive functions, such as the ability to plan and organize. Memory may be less impaired.

Lifestyle behaviors remain an important avenue for preventing vascular dementia, she said. Controlling blood pressure, cholesterol and blood sugar levels and making other lifestyle changes, such as quitting smoking, exercising, eating a nutritious diet and losing weight – metrics the AHA has dubbed Life’s Simple 7 – all have been shown to help maintain good brain health as people age.

This has to start early, Elkind said. “It’s not your blood pressure in your 70s and 80s that causes dementia, but what it was in your 40s and 50s.”

One of the best things people can do is exercise, Lemere said. “It promotes cardiovascular health, which is related to brain health. It’s anti-inflammatory and it promotes better sleep. Lack of sleep is a risk factor for Alzheimer’s disease, and exercise is one of the biggest ways people can stave off or reduce their risk for dementia.”

Source: American Heart Association