Alzheimers News

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Inhibition of meprin β enzyme linked to the development of Alzheimer's disease analyzed

Findings of researchers at Mainz University could lead to the creation of new drugs

Johannes Gutenberg Universitaet Mainz

4/20/21 ... 042021.php

Researchers at Johannes Gutenberg University Mainz (JGU) in Germany and the Institute of Molecular Biology of Barcelona in Spain have discovered how the blood plasma protein fetuin-B binds to the enzyme meprin β and used a computer model to visualize their findings. These results could lead to the development of new drugs to treat serious diseases such as Alzheimer's and cancer. Meprin β releases proteins from cell membranes, thus controlling important physiological functions in the human body. However, a dysregulation of this process can trigger the development of Alzheimer's and cancer. Meprin β is regulated by fetuin-B binding to the enzyme when required, thereby preventing the release of other proteins. Presenting their findings in the journal "Proceedings of the National Academy of Sciences", the researchers are now the first to describe this binding in detail.

The team at Mainz University produced both meprin β and fetuin-B in insect cells and then allowed them to react with one other in a test tube. By means of measurement of enzyme kinetics and biophysical analyses, the researchers determined that this reaction resulted in an exceptionally stable, high-molecular-mass complex. Their colleagues in Barcelona subsequently managed to crystallize the complex and determine its three-dimensional structure using X-ray crystallography. This involved X-rays being fired at the protein crystals, which allowed the atomic structure of the crystals to be calculated from the diffraction of the X-rays. A computer model of the structure was then generated. "Thanks to the model, we can now see exactly how meprin β and fetuin-B bind together," said Professor Walter Stöcker, who conducted the research at JGU together with Dr. Hagen Körschgen and Nele von Wiegen. "This research represents an excellent starting point for gaining a better understanding of diseases such as Alzheimer's and for developing the drugs to combat them." Meprin β is already known to be involved in the formation of so-called beta-amyloid plaques, which are a characteristic feature of the condition. Moreover, people with Alzheimer's disease have relatively little fetuin-B in their blood, which in turn may lead to a lack of regulation of meprin β. "If it is possible to develop a drug that binds to the enzyme and inhibits it in a similar way to fetuin-B, this could be a new way of treating Alzheimer's," concluded Stöcker.
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Re: Alzheimers News

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In surprising twist, some Alzheimer's plaques may be protective, not destructive

Scientists find brain's immune cells form some plaques as a defense in Alzheimer's, suggesting a new therapeutic direction

4/15/21 ... 114143.htm

One of the characteristic hallmarks of Alzheimer's disease (AD) is the buildup of amyloid-beta plaques in the brain. Most therapies designed to treat AD target these plaques, but they've largely failed in clinical trials. New research by Salk scientists upends conventional views of the origin of one prevalent type of plaque, indicating a reason why treatments have been unsuccessful.

The traditional view holds that the brain's trash-clearing immune cells, called microglia, inhibit the growth of plaques by "eating" them. The Salk scientists show instead that microglia promote the formation of dense-core plaques, and that this action sweeps wispy plaque material away from neurons, where it causes cell death. The research, which was published in Nature Immunology on April 15, 2021, suggests that dense-core plaques play a protective role, so treatments to destroy them may do more harm than good.

"We show that dense-core plaques don't form spontaneously. We believe they're built by microglia as a defense mechanism, so they may be best left alone," says Greg Lemke, a professor in Salk's Molecular Neurobiology Laboratory. "There are various efforts to get the FDA to approve antibodies whose main clinical effect is reducing dense-core plaque formation, but we make the argument that breaking up the plaque may be doing more damage."

Alzheimer's disease is a neurological condition that results in memory loss, impairment of thinking, and behavioral changes, which worsen as we age. The disease seems to be caused by abnormal proteins aggregating between brain cells to form the hallmark plaques, which interrupt activity that keeps the cells alive.

There are numerous forms of plaque, but the two most prevalent are characterized as "diffuse" and "dense-core." Diffuse plaques are loosely organized, amorphous clouds. Dense-core plaques have a compact center surrounded by a halo. Scientists have generally believed that both types of plaque form spontaneously from excess production of a precursor molecule called amyloid precursor protein (APP).

But, according to the new study, it is actually microglia that form dense-core plaques from diffuse amyloid-beta fibrils, as part of their cellular cleanup.

This builds on a 2016 discovery by the Lemke lab, which determined that when a brain cell dies, a fatty molecule flips from the inside to the outside of the cell, signaling, "I'm dead, eat me." Microglia, via surface proteins called TAM receptors, then engulf, or "eat" the dead cell, with the help of an intermediary molecule called Gas6. Without TAM receptors and Gas6, microglia cannot connect to dead cells and consume them.

The team's current work shows that it's not only dead cells that exhibit the eat-me signal and Gas6: So do the amyloid plaques prevalent in Alzheimer's disease. Using animal models, the researchers were able to demonstrate experimentally for the first time that microglia with TAM receptors eat amyloid plaques via the eat-me signal and Gas6. In mice engineered to lack TAM receptors, the microglia were unable to perform this function.

Digging deeper, they traced the dense-core plaques using live imaging. Much to their surprise, the team discovered that after a microglial cell eats a diffuse plaque, it transfers the engulfed amyloid-beta to a highly acidic compartment and converts it into a highly compacted aggregate that is then transferred to a dense-core plaque. The researchers propose that this is a beneficial mechanism, organizing diffuse into dense-core plaque and clearing the intercellular environment of debris.

"Our research seems to show that when there are fewer dense-core plaques, there seem to be more detrimental effects," says Youtong Huang, first author on the paper. "With more-diffuse plaques, there's an abundance of dystrophic neurites, a proxy for neuronal damage. I don't think there's a distinct clinical decision on which form of plaque is more or less detrimental, but through our research, we seem to find that dense-core plaques are a bit more benign."

Their findings suggest new ways of developing a treatment for Alzheimer's disease, such as boosting expression of TAM receptors on microglia to accelerate dense-core plaque formation. The team would like to conduct cognitive studies to see if increasing the activity of microglial TAM receptors would alleviate the effects of AD.

Lemke, who holds the Françoise Gilot-Salk Chair, believes that the current failure rate of most Alzheimer's drug trials is about to end. "Some people are saying that the relative failure of trials that bust up dense-core plaques refutes the idea that amyloid-beta is a bad thing in the brain," says Lemke. "But we argue that amyloid-beta is still clearly a bad thing; it's just that you've got to ask whether dense-core plaques are a bad thing."

Lemke suggests that scientists looking for a cure for Alzheimer's should stop trying to focus on breaking up dense-core plaques and start looking at treatments that either reduce the production of amyloid-beta in the first place or therapies that facilitate transport of amyloid-beta out of the brain altogether.

Journal Reference:

Youtong Huang, Kaisa E. Happonen, Patrick G. Burrola, Carolyn O’Connor, Nasun Hah, Ling Huang, Axel Nimmerjahn, Greg Lemke. Microglia use TAM receptors to detect and engulf amyloid β plaques. Nature Immunology, 2021; DOI: 10.1038/s41590-021-00913-5
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Re: Alzheimers News

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These Signs May Indicate Early Dementia or Alzheimer’s Disease

4/19/21 ... -symptoms/

by Ray Burow

While aging is the greatest risk factor associated with Alzheimer’s disease, the disease is not a normal part of aging.

Most people with Alzheimer’s are 65 or older. But this is not an indication that Alzheimer’s is strictly a disease of old age. Thousands of younger people have been diagnosed with Alzheimer’s, too.

Nearly 200,000 people in the United States under 65 — and some as young as 40 — have been diagnosed with early-onset Alzheimer’s. Many also care for loved ones who have been diagnosed, and they likely would recognize the signs and symptoms of the disease.

Perhaps you or a loved one has noticed signs that dementia or Alzheimer’s might be on your horizon. It’s a scary thought, but if the signs are appearing, they can’t be ignored.

Do not ignore early signs of dementia

The signs and symptoms of dementia can be subtle. They don’t appear as they do in a person with a more advanced stage of the disease. Sometimes, even a healthcare provider might miss the opportunity to pursue an early diagnosis because they’re unfamiliar with how the stages progress.

When quizzing a patient during an assessment, a doctor who doesn’t specialize in cognitive health and brain function might ask questions a person in the later stages of the disease won’t have the ability to answer correctly. However, a person with early-onset dementia can answer simple questions, which may result in a misdiagnosis.

A critical early diagnosis might also be missed when the person experiencing symptoms, or their loved ones, choose to ignore the signs. People with early-onset Alzheimer’s can often recognize when something isn’t right. The signs are there, but they’re either ignored or denied outright.

By veiling mistakes and missteps with excuses, a person can remain in denial and fail to be diagnosed. It is difficult to do, but facing these symptoms head-on is the best way to combat the changes taking place in the brain and prepare for the future.

Understand and acknowledge dementia symptoms

If you believe you may be experiencing symptoms, do not dismiss the changes taking place in your brain, and don’t write them off as a normal part of aging. If you’re experiencing the following symptoms or notice them in a loved one’s behavior, seek medical attention.

Memory loss negatively affects daily life

Memory loss is the primary symptom of Alzheimer’s and dementia, but occasionally misplacing the car keys or forgetting where your car is parked aren’t definitive signs. Memory loss that continues to negatively affect daily life could be a signal.

Do you or a loved one, having forgotten the answer to a recently asked question, ask it again, perhaps several times? Are you relying on memory tricks to help you hold on to things you’d normally remember? Are you making an inordinate number of lists to remind yourself of this or that?

This may not be normal behavior and may be a sign of cognitive issues that should be addressed.

A loss for words

While putting words together has never been a problem in the past, suddenly a person might find themselves searching for the right word to use in conversation. They may use the wrong word in place of another or call an object by the wrong name. The name given the object might be similar to what it actually is, or perhaps it is more a definition than a name or title.

For example, rather than calling a watch by its common name, the person might define it as “arm clock” or “wrist clock.” They also might have a hard time following a conversation.

Simple tasks become complicated

A person with early-onset dementia might take a long way home because they momentarily forgot the way. They might fail to remember a recipe they’ve made by memory a thousand times, or forget how to play a simple card game.

Keeping up with a storyline might be difficult. Little things might have become confusing, and foggy moments could occur.

Loss of interest in a favorite hobby or pastime

A person may experience a loss of motivation. They might not have a desire to do much of anything and seem satisfied to sit in one place for long periods rather than being active. They’re often less engaged.

Poor judgment

Personal decisions can make less sense, and choices might stray from how the person normally would react in certain situations. Poor choices are made. A person with early signs of dementia may become suspicious of a spouse, child, or close friend.

Personality changes

A change in personality often signals changes in the brain. Bouts with anger, depression, anxiousness, or any trait that is opposite to what the person usually exhibits might be a sign that cognitive changes are taking place.

The above symptoms can be signs of dementia, but also of treatable conditions. Speak with a qualified health professional to be diagnosed, particularly one who specializes in cognitive issues that affect the brain.
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Draining brain's debris enhances Alzheimer's therapies in mice

Impaired drainage also may play a role in Alzheimer's in people

4/28/21 ... 113753.htm

Experimental Alzheimer's drugs have shown little success in slowing declines in memory and thinking, leaving scientists searching for explanations. But new research in mice has shown that some investigational Alzheimer's therapies are more effective when paired with a treatment geared toward improving drainage of fluid -- and debris -- from the brain, according to a study led by researchers at Washington University School of Medicine in St. Louis.

The findings, published April 28 in the journal Nature, suggest that the brain's drainage system -- known as the meningeal lymphatics -- plays a pivotal but underappreciated role in neurodegenerative disease, and that repairing faulty drains could be a key to unlocking the potential of certain Alzheimer's therapies.

"The lymphatics are a sink," said co-senior author Jonathan Kipnis, PhD, the Alan A. and Edith L. Wolff Distinguished Professor of Pathology & Immunology and a BJC Investigator. "Alzheimer's and other neurodegenerative diseases such as Parkinson's and frontotemporal dementia are characterized by protein aggregation in the brain. If you break up these aggregates but you have no way to get rid of the debris because your sink is clogged, you didn't accomplish much. You have to unclog the sink to really solve the problem."

Sticky plaques of the protein amyloid start forming in the brains of people with Alzheimer's two decades or more before symptoms such as forgetfulness and confusion arise. For years, scientists have tried to treat Alzheimer's by developing therapies that clear away such plaques but have had very limited success. One of the most promising candidates, aducanumab, recently proved effective at slowing cognitive decline in one clinical trial but failed in another, leaving scientists baffled.

Kipnis, who is also a professor of neurosurgery, of neurology and of neuroscience, identified meningeal lymphatics as the brain's drainage system in 2015. A few years later, in 2018, he demonstrated that damage to the system increases amyloid buildup in mice. He suspects that the mixed and often disappointing performance of anti-amyloid drugs can be explained by differences in lymphatic function among Alzheimer's patients. But proving this hunch has been challenging, as there are no tools to measure the health of a person's meningeal lymphatics directly.

In this study, Kipnis and colleagues took an indirect approach to checking the drainage system in the brains of Alzheimer's patients. The study was undertaken in collaboration with biotherapeutics company PureTech Health.

Thinking that the effects of a clogged drain might spill over onto microglia, the cells that serve as the brain's cleanup crew, the researchers looked for evidence of lymphatic damage in the form of altered patterns of microglial gene expression. Microglia play a complicated role in Alzheimer's disease: They seem to slow the growth of amyloid plaques early in the course of the disease but worsen neurological damage later on. The researchers disabled the meningeal lymphatics of a group of mice genetically prone to forming amyloid plaques, leaving the lymphatics functional in another group of mice for comparison, and analyzed the patterns of genes expressed by microglia.

Lymphatic dysfunction shifted microglia toward a state that was more likely to promote neurodegeneration. Further, when co-senior author Oscar Harari, PhD, an assistant professor of psychiatry and of genetics, compared the gene-expression patterns in microglia from mice and people -- including 53 people who died with Alzheimer's disease and nine who died with healthy brains -- the people's microglia most resembled those from mice with damaged lymphatics.

"There was a signature we found in the microglia from mice with ablated meningeal lymphatics," Harari said. "When we harmonized the human and mouse microglial data, we found the same signature in the human data."

Another cell type, endothelial cells that line the inside of lymphatic vessels, provided additional evidence for the importance of the brain's drainage system. Co-senior author Carlos Cruchaga, PhD, a professor of psychiatry, of genetics and of neurology, identified the genes most highly expressed in lymphatic endothelial cells from mice. He discovered that genetic variations in many of the same genes have been linked to Alzheimer's in people, suggesting that problems with the lymphatics might contribute to the disease.

"In the end, even though we're looking at specific cell types and specific pathways, the brain is one big organ," Cruchaga said. "The lymphatic system is how the garbage is cleaned out of the brain. If it's not working, everything gets gummed up. If it starts working better, then everything in the brain works better. I think this is a very good example of how everything is connected, everything impacts brain health."

To find out whether bolstering lymphatic function could help treat Alzheimer's disease, the researchers studied mice genetically prone to developing amyloid plaques and whose lymphatics were impaired due to age or injury. They treated the animals with mouse versions of the experimental Alzheimer's drugs aducanumab or BAN2401, along with vascular endothelial growth factor C, a compound that promotes the growth of lymphatic vessels. Combination therapy reduced amyloid deposits more than the anti-amyloid drugs alone.

"There have been several antibodies that appear very effective at reducing amyloid deposits in mouse studies and now in humans," said co-author David Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology. "Some now also appear to slow cognitive decline in people with very mild dementia or mild cognitive impairment due to Alzheimer's. However, the cognitive effects are not large, and one wonders if meningeal lymphatic system dysfunction may be related in part to the somewhat limited effects on cognition currently being observed. The meningeal lymphatic system seems to be influencing not just the progression of the amyloid component of Alzheimer's pathology but also the response to immunotherapy. Maybe an understanding of this system is a part of what the field of Alzheimer's drug development has been missing, and with increased attention to it we will better translate some of these promising drug candidates into therapies that provide meaningful benefits to people living with this devastating disease."

Story Source:

Materials provided by Washington University School of Medicine. Original written by Tamara Bhandari. Note: Content may be edited for style and length.

Journal Reference:

Da Mesquita, S., Papadopoulos, Z., Dykstra, T. et al. Meningeal lymphatics affect microglia responses and anti-Aβ immunotherapy. Nature, 2021 DOI: 10.1038/s41586-021-03489-0
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Re: Alzheimers News

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Partially sighted may be at higher risk of dementia

4/29/21 ... entia.html

Older people with vision loss are significantly more likely to suffer mild cognitive impairment, which can be a precursor to dementia, according to a new study published in the journal Ageing Clinical and Experimental Research.

The research by Anglia Ruskin University (ARU) examined World Health Organisation data on more than 32,000 people and found that people with loss in both near and far vision were 1.7 times more likely to suffer from mild cognitive impairment.

People with impairment of their near vision were 1.3 times more likely to suffer from mild cognitive impairment than someone with no vision impairment.

However, people who reported only loss of their far vision did not appear to have an increased risk.

Dr. Lee Smith, Reader in Physical Activity and Public Health at ARU, said: "Our research shows for the first time that vision impairment increases the chances of having mild cognitive impairment. Although not everyone with mild cognitive impairment will go on to develop it, there is a likelihood of progression to dementia, which is one of the major causes of disability and dependency in the older population."

Co-author Shahina Pardhan, Director of the Vision and Eye Research Institute at ARU, said: "Research now needs to focus on whether intervention to improve quality of vision can reduce the risk of mild cognitive impairment, and ultimately dementia. More work needs to be done to examine any possible causation, and what the reasons might be behind it."

The researchers examined population data from China, India, Russia, South Africa, Ghana and Mexico from the WHO's Study on Global Ageing and Adult Health (SAGE). The overall prevalence of mild cognitive impairment was 15.3% in the study sample of 32,715 people, while around 44% of the total number of people surveyed had vision impairment.

More information:
Lee Smith et al, The association between objective vision impairment and mild cognitive impairment among older adults in low- and middle-income countries, Aging Clinical and Experimental Research (2021). DOI: 10.1007/s40520-021-01814-1
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Re: Alzheimers News

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New algorithm for the diagnostics of dementia

4/29/21 ... entia.html

Researchers from the University of Eastern Finland and the University of Oulu in collaboration with an international team have created a new diagnostic biomarker-based algorithm for the diagnostics of dementia. The team is led by Professor Barbara Borroni from the University of Brescia, Italy. The article was published in the Diagnostics journal.

The accurate diagnosis of different types of dementia is frequently complicated and often cannot be set at the early phases of the disease due to the lack of practical and specific diagnostic tools. In addition, the clinical symptoms of patients with various neurodegenerative diseases often overlap and thus, the accurate diagnosis is not always possible.

The precise diagnosis, however, is needed to enable the management of the disease in the best possible way. For example, the widely used pharmaceutical cholinesterase inhibitors are beneficial in the symptomatic treatment and help maintaining activities of daily living in Alzheimer's disease patients. However, they worsen the clinical and neuropsychiatric symptoms in patients with frontotemporal dementia.

In the future, disease modifying drugs will be available for the individualized management of dementia. Those patients that benefit from these interventions should be recognized as early as possible to prevent irreversible neuronal damage and loss associated with cognitive decline and diminished capability for independent life.

The present novel diagnostic algorithm will help to reliably differentiate patients with different types of dementia and is useful in selecting patients for clinical drug trials as well.

New biomarkers are more sensitive and specific, but not yet largely available

The cerebrospinal fluid-based Alzheimer's disease biomarkers developed at the end of last century had a ground-breaking impact on the diagnostics of dementia. However, it has recently been shown that the specificity of these biomarkers in differentiating dementing diseases from each other is low, which has increased the pressure to develop new, improved biomarkers for the diagnostics of dementia.

The new generation biomarkers are based widely on the utilization of blood samples instead of the invasive cerebrospinal fluid samples. Based on the present algorithm, the researchers recommend the utilization of blood neurofilament light chain levels in the screening of dementias. Also, the new algorithm allows the diagnosis of the most common type of dementia, Alzheimer's disease, based on blood sample analysis. Later on, cerebrospinal fluid-based analyses might only be needed for the diagnostics of rarer forms of dementia.

"New biomarkers will enable ground-breaking next-generation diagnostics. Moreover, the currently time-taking diagnostic procedures will accelerate. This will diminish the humane burden of patients and their next-of-kin, when we can provide a precise diagnosis instead of prolonged uncertainty for the families," says the leading author of the article, Adjunct Professor Eino Solje from the University of Eastern Finland.

The published algorithm cannot yet be applied in the daily clinical work, since most of the biomarkers are not so far widely available in the clinical laboratories. Nevertheless, the researchers believe that the promising results will accelerate the accessibility of these biomarker measurements in the near future.

More information: Eino Solje et al. State-of-the-Art Methods and Emerging Fluid Biomarkers in the Diagnostics of Dementia—A Short Review and Diagnostic Algorithm, Diagnostics (2021). DOI: 10.3390/diagnostics11050788
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Study examines the accuracy and reliability of virtual cognitive assessments for diagnosing dementia

5/5/21 ... entia.aspx

Virtual care provided through telephone or videoconference has been broadly implemented in recent months because of the COVID-19 pandemic.

A new analysis of published studies has examined the accuracy and reliability of virtual compared with in-person cognitive assessments for diagnosing dementia or mild cognitive impairment.

The analysis, which is published in the Journal of the American Geriatrics Society, included 121 studies. Three studies comparing videoconference with in-person cognitive assessments demonstrated good reliability and accuracy of virtual cognitive assessments in diagnosing dementia. Investigators did not identify any studies comparing telephone with in-person cognitive assessments.

The analysis also allowed the researchers to identify virtual cognitive test cut-offs suggestive of dementia or mild cognitive impairment, as well as barriers to implementing cognitive assessments for older adults.

" Our results highlight serious knowledge gaps and challenges associated with implementing virtual care for older adults--especially when you consider that the majority of older adults continue to access virtual care via the telephone."

- Jennifer A. Watt, MD, PhD, Study Lead Author, St. Michael's Hospital-Unity Health Toronto, Canada



Journal reference:

Watt, J. A., et al. (2021) Diagnostic accuracy of virtual cognitive assessment and testing: Systematic review and meta‐analysis. Journal of the American Geriatrics Society.
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Trouble managing money may be an early sign of dementia

5/5/21 ... entia.aspx

After Maria Turner's minivan was totaled in an accident a dozen years ago, she grew impatient waiting for the insurance company to process the claim. One night, she saw a red pickup truck on eBay for $20,000. She thought it was just what she needed. She clicked "buy it now" and went to bed. The next morning, she got an email about arranging delivery. Only then did she remember what she'd done.

Making such a big purchase with no forethought and then forgetting about it was completely out of character for Turner, then a critical care nurse in Greenville, South Carolina. Although she was able to back out of the deal without financial consequences, the experience scared her.

"I made a joke out of it, but it really disturbed me," Turner said.

It didn't stop her, though. She shopped impulsively online with her credit card, buying dozens of pairs of shoes, hospital scrubs and garden gnomes. When boxes arrived, she didn't remember ordering them.

Six years passed before Turner, now 53, got a medical explanation for her spending binges, headaches and memory lapses: Doctors told her that imaging of her brain showed all the hallmarks of chronic traumatic encephalopathy. CTE is a degenerative brain disease that in Turner's case may be linked to the many concussions she suffered as a competitive horseback rider in her youth. Her doctors now also see evidence of Alzheimer's disease and frontotemporal dementia, which affects the frontal and temporal lobes of the brain. These may have roots in her CTE.

Turner's money troubles aren't unusual among people who are beginning to experience cognitive declines. Long before they receive a dementia diagnosis, many people start losing their ability to manage their finances and make sound decisions as their memory, organizational skills and self-control falter, studies show. As people fall behind on their bills or make unwise purchases and investments, their bank balances and credit rating may take a hit.

Mental health experts say the covid pandemic may have masked such early lapses during the past year. Many older people have remained isolated from loved ones who might be the first to notice unpaid bills or unopened bank notices.

"That financial decision-making safety net may have been weakened," said Carole Roan Gresenz, interim dean at Georgetown University's School of Nursing and Health Studies, who co-authored a study examining the effect of early-stage Alzheimer's disease on household finances. "We haven't been able to visit, and while technology can provide some help, it's not the same … as sitting next to people and reviewing their checking account with them."

Even during times that aren't complicated by a global health crisis, families may miss the signs that someone is struggling with finances, experts say.

"It's not uncommon at all for us to hear that one of the first signs that families become aware of is around a person's financial dealings," said Beth Kallmyer, vice president for care and support at the Alzheimer's Association.

Early in the disease, Kallmyer said, dementia robs people of the abilities they need to manage money: "executive functioning" skills like planning and problem-solving, as well as judgment, memory and the ability to understand context.

People who live alone may be the most likely to slip through the cracks, their lapses unnoticed, Kallmyer said. And many adult children may be reluctant to discuss personal finances with their parents, who often guard their independence.

About 6 million Americans are living with Alzheimer's disease, the most common cause of dementia. Dementia is an umbrella term for a range of conditions associated with declines in mental abilities that are severe enough to interfere with daily life. There is no cure. Alzheimer's, which killed more than 133,000 Americans in 2020, is the seventh-leading cause of death in the U.S.

Many people have mild symptoms for years before they are diagnosed. During this stage, before obvious impairment, they may make substantial errors managing their finances.

In Gresenz's study, researchers linked data from Medicare claims between 1992 and 2014 with results from the federally funded Health and Retirement Study, which regularly surveys older adults about their finances, among other things. Her study, published in the journal Health Economics in 2019, found that during early-stage Alzheimer's, people were up to 27% more likely than cognitively healthy people to experience a large decline in their liquid assets, such as savings and checking accounts, stocks and bonds.

Another study, published in JAMA Internal Medicine in November, linked Medicare claims data to the Federal Reserve Bank of New York/Equifax Consumer Credit Panel to track people's credit card payments and credit scores. The study found that people with Alzheimer's and related dementias were more likely to miss bill payments up to six years before they were diagnosed than were people who were never diagnosed. The researchers also noted that the people later diagnosed with dementia started to show subprime credit scores 2.5 years before the others.

"We went into the study thinking we might be able to see these financial indicators," said Lauren Hersch Nicholas, an associate professor of public health at the University of Colorado, who co-authored the study. "But we were sort of surprised and dismayed to find that you really could. That means it's sufficiently common because we're picking it up in a sample of 80,000 people."

For decades, Pam McElreath kept the books for the insurance agency that she and her husband, Jimmy, owned in Aberdeen, North Carolina. In the early 2000s, she started having trouble with routine tasks. She assigned the wrong billing codes to expenditures, filled in checks with the wrong year, forgot to pay the premium on her husband's life insurance policy.

Everyone makes mistakes, right? It's just part of aging, her friends would say.

"But it's not like my friend that made that one mistake, one time," said McElreath, 67. "Every month I was having to correct more mistakes. And I knew something was wrong."

She was diagnosed with mild cognitive impairment in 2011, at age 56, and with early-onset Alzheimer's two years later. In 2017, doctors changed her diagnosis to frontotemporal dementia.

Receiving a devastating diagnosis is hard enough, but learning to cope with it is also hard. Eventually both McElreath and Maria Turner put mechanisms in place to keep their finances on an even keel.

Turner, who has two adult children, lives alone. After her diagnosis, she hired a financial manager, and together they set up a system that provides Turner with a set amount of spending money every month and doesn't allow her to make large withdrawals on impulse. She ditched her credit cards and removed eBay and Amazon from her phone.

Though not a micromanager, Turner's financial adviser keeps an eye on her spending and questions her when something seems off.

"Did you realize you spent X?" she'll ask, Turner said.

"And I'll be like, 'No, I didn't.' And that's the thing. I'm aware but I'm not aware," she added.

In 2017, Pam and Jimmy McElreath sold their insurance agency to spend more time together and moved west to Sugar Grove, in the Blue Ridge Mountains. They worked with a therapist to figure out how to ensure Pam is able to continue to do as much as possible.

These days, Pam still signs their personal checks, but now Jimmy looks them over before sending them out. The system is working so far.

"At first I was mad, and I went through this dark time," Pam said, adding: "But the more that you come to accept your problem, the easier it is to say, 'I need help.'"

Jimmy's gentle approach helped. "He was so good about telling me when I did something wrong but doing it in such a kind way, not blaming me for making mistakes. We've been able to work it out."

Tips for helping a loved one

It's not easy to broach financial management issues with an elderly parent or other relative experiencing cognitive trouble. Ideally, you and they will have these conversations before problems develop.

As an adult child, you might mention you've been talking with a financial adviser about managing your own finances to ease into a conversation about what your elder is doing, said Beth Kallmyer of the Alzheimer's Association.

Or suggest that allowing a shared financial management arrangement would eliminate the hassle of tracking and paying bills.

"Often people are open to the idea of making their lives easier," Kallmyer said.

Whatever the approach, it's important to plan and take steps to protect assets.

"Part and parcel of any legal or estate planning is protecting oneself in the event of incapacity," said Jeffrey Bloom, an elder law attorney at Margolis & Bloom in the Boston area.

Specific steps depend on the family and their financial situation, but here are some to consider:

Encourage the parent in need of help to sign a financial power of attorney.

These legal documents authorize you or another person to act on a parent's behalf in financial matters. The terms may be narrow or broad, allowing you to make all financial decisions or to perform specific duties like paying bills, making account transfers or filing taxes.

A "durable" power of attorney allows you to make decisions even if your parent becomes incapacitated. In some states, power of attorney documents are automatically considered durable.

Put assets in a trust.

A trust is a legal vehicle that can hold a range of assets and property. It can spell out how those assets are managed and distributed while people are alive or after they die.

"We do believe in the power of attorney, but we believe in the trust as an even better tool in the event of incapacity," Bloom said.

Trusts can be tailored to a client's concerns and provide more guidance than a power of attorney document about what money can be spent on and who has access under what circumstances, among other things.

You might be a co-trustee on major distributions, for example, or there may be rules that provide for you or others to review and be notified of any changes, Bloom said.

The Alzheimer’s Association recommends working with an attorney who specializes in trusts to ensure all laws and regulations are followed, Kallmyer said.

Have your name added as another user on a parent's bank accounts, credit cards or other financial accounts.

This may be a convenient way to make payments or monitor activity. But a shared account can be problematic if children are sued, for example, or wish to withdraw the money for their own use.

The funds typically belong to all parties whose names are on the account. Unlike a power of attorney, the child isn't obligated to act in a parent's best interest.

Each of these setups may help protect a parent's assets. But parents may not welcome what they see as interference, no matter how well meaning family members are. Typically, they can refuse to permit children's access to their financial information or revoke permission previously granted.

Finding a balance between protecting someone and usurping their rights is hard, said Bloom. The only way to ensure financial control is to go to court to establish guardianship or conservatorship. But that is a serious step not to be taken lightly.

"You only want to do that if there's a major risk."
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