Archives for March 2017

Answers to Tax Questions Caregivers Ask Most

( With tax time comes rules, exceptions, exemptions, requirements – and lots of confusion. AgingCare has gathered a list of frequently asked questions that caregivers ask most, with responses from the IRS website.

Q: Can I claim my elderly parent who lives in my home as a dependent on my tax return?

A: You may claim your parent as a dependent if the following tests are met:

  1. You are not a dependent of another taxpayer.
  2. Your parent does not file a joint return.
  3. Your parent is a U.S. citizen, U.S. national, U.S. resident, or a resident of Canada or Mexico.
  4. You paid more than half of your parent’s support for the calendar year.
  5. Your parent’s gross income for the calendar year was less than the exemption amount.
  6. Your parent DOES NOT have to live with you in order to claim them as a dependent, if you’ve meet the above criteria. Relatives who quality who do not have to live with you include: mother, father, grandparent, stepmother, stepfather, mother-in-law, father-in-law.

(See Publication 17, Your Federal Income Tax, and Table 3-1 on page 27, “Overview of the Rules for Claiming an exemption for a Dependent.”)

Q: I am a caregiver and my elderly parent lives in my home. Can I file as head of household?

A: You may file as head of household if you meet the following requirements:

  1. You are unmarried or “considered unmarried” on the last day of the year.
  2. You may claim a dependency exemption for your parent.
  3. You paid more than half the cost of keeping up a home for your parent for the tax year.

Your dependent parent does not have to live with you. Your parent DOES NOT have to live with you in order to claim them as a dependent, if you’ve meet the above criteria. Relatives who quality who do not have to live with you include: mother, father, grandparent, stepmother, stepfather, mother-in-law, father-in-law.

(See Special rule for Parent , in Publication 17, under Qualifying Person. See also Publication 501: Exemptions, Standard Deduction, and Filing Information.)

Q: Can I claim modifications to my home to accommodate my parent’s medical condition as a medical expense?

Yes, but only if your parent was your dependent at the time the medical services were provided or at the time you paid the expense. Also, the amount of the allowable medical expense is the cost of the modification decreased by any resulting increase to the value of your home. Finally, your total deduction for medical and dental expenses must be reduced by 10 percent of your adjusted gross income (7.5 percent if either you or your spouse was born before January 2, 1949).

(See Publications 17 and 502 for additional information.)

Q: My parents occasionally give me money to offset some of the cost of their care. Do I have to pay taxes on these funds?

A: An amount of money that your parents give you to offset their expenses is not taxable to you, however, you should take this amount into account in determining whether your parents are your dependents.

(See Publication 501, Exemptions, Standard Deduction, and Filing Information)

Q: I pay for some of my parent’s expenses medical expenses. Can I deduct these expenses on my tax return?

A: If you can claim your parent as a dependent, you also may be able to claim a deduction for the portion of your parent’s medical or dental expenses that you paid. However, your total deduction for medical and dental expenses must be reduced by 10 percent of your adjusted gross income (7.5 percent if either you or your spouse was born before January 2, 1949).

(See Publication 17, pages 140-144, for additional information. See also Publication 501, Exemptions, Standard Deduction, and Filing Information; Publication 502, Medical and Dental Expenses.)

Q: As a condition of acceptance to their assisted-living facility, my parents relinquished all home ownership rights to the community. Does this arrangement have any tax consequences?

A: Yes, this transaction will be considered a sale of their home. The property was transferred for services.

(See Publication 523 “Selling your Home” for additional information.)

Q: My parent is suffering from dementia. I cash his/her monthly social security check and use the proceeds for his/her care. What are the tax consequences?

A: Your parent’s social security benefits are not taxable to you. However, in determining whether your parent is your dependent, you should consider the benefits used for your parent’s support as support provided by your parent.

(See Publication 501, Exemptions, Standard Deduction, and Filing Information, for additional information.)

Q: My parent signed his/her home over to me. Does this transaction have to be reported to the IRS?

A: Yes. If certain conditions apply, this transaction would be considered a taxable gift from your parent to you. Generally, your parent must file a gift tax return ( Form 709) if any of the following apply:

  1. Your parent gave gifts to at least one person (other than his/her spouse) that are more than the annual exclusion for the year. Check Publication 950 for the annual exclusion.
  2. Your parent and his/her spouse are splitting a gift.
  3. Your parent gave someone (other than his/her spouse) a gift of a future interest that he or she cannot actually possess, enjoy, or receive income from until some time in the future.
  4. Your parent gave his/her spouse an interest in property that will be ended by some future event

NOTE: If any of the above conditions apply, your parent is required to file a Form 709, even if a gift tax is not payable.

(See Publication 950 for additional information on gifts.)

Q: I received a death benefit from my parent’s life insurance policy. Do I have to pay taxes on that money?

A: Life insurance proceeds paid to you because of the death of the insured person are not taxable unless the policy was turned over to you for a price. This is true even if the proceeds were paid under an accident or health insurance policy or an endowment contract. However, interest income received as a result of life insurance proceeds may be taxable.

(See Publication 525 for additional information.)

Links to IRS Documents Referenced in this Article

Publication 17: Your Federal Income Tax

Publication 501: Exemptions, Standard Deductions and Filing Information

Publication 502: Medical and Dental Expenses

Publication 523: Selling Your Home

Publication 525: Taxable and Non-Taxable Income

Publication 950: Estate and Gift Taxes


By Marlo Sollitto

Copyright 2016 AgingCare, LLC.


‘Jumping Genes’ May Set Stage for Brain Cell Death in Alzheimer’s, Other Diseases

(Duke University) The latest round of failed drug trials for Alzheimer’s has researchers questioning the reigning approach to battling the disease, which focuses on preventing a sticky protein called amyloid from building up in the brain.

Duke University scientists have identified a mechanism in the molecular machinery of the cell that could help explain how neurons begin to falter in the initial stages of Alzheimer’s, even before amyloid clumps appear.

This rethinking of the Alzheimer’s process centers on human genes critical for the healthy functioning of mitochondria, the energy factories of the cell, which are riddled with mobile chunks of DNA called Alu elements.

If these “jumping genes” lose their normal controls as a person ages, they could start to wreak havoc on the machinery that supplies energy to brain cells — leading to a loss of neurons and ultimately dementia, the researchers say.

And if this “Alu neurodegeneration hypothesis” holds up, it could help identify people at risk sooner, before they develop symptoms, or point to new ways to delay onset or slow progression of the disease, said study co-author Peter Larsen, senior research scientist in biology professor Anne Yoder’s lab at Duke.

The dominant idea guiding Alzheimer’s research for 25 years has been that the disease results from the abnormal buildup of hard, waxy amyloid plaques in the parts of the brain that control memory. But drug trials using anti-amyloid drugs have failed, leading some researchers to theorize that amyloid buildup is a byproduct of the disease, not a cause.

The Duke study builds on an alternative hypothesis. First proposed in 2004, the “mitochondrial cascade hypothesis” posits that changes in the cellular powerhouses, not amyloid buildup, are what cause neurons to die.

Like most human cells, neurons rely on mitochondria to stay healthy. But unlike other cells, most neurons stop dividing after birth, so they can’t be replaced if they’re damaged.

Alzheimer’s disease causes neurons in the brain to stop working, lose connections with other neurons and die. Duke University researchers have identified a molecular mechanism that may be responsible for setting the damage in motion.

Alzheimer’s disease causes neurons in the brain to stop working, lose connections with other neurons and die. Duke University researchers have identified a molecular mechanism that may be responsible for setting the damage in motion.

In Alzheimer’s patients, the thinking goes, the mitochondria in neurons stop working properly. As a result they are unable to generate as much energy for neurons, which starve and die with no way to replenish them. But how mitochondria in neurons decline with age is largely unknown.

Most mitochondrial proteins are encoded by genes in the cell nucleus before reaching their final destination in mitochondria. In 2009, Duke neurologist and study co-author Allen Roses (now deceased) identified a non-coding region in a gene called TOMM40 that varies in length. Roses and his team found that the length of this region can help predict a person’s Alzheimer’s risk and age of onset.

Larsen wondered if the length variation in TOMM40 was only part of the equation. He analyzed the corresponding gene region in gray mouse lemurs, teacup-sized primates known to develop amyloid brain plaques and other Alzheimer’s-like symptoms with age. He found that in mouse lemurs alone, but not other lemur species, the region is loaded with short stretches of DNA called Alus.

Found only in primates, Alus belong to a family of retrotransposons or “jumping genes,” which copy and paste themselves in new spots in the genome. If the Alu copies present within the TOMM40 gene somehow interfere with the path from gene to protein, Larsen reasoned, they could help explain why mitochondria in nerve cells stop working.

“Alu elements are a double-edged sword,” Larsen said. Once dismissed as selfish or junk DNA, they are now recognized as contributors to the diversity and complexity of the human brain.

“They can provide new and beneficial gene functions,” Larsen said.

“They have helped humans evolve higher cognitive function, but perhaps at the cost of neuron vulnerability that increases with age.”

When the researchers looked across the human genome, they found that Alus were more likely to be lurking in and around genes essential to mitochondria than in other protein-coding genes.

Alus are normally held in check by clusters of atoms called methyl groups that stick to the outside of the DNA and shut off their ability to jump or turn genes on or off. But in aging brains, DNA methylation patterns change, which allows some Alu copies to re-awaken, Larsen said.

The TOMM40 gene encodes a barrel-shaped protein in the outer membrane of mitochondria that forms a channel for molecules — including the precursor to amyloid — to enter. Larsen used 3D modeling to show that Alu insertions within the TOMM40 gene could make the channel protein it encodes fold into the wrong shape, causing the mitochondria’s import machinery to clog and stop working.

Such processes likely get underway before amyloid builds up, so they could point to new or repurposed drugs for earlier intervention, said study co-author Michael Lutz, assistant professor of neurology at Duke.

The TOMM40 gene is one example, the researchers say, but if Alus disrupt other mitochondrial genes, the same basic mechanism could help explain the initial stages of other neurodegenerative diseases too, including Parkinson’s disease, Huntington’s disease and amyotrophic lateral sclerosis (ALS).

Alus within the TOMM40 gene could make the channel protein it encodes misfold.

Alus within the TOMM40 gene could make the channel protein it encodes misfold.

The researchers describe the Alu neurodegeneration hypothesis in a paper published online by Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.

“We need to start thinking outside of the box when it comes to treating neurological diseases like Alzheimer’s,” said Larsen, who has filed a provisional patent that focuses on preserving mitochondrial function by keeping Alus in check.


By Robin A. Smith

Other authors include Kelsie Hunnicutt, Mirta Mihovilovic and Ann Saunders of Duke. This research was supported by a seed grant from Allen Roses and Duke funds to Anne Yoder.

© Copyright 2016 Duke University.


Cancer Drug That Might Slow Parkinson’s, Alzheimer’s Headed For Bigger Tests

( Scientists are hoping that a single drug can treat two devastating brain diseases: Parkinson’s and Alzheimer’s.

The drug is nilotinib, which is approved to treat a form of leukemia.

In late 2015, researchers at Georgetown University Medical Center found that small doses of the drug appeared to help a handful of people with Parkinson’s disease and a related form of dementia. They’d tried the unlikely treatment because they knew nilotinib triggered cells to get rid of faulty components — including the ones associated with several brain diseases.

A colored magnetic resonance imaging (MRI) scans of the brain of a 76-year-old patient with dementia shows the brain has atrophied and the dark brown fluid-filled spaces have become enlarged. Zephyr/Science Source

Results of that preliminary study generated a lot of excitement because there is currently no treatment that can slow or halt the brain damage caused by either Parkinson’s or Alzheimer’s.

“Our phones were basically (ringing) off the hook,” says Fernando Pagan, medical director of the translational neurotherapeutics program at Georgetown.

Many researchers were cautious, though.

“It was such a small trial, there was no placebo control and it really wasn’t designed to assess efficacy,” says J. Paul Taylor, chair of the cell and molecular biology department at St. Jude Children’s Research Hospital in Memphis.

So Georgetown is launching two larger and more rigorous trials of nilotinib, both designed with input from the Food and Drug Administration. One of the trials will enroll 75 patients with Parkinson’s disease, the other will enroll 42 patients with Alzheimer’s.

“This is going to help us identify what might have been a placebo effect and what is truly the effect of the medication,” Pagan says.

Nilotinib seems to work by eliminating toxic proteins that build up in the brains of people with Parkinson’s and Alzheimer’s. The drug activates a mechanism in brain cells that acts like a sort of garbage disposal, Pagan says.

“Our drug goes into the cells to turn on that garbage disposal mechanism,” Pagan says.

“And if we’re able to degrade these proteins, we could potentially stop the progression of this disorder.”

The primary goal of the studies is to learn whether this powerful cancer drug is safe enough for patients with brain diseases. But the new studies should also provide better evidence about whether the drug really works.

That possibility attracts patients like Jonathan Lessin, a former anesthesiologist in the Washington D.C. area. Lessin was diagnosed with Parkinson’s 14 years ago, when he was just 38.

Parkinson’s gradually kills off brain cells that control movement. And for a decade after his diagnosis, drugs and a treatment called deep brain stimulation allowed Lessin to continue working. He retired several years ago, when his symptoms progressed to the point that he feared he might not be able to provide first-rate care for his patients.

Since then, the disease has caused Lessin’s speech to become slightly slurred. “It’s slowly progressing,” he says. “My balance is getting worse and worse. I’m falling more and more during the day. But I’m still able to do things like rock climb and ski and bike.”

Lessin has been able to stay active thanks to treatments that help control symptoms. But the disease continues to eat away areas of his brain.

So Lessin was excited to learn about the Georgetown study, which held the tantalizing prospect of a drug that just might slow or halt that process.

“I’ve always been riding the leading edge of treatment,” Lessin says. “And I just figured I’d go for it.”

As a former physician, Lessin fully understands the limitations of the earlier trial, and the risks of taking a powerful cancer drug. But as someone with Parkinson’s, he sees an opportunity.

“I’m very optimistic,” he says. “I’ve seen it cure Parkinson’s in mice. I’ve seen people who can talk again, walk again, which is very encouraging.”

There’s good reason for patients with Parkinson’s, Alzheimer’s and other neurodegenerative diseases to be optimistic these days, Taylor says.

Drugs like nilotinib are coming along because years of research have provided a much better understanding of how these damage the brain, he says.

“Now we’re in the payoff phase.”

Taylor still isn’t sure whether nilotinib will live up to its early promise. But, he says,

“If the results of this trial don’t turn out to be as exciting as the very tiny trial suggested, I would not get too pessimistic because there are other developments that are in the wings.”

The Georgetown studies are enrolling patients now and will take more than a year to complete.

Information about the Parkinson’s study can be found here. Information about the Alzheimer’s study is available here.


By Jon Hamilton

© 2017 npr


Alzheimer’s Disease and When to Stop Driving

(Mayo Clinic) If your loved one has Alzheimer’s, he or she may not be safe on the road. Explain the risks — then provide other ways to get around.

Driving is a powerful symbol of competence and independence, besides being a routine part of adult life. But the focused concentration and quick reaction time needed for safe driving tends to decline with age. Alzheimer’s disease accelerates this process dramatically. If you’re caring for a loved one living with Alzheimer’s, you may need to modify his or her driving – or stop his or her driving completely.

More than Memory Problems

Dimmed short-term memory makes it easy for a driver who has Alzheimer’s to get lost, even in familiar surroundings. Perhaps more dangerous, however, is a decline in the ability to judge distances and predict upcoming traffic problems. A driver who has Alzheimer’s may also have trouble prioritizing visual cues. An irrelevant sight, such as a dog jumping behind a fence, may distract the driver from important cues — such as brake lights or traffic signs.

When to Stop Driving

Driving concerns often surface during the early stages of memory changes. People with dementia are especially likely to minimize the complexity of driving and overestimate their abilities. Opinions vary on whether driving should be allowed at all after an Alzheimer’s diagnosis. Research indicates that drivers with Alzheimer’s disease are more likely to get into motor vehicle accidents. For some people, it may be easier to give up the wheel early on, when they can still grasp the potential hazards. On the other hand, people in the early stages of the disease may be able to safely limit their driving to short daytime trips in familiar surroundings.

If your loved one continues to drive, pay attention to warning signs of unsafe driving, such as:

  • Difficulty navigating to familiar places
  • Inappropriate lane changing
  • Confusing the brake and gas pedals
  • Failing to observe traffic signals
  • Making slow or poor decisions
  • Hitting the curb while driving
  • Driving at an inappropriate speed (often too slow)
  • Becoming angry or confused while driving

According to a report from the American Academy of Neurology, one of the more accurate predictors of driving trouble is a caregiver’s assessment. If a caregiver (generally a spouse) believes that his or her relative with dementia is driving unsafe, the caregiver is likely to be correct. If you’re not sure whether it’s safe for your loved one to drive, ask yourself whether you feel safe riding in a vehicle driven by the person who has Alzheimer’s — or if you’d feel safe having your children or others drive with that person. If the answer is no, then you know it’s time for him or her to retire from driving.

How to Ease the Transition

When your loved one stops driving, arrange for alternative transportation. Perhaps family members and friends can run errands with your loved one, or you can arrange transportation through a senior van route. You may be able to establish a payment account with a taxi service so that your loved one can go places, but won’t have to handle money.

Also consider ways to limit your loved one’s need to drive. Many items — such as groceries, meals and prescriptions — can be delivered to your loved one’s home. Some barbers and hairdressers make house calls as well.

Remain Firm as the Disease Progresses

If your loved one wants to continue driving despite the hazards — or begins driving again after a period off the road — consider these strategies to keep him or her out of the driver’s seat:

  • Get it in writing. Sometimes it helps if an authority figure — physician, lawyer or insurance agent — tells your loved one to stop driving. Having something in writing can be a useful reminder.
  • Keep keys out of sight. Park the vehicle around the corner or in a closed garage, and don’t keep keys in plain sight. If your loved one insists on carrying a set of keys, offer old keys that won’t start the vehicle.
  • Disable the vehicle. Remove a battery cable to prevent the car from starting, or ask a mechanic to install a “kill switch” that must be engaged before the car will start.
  • Sell the vehicle. If you can make do without your loved one’s vehicle, consider selling it.

Whether your loved one stops driving all at once or in stages, he or she will probably grieve the loss of independence. Be as patient as you can, but remember to stand firm. The consequences of unsafe driving can be devastating.



  1. Driving. Alzheimer’s Association. Accessed March 14, 2013.
  2. Martin AJ, et al. Driving assessment for maintaining mobility and safety in drivers with dementia. Cochrane Database of Systematic Reviews. Accessed March 14, 2013.
  3. Snyder CH. Dementia and driving: Autonomy versus safety. Journal of the American Academy of Nurse Practitioners. 2005;17:393.
  4. Ott BR, et al. A longitudinal study of drivers with Alzheimer disease. Neurology. 2008;70:1171.
  5. Iverson DJ, et al. Practice parameter update: Evaluation and management of driving risk in dementia. Neurology. 2010;74:1316.
  6. AskMayoExpert. Alzheimer’s disease: Should patients with Alzheimer’s dementia be allowed to drive? Rochester, Minn.: Mayo Foundation for Medical Education and Research;2012.

© 1998-2017 Mayo Foundation for Medical Education and Research. All rights reserved.


Mayo Clinic Publishes Genetic Screen for Alzheimer’s in African-Americans

(Journal of Alzheimer’s Disease) A Mayo Clinic research team has found a new gene mutation that may be a risk factor for late-onset Alzheimer’s disease in African-Americans. This is the first time this gene has been implicated in the development of this disease in this population. Alzheimer’s disease has been understudied in African-Americans, despite the fact that the disease is twice as prevalent in African-Americans, compared to Caucasians and other ethnic groups.

This likely pathogenic variant may be unique to the African-American population, the researchers say. It has not been found in Caucasians with Alzheimer’s disease or in gene repositories from more than 60,000 subjects who are not African-Americans.

The findings, published in the February issue of the Journal of Alzheimer’s Disease, represent the first comprehensive genetic screening in African-Americans for potentially pathogenic variants in known Alzheimer’s genes.

Mayo Clinic Alzheimer’s research seeks to paint a more complete genetic picture of genes that confer risk for Alzheimer’s and genes that protect against that risk in different populations, says neurogeneticist Minerva Carrasquillo, Ph.D., who is the co-author.

“Currently, at least 5 million Americans are affected by Alzheimer’s disease, and the rate of this devastating dementia is expected to rise dramatically in the coming decades,” says Dr. Carrasquillo.

“By uncovering genetic factors that modify the risk of Alzheimer’s disease, there is the potential to identify druggable gene targets and genetic variants that could be used for early disease detection and prevention.”

The research team’s approach is to look at genetic factors known to be involved in early-onset Alzheimer’s disease — dementia that occurs before 65 and sometimes in people as young as 30-40 years of age. Up to 5 percent of Alzheimer’s disease has this early form, and a substantial number of these cases have been shown to be caused by genetic irregularities.

The investigators hypothesized that early-onset Alzheimer’s disease genes may also be involved in late-onset Alzheimer’s disease in African-Americans, although a comprehensive screen has not been done previously.

In this study, researchers looked for genetic mutations in three genes known to contribute to early-onset Alzheimer’s disease. The three genes ─ APP, PSEN1 and PSEN2 ─ are involved in producing and cutting apart proteins as part of normal brain function. But mutations in these genes can result in increasing the amount of the amyloid beta peptide (Abeta) that leads to the amyloid plaques that build up in the brain of Alzheimer’s patients. The rise in brain plaque quantity mirrors progression of Alzheimer’s dementia.

While 200 early-onset Alzheimer’s disease mutations in these three genes have been identified in Caucasians with Alzheimer’s disease, only three have been found in African-Americans with Alzheimer’s disease — one APP mutation in a single family and two PSEN1 mutations.

Of the two PSEN1 mutations, one was within a single African-American family, and one was in a female early-onset Alzheimer’s disease patient. Before this study, no PSEN2 mutations had been found in African-American patients.

In this study, the team sequenced the genome of 238 African-Americans participants. This group was divided between 131 patients with late-onset Alzheimer’s disease and 107 control participants. Investigators found six variants within the early-onset Alzheimer’s disease genes in the patients, but not in the control group.

Researchers then looked for these six gene variants in a second independent group of 300 African-Americans participants (67 with late-onset Alzheimer’s disease and 233 controls) and found that four of the variants were in the control group. That means two variants ─ one in a shorter form of PSEN1 and one in PSEN2 ─ may pose risk for late-onset Alzheimer’s disease in African-Americans.

PSEN1 variants had been found before in African-Americans with the disease, but this discovery of a likely pathogenic PSEN2 gene variant is new in this population, says Dr. Carrasquillo. “And as far as we know, it has not been found in other populations with late onset Alzheimer’s disease.”

“This study opens the door to further analysis of this gene variant ─ both in African-Americans with Alzheimer’s and in other populations,” she says.

“These findings, which require replication, represent an important step in expanding genetic research in Alzheimer’s disease to minority populations,” says the study’s senior investigator, neurogeneticist and neurologist Nilufer Ertekin-Taner, M.D., Ph.D.


This work was supported by the Florida Department of Health, the Ed and Ethel Moore Alzheimer’s Disease Research Program (AZ03), the Mentored New Investigator Research Grant to Promote Diversity Alzheimer’s Association grant, Mayo Clinic Office of Health Disparities Research, Mayo Alzheimer’s Disease Research Center (P50 AG0016574), National Institute on Aging (RF1 G051504 and U01 AG046139), and National Institute of Neurological Disorders and Stroke (R01 NS080820).

N’Songo A, Carrasquillo MM, Wang X, Nguyen T, Asmann Y, Younkin SG, Allen M, Duara R, Custo MT, Graff-Radford N, Ertekin-Taner N (2017) Comprehensive Screening for Disease Risk Variants in Early-Onset Alzheimer’s Disease Genes in African Americans Identifies Novel PSEN Variants. J Alzheimers Dis 56, 1215-1222.

Journal of Alzheimer’s Disease is published by IOS Press

Copyright © 2017


Autoimmune Conditions and Dementia: What’s the Link?

(MedicalNewsToday) A recent large-scale study concludes that individuals with autoimmune conditions may have an increased risk of developing dementia later in life. Although the effect size is relatively small, if the findings are replicated, they will have important clinical implications.

Dementias are a range of conditions, the most prevalent of which is Alzheimer’s. They are characterized by a progressive loss of memory function and other cognitive skills, eventually leading to an inability to perform everyday activities.

Currently, an estimated 47.5 million people are living with dementia, worldwide. Due to increasing lifespans, this figure is predicted to triple by the year 2050.

This steep rise in the number of cases is being referred to by some as a dementia epidemic, and for this reason, there is a great deal of focus on identifying the precise causes.

Certain factors are known to increase the risk of dementia. Advanced age, alcohol use, diabetes, and hypertension (high blood pressure) have all been said to contribute to this risk. However, there is still much to learn about how and why dementia arises.

Autoimmune Disease and Dementia

Over recent years, another potential risk factor has received some attention: autoimmune diseases.

Autoimmune diseases are conditions in which the body’s own immune system attacks healthy cells and tissues. Some evidence has shown that individuals with these types of diseases have an increased risk of developing dementia.

A research team from the University of Oxford in the United Kingdom set out to examine this question in more detail. Utilizing hospital admissions data taken from U.K. hospitals between 1998 and 2012, they investigated whether being admitted to a hospital with one of 25 autoimmune diseases was associated with an increased risk of a dementia admission later in time.

Across the 14-year time sample, there were more than 1.8 million admissions to hospitals because of an autoimmune disorder. This included more than 300,000 people with rheumatoid arthritis (RA) and around 1,000 with Goodpasture’s syndrome, a rare condition that attacks the lungs and kidneys.

Increased Dementia Risk Identified

Once the data were analyzed, the researchers found that an initial admission due to an autoimmune condition increased the risk of a later admission due to dementia by 20 percent.

Of the 25 autoimmune conditions analyzed, 18 were shown to be significantly associated with dementia. These include:

  • Addison’s disease – 48 percent increased risk
  • Polyarteritis nodosa – 43 percent increased risk
  • Multiple sclerosis – 97 percent increased risk
  • Psoriasis – 29 percent increased risk
  • Systemic lupus erythematosus – 46 percent increased risk
  • Thyrotoxicosis – 31 percent increased risk.

The majority of these associations were still significant 5 or more years after the initial admission for an autoimmune disease. In other words, the dementia was not picked up during the initial hospital examination.

Although the exact dementia diagnosis was not always noted, the risk was 6 percent higher for Alzheimer’s and 28 percent higher for vascular dementia.

The researchers believe that the higher risk associated with vascular dementia might be due to associations between autoimmune diseases and risk factors for cardiovascular and cerebrovascular diseases in general.

For instance, individuals with an autoimmune disease were more likely to receive a subsequent hospital admission for coronary heart disease and stroke (53 percent and 46 percent, respectively).

An interesting exception to these results was RA; in this case, a hospital admission for RA seemed to protect against Alzheimer’s disease. The researchers believe that this might be due to the nonsteroidal anti-inflammatory drugs often taken by individuals with RA, such as aspirin and paracetamol. These medications have previously been shown to reduce Alzheimer’s risk.

“If our findings are confirmed in other studies, clinicians and epidemiologists will wish to know that some people with some autoimmune diseases have an elevated risk of dementia.”

The study is observational and, therefore, cannot prove cause and effect. Furthermore, although the large sample size makes the interaction worthy of further study, as the authors emphasize, the effect size was small. The authors write that their

“findings should be considered as indicative rather than definitive.”


Written by Tim Newman

© 2004-2017 All rights reserved. MNT is the registered trade mark of Healthline Media.


Alzheimer’s Death Toll Nearly Doubles in 15 Years

(WebMD) Alzheimer’s disease claims nearly twice as many American lives annually as it did just 15 years ago, a new report shows.

“And that’s frankly alarming,” said Keith Fargo, director of scientific programs and outreach at the Alzheimer’s Association, which produced the report.

“Now, a lot of people will think it’s because we’re living longer,” he added.

“And there is some truth to that. But there’s also an assumption that we should just expect to get Alzheimer’s disease as we get older. And that’s not true.

“Most people do not get Alzheimer’s, even if they live into their 80s or 90s. It’s not normal. It’s not something that we should accept. We’ve definitely got to do something about it,” Fargo said.

The report also found that more than 5 million American seniors aged 65 and older now live with the memory-robbing disease.

That represents approximately 10 percent of all the nation’s seniors, and that number is projected to jump to nearly 14 million by 2050. In fact, nearly half a million seniors are expected to develop the disease in 2017 alone.

Another 200,000 Americans under the age of 65 also struggle with the disease, the report found.

And those statistics come with a hefty price tag: It costs $259 billion a year for Alzheimer’s care. That amount is expected to reach $$1.1 trillion by 2050, the report estimated.

Dr. Anton Porsteinsson is director of the Alzheimer’s Disease Care, Research and Education Program at the University of Rochester School of Medicine in Rochester, N.Y. He said the rising numbers likely reflect a number of different factors in play.

“Partly, it is due to increasing numbers of older individuals, partly due to success in treating other leading causes of death, and partly due to increasing awareness that AD [Alzheimer’s] is a lethal disease,” Porsteinsson said.

Among the report’s additional findings: Alzheimer’s is now the fifth leading cause of death among seniors; the sixth leading cause of fatalities among all Americans; and the only disease among the nation’s top 10 biggest killers for which there is no prevention, no way to slow progression and no cure.

“And the costs are now completely out of control,” added Fargo, with the total annual cost for Alzheimer’s and dementia care in excess of a quarter trillion dollars.

Another highlighted concern: the “especially burdensome” ordeal Alzheimer’s caregivers experience while attending to the needs of loved ones as the patient suffers across-the-board mental and physical decline.

In 2016, more than 15 million Alzheimer’s caregivers provided just over 18 billion hours of unpaid care, valued at $230 billion.

And those caregivers suffer their own health consequences: More than a third (35 percent) report their health has worsened since assuming caregiver duties, compared with 19 percent of caregivers for older people without dementia. Depression and anxiety also plague dementia caregivers more often, the report found.

Still, the report was not entirely bleak, spotlighting growing efforts to identify telltale signs of developing disease.

The goal is to hone in on neurological signs — including changes in brain size, shifts in spinal fluid content, and/or the growth of nerve plaques in the brain — that could allow rapid detection of pre-symptomatic Alzheimer’s.

“It’s a window into the future,” Fargo said.

“If you ask where Alzheimer’s disease research is headed, that’s where it’s headed.”

“We believe that in the coming years we’ll have tests that you can do in the doctor’s office that will let you know your risk for Alzheimer’s,” he noted. And that, he suggested, “could open the door for prevention.”

Fargo noted that, even in the absence of effective treatments or a cure, early diagnosis would be a boon for research and would give patients a head start on planning for their future.

Yet, Porsteinsson suggested that the future of these telltale signs, known as biomarkers, remains unclear.

“Biomarkers are particularly important when it comes to research and development of future potential treatments,” he said.

On the other hand, he stressed that “the utility of biomarkers in current care is intensely debated.

“The biomarkers are expensive,” Porsteinsson noted.

“And it is a question how much a positive or negative finding will change approach to care.

“Having said that,” he added, “it often matters greatly to patients and their families to know exactly what they have and what to expect.”


SOURCES: Keith Fargo, Ph.D., director, scientific programs and outreach, Alzheimer’s Association, New York City; Anton Porsteinsson, M.D., professor, psychiatry, and director, Alzheimer’s Disease Care, Research and Education Program, University of Rochester School of Medicine, Rochester, N.Y.; March 7, 2017, 2017 Alzheimer’s Disease Facts and Figures

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