Wednesday, July 18, 2018

Prevent vascular dementia with these foods

Caregivers, and healthcare professionals,here is some great information

Here is a great dementia resource for caregivers and healthcare professionals,

Your residents will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

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The Dementia Caregiver's Little Book of Hope [Kindle Edition]

DIET & NUTRITION: A diet that combines unsaturated fats with nitrite-rich vegetables, such as olive oil and lettuce, can protect you from hypertension and vascular dementia. Learn which foods are helpful and why.

A diet that combines unsaturated fats with nitrite-rich vegetables, such as olive oil and lettuce, can protect you from hypertension, suggests a dietary study led by King's College London. Hypertension is a major risk factor for vascular dementia.

The findings, published in the journal PNAS, help to explain why some previous studies have shown that a Mediterranean diet can reduce blood pressure.

The Mediterranean diet typically includes unsaturated fats found in:
  • olive oil,
  • nuts
  • avocados,
along with vegetables that are rich in nitrites and nitrates like: 
  • spinach,
  • celery
  • carrots.
When these two food groups are combined, the reaction of unsaturated fatty acids with nitrogen compounds in the vegetables results in the formation of nitro fatty acids.

The study, supported by the British Heart Foundation, used mice to investigate the process by which these nitro fatty acids lower blood pressure, looking at whether they inhibited an enzyme known as soluble Epoxide Hydrolase which regulates blood pressure.

Mice genetically engineered to be resistant to this inhibitory process were found to maintain their high blood pressure despite being fed the type of nitro fatty acids that normally form when a Mediterranean diet is consumed. However, nitro fatty acids were found to lower the blood pressure of normal mice following the same diets.

Thus, the study concludes that the protective effect of the Mediterranean diet, combining unsaturated fats and vegetables abundant in nitrite and nitrate, comes at least in part from the nitro fatty acids generated which inhibit soluble Epoxide Hydrolase to lower blood pressure.

Professor Philip Eaton, Professor of Cardiovascular Biochemistry at King's College London, said: 
"The findings of our study help to explain why previous research has shown that a Mediterranean diet supplemented with extra-virgin olive oil or nuts can reduce the incidence of cardiovascular problems like stroke, heart failure and heart attacks."


Journal Reference:
  1. Rebecca L. Charles, Olena Rudyk, Oleksandra Prysyazhna, Alisa Kamynina, Jun Yang, Christophe Morisseau, Bruce D. Hammock, Bruce A. Freeman, and Philip Eaton. Protection from hypertension in mice by the Mediterranean diet is mediated by nitro fatty acid inhibition of soluble epoxide hydrolasePNAS, May 2014 DOI: 10.1073/pnas.1402965111

Monday, July 16, 2018

Will you get dementia?

Caregivers, and healthcare professionals,here is some great information

Here is a great dementia resource for caregivers and healthcare professionals,

Your residents will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two

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The Dementia Caregiver's Little Book of Hope [Kindle Edition]

NewsMax Health

Experts say that dementia, the general term for a severe decline in mental ability, affects 47.5 million people worldwide and the numbers are growing. Dementia, like cancer, is an umbrella term that includes Alzheimer’s disease, vascular dementia which occurs after a stroke, and many other conditions that can cause symptoms of dementia, including some that are reversible, such as thyroid problems and vitamin deficiencies.
However, new research shows that many cases of dementia are triggered by treatable conditions. Incredibly, experts say that one-third or more of the Alzheimer’s and dementia cases may be prevented by better management of lifestyle factors.
"Dementia is the greatest global challenge for health and social care in the 21st century," Dr. Dean Hartley, Ph.D, Director of Science Initiatives at the Alzheimer’s Association tells Newsmax. "One in nine people at age 65 suffers from dementia and that number leaps to one in three by the age of 85. Now that we know the scientifically proven lifestyle factors to prevent the disease, the earlier we adopt these changes the more we can reduce our risk."

 And top neurosurgeon Dr. Joseph Maroon, a sports medicine expert who served as the team neurosurgeon for the Pittsburgh Steelers for over 20 years, tells Newsmax that in his best selling book, "Square One: A Simple Guide to a Balanced Life", he outlines the steps we can take to stay clear minded and healthy.

"Too many people take not only a fatalistic but also a nihilistic approach to getting old and dementia," he says. "There are scientifically proven ways to markedly contribute to brain health and the prevention of dementia." Here are five fixable factors that can lead to dementia:
  1. Drinking alcohol. Alcohol when used in moderation may not pose significant impairment but as we age, it interacts differently with our bodies. Experts say that prolonged alcohol abuse in older adults can result in deficiencies in memory and damage to the kidneys, liver and brain.
  2. Eating lots of sugar. Eating too much sugar in your diet is dangerous, says Maroon. Sugar is directly involved with the brain and can cause major changes including increased risk for stroke which can lead to vascular dementia.
  3. Lack of exercise. Maroon, a renowned triathlete, says that exercise saved him from depression. But it can also help stave off dementia by boosting immunity and tamping down inflammation, he says. "Even Plato, the ancient Greek philosopher, emphasized the mind-body connection," he says.
  4. Not getting enough sleep. Your brain needs time to rest and recuperate, just like your body, so it is essential to get a good night’s sleep to keep the brain healthy. "Keep a sleep journal and practice good sleep hygiene," says Maroon. "Establish regular sleep patterns and turn off all electronics at least an hour before bedtime.
  5. Spending too much time alone. A recent study published in the American Journal of Public Health found that older women who maintained large social networks reduced their risk of dementia or prevented cognitive impairment. The results showed that the women were actually 26 percent less likely to develop dementia -- a case in point for keeping socially active as we age, says Maroon.
© 2018 NewsmaxHealth. All rights reserved. 

Saturday, July 14, 2018

Scam protection for those with dementia

Caregivers, and healthcare professionals,here is some great information

Here is a great dementia resource for caregivers and healthcare professionals,

Your residents will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or follow
. alzheimersideas on twitter

The Dementia Caregiver's Little Book of Hope [Kindle Edition]

  • The Alzheimer’s Disease Education and Referral (ADEAR) Center - a service of the National Institute on Aging, part of the National Institutes of Health.


We've all heard stories of crooks taking advantage of people with Alzheimer's. See how to protect people with dementia from scammers. 

People with Alzheimer’s may be victims of financial abuse or scams by dishonest

Guard Against Financial Abuse and Fraud 

Sometimes, the person behind the scam is a “friend” or family member. Telephone, e-mail, or in-person scams can take many forms, such as:
  • Identity theft
  • Get-rich-quick offers 
  • Phony offers of prizes or home or auto repairs 
  • Insurance scams 
  • Health scams such as ads for unproven memory aids 
  • Threats 

Warning Signs

Look for signs that the person with Alzheimer’s may be a victim of financial abuse or fraud:
  1. Signatures on checks or other papers don’t look like the person’s signature. 
  2. The person’s will has been changed without permission. 
  3. The person’s home is sold, and he or she did not agree to sell it. 
  4. The person has signed legal papers (such as a will, power of attorney, or joint deed to a house) without knowing what the papers mean. 
  5. Things that belong to you or the person with Alzheimer’s, such as clothes or jewelry, are missing from the home. 
If you think a person with Alzheimer’s may be the victim of a scam, contact your local police department. You can also contact the State consumer protection office or Area Agency on Aging office. 

  • The Alzheimer’s Disease Education and Referral (ADEAR) Center - a service of the National Institute on Aging, part of the National Institutes of Health.

Thursday, July 12, 2018

How do viruses affect Alzheimer's

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American researchers found 'unusually high' levels of two strains of human herpes virus 6A (HHV-6A) and human herpes virus 7 (HHV-7) in brains of Alzheimer's sufferers, compared to those free of the disease. This opens up a robust array of new targets in the search for a cure to Alzheimer's. 

The quest to understand what causes Alzheimer's disease--and to treat it--is complicated by the disease's long, slow progression and the difficulty of collecting brain tissue samples. But in a large-scale analysis published June 21 in the journal Neuron, researchers at the Icahn School of Medicine at Mount Sinai use data from three different brain banks to suggest that human herpesviruses are more abundant in the brains of Alzheimer's patients and may play a role in regulatory genetic networks that are believed to lead to the disease. This work lends support to the controversial hypothesis that viruses are involved in Alzheimer's disease and offers potential new paths for treatment.

"All I Found Were These Lousy Viruses"

"The title of the talk that I usually give is, 'I Went Looking for Drug Targets and All I Found Were These Lousy Viruses.' We didn't set out to find what we found. Not even close. We were trying to find drugs that could be repurposed to treat Alzheimer's patients, but the patterns that emerged from our data-driven analysis all pointed towards these viral biology themes," says co-senior author and geneticist Joel Dudley. who is also a member of the ASU-Banner Neurodegenerative Disease Research Center

The researchers analyzed data from three major brain banks courtesy of the National Institutes of Health's Accelerating Medicines Partnership - Alzheimer's Disease (AMP-AD) consortium, which allowed them to look at raw genomic data for large numbers of Alzheimer's patients in different cohorts. They constructed, mapped, and compared regulatory gene networks in areas of the brain known to be affected by Alzheimer's on multiple levels, looking at DNA, RNA, and proteins.

Search for Sequences from Hundreds of Different Viruses

"This kind of analysis was only possible because the consortium had coordinated for all of these other groups to put their sequencing data in the AMP-AD Knowledge Portal in a precompetitive environment that let us very quickly replicate our work across all these different cohorts. We needed access to sequences that are usually discarded in the course of studying the human genome. We needed to search for sequences from hundreds of different viruses, so having access to that raw, unprocessed data was absolutely key," says first author Ben Readhead. 

They found that human herpesvirus DNA and RNA were more abundant in the brains of those diagnosed postmortem with Alzheimer's disease and that abundance correlated with clinical dementia scores. And the two viruses they found to be most strongly associated with Alzheimer's, HHV-6A and HHV-7, were not as abundant in the brains of those with other neurodegenerative disorders. When they constructed networks that modeled how the viral genes and human genes interacted, they were able to show that the viral genes were regulating and being regulated by the human genes--and that genes associated with increased Alzheimer's risk were impacted.

Viruses are Accelerating the Brain Towards Alzheimer's

The brain is shown here as a complex network of interactions, with disruption of connections by the key viral species (HHV-6A, HHV-6B, HHV-7) identified in this study. (CREDIT: Readhead et al. Click to enlarge.)
"Previous studies of viruses and Alzheimer's have always been very correlative. But we were able to do statistical causal inference testing and more sophisticated analysis, which allowed us to identify how the viruses are directly interacting with or coregulating or being regulated by Alzheimer's genes. I don't think we can answer whether herpesviruses are a primary cause of Alzheimer's disease. But what's clear is that they're perturbing networks and participating in networks that directly accelerate the brain towards the Alzheimer's topology," says Dudley. 

The researchers believe that their findings align with other current research in the Alzheimer's field on the role of innate immunity in the disease, particularly recent findings that beta-amyloid protein--the culprit behind the plaques that build up in the Alzheimer's-affected brain--may accumulate as part of a defense against infections. In their study, they found that herpesviruses were involved in networks that regulate amyloid precursor proteins.

No New Worries

They argue, however, that their work shouldn't make anyone worried. "While these findings do potentially open the door for new treatment options to explore in a disease where we've had hundreds of failed trials, they don't change anything that we know about the risk and susceptibility of Alzheimer's disease or our ability to treat it today," says co-senior author and Alzheimer's disease specialist Sam Gandy. 

This is especially true because HHV-6A and HHV-7 are extremely common and often latent or asymptomatic: in North America, almost 90% of children have one of these viruses circulating in their blood by the time they're a few years old. "There are still a lot of unanswered questions around how we go from being able to detect it circulating in someone's blood to knowing whether it's active in a state that might be relevant to Alzheimer's disease," says Readhead.

Alzheimer's & Viruses: Specific and Testable

But even if questions remain, this research offers strong support for a long-controversial hypothesis that viruses might be involved in the development of Alzheimer's disease. "We didn't have a horse in this virus race whatsoever. It's the data that took us there. And now, not only is the viral hypothesis resurrected: it has specific testable pathways and networks and interactions that can be explored and reconciled with the rest of the work emerging in Alzheimer's," says Dudley. 

"All these Alzheimer's brains in these separate, major brain banks have previously unsuspected substantial populations of herpesvirus genomes and that deserves an explanation wherever it falls in the pathogenesis. It doesn't deserve to just be brushed away," says Gandy.

“The hypothesis that viruses play a part in brain disease is not new, but this is the first study to provide strong evidence based on unbiased approaches and large data sets that lends support to this line of inquiry,” said NIA Director Richard J. Hodes, M.D. “This research reinforces the complexity of Alzheimer’s disease, creates opportunities to explore Alzheimer’s more thoroughly, and highlights the importance of sharing data freely and widely with the research community.” 

Alzheimer’s disease is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills and, eventually, the ability to carry out simple tasks. More evidence is accumulating to indicate that this loss of cognitive functioning is a mix of many different disease processes in the brain, rather than just one, such as buildup of amyloid or tau proteins. Identifying links to viruses may help researchers learn more about the complicated biological interactions involved in Alzheimer’s, and potentially lead to new treatment strategies. 

The research group, which included experts from Icahn School of Medicine at Mount Sinai, New York City, and Arizona State University, Phoenix, originally set out to find whether drugs used to treat other diseases can be repurposed for treating Alzheimer’s. They designed their study to map and compare biological networks underlying Alzheimer’s disease. What they found is that Alzheimer’s biology is likely impacted by a complex constellation of viral and host genetic factors, adding that they identified specific testable pathways and biological networks.

Robust Findings

“The robust findings by the Mount Sinai team would not have been possible without the open science data resources created by the AMP-AD program–particularly the availability of raw genomic data,” said NIA Program Officer Suzana Petanceska, Ph.D., who leads the AMP-AD Target Discovery and Preclinical Validation Project. “This is a great example of the power of open science to accelerate discovery and replication research.” 

The researchers used multiple layers of genomic and proteomic data from several NIA-supported brain banks and cohort studies. They began their direct investigation of viral sequences using data from the Mount Sinai Brain Bank and were able to verify their initial observations using datasets from

They were then able to incorporate additional data from the Emory Alzheimer’s Disease Research Center to understand viral impacts on protein abundance. Through the application of sophisticated computational modeling the researchers made several key findings, including:
  1. Human herpesvirus 6A and 7 were more abundant in Alzheimer’s disease samples than non-Alzheimer’s.
  2. There are multiple points of overlap between virus-host interactions and genes associated with Alzheimer’s risk.
  3. Multiple viruses impact the biology of Alzheimer’s disease across domains such as DNA, RNA and proteins.

No Evidence to Reassess Risk

Important roles for microbes and viruses in Alzheimer’s disease have been suggested and studied for decades, the authors noted. Since the 1980s, hundreds of reports have associated Alzheimer’s with bacteria and viruses. These studies combined suggest a viral contribution but have not explained how the connection works. 

While the current findings are more specific, they do not provide evidence to change how risk and susceptibility are assessed, nor the diagnosis and treatment of Alzheimer’s, the authors said. Rather, the research gives scientists reason to revisit the old pathogen hypothesis and will be the basis for further work that will test whether herpes virus activity is one of the causes of Alzheimer’s.

  • Note: This article describes a basic research finding. Basic research increases our understanding of human behavior and biology, which is foundational to advancing new and better ways to prevent, diagnose, and treat disease. Science is an unpredictable and incremental process — each research advance builds on past discoveries, often in unexpected ways. Most clinical advances would not be possible without the knowledge of fundamental basic research.
  • About AMP-AD: The Accelerating Medicines Partnership is a joint venture among the National Institutes of Health, the Food and Drug Administration, 12 biopharmaceutical and life science companies and 13 non-profit organizations, managed by the Foundation for the NIH, to identify and validate promising biological targets of disease. AMP-AD is one of the four initiatives under the AMP umbrella; the other three are focused on type 2 diabetes (AMP-T2D), rheumatoid arthritis and systemic lupus erythematosus (AMP-RA/SLE) and Parkinson’s disease (AMP-PD). The AMP-AD knowledge portal already has over 1,300 total users. To learn more about the AMP-AD Target Discovery and Preclinical Validation Project, visit:
  • About the National Institute on Aging: The NIA leads the federal government effort conducting and supporting research on aging and the health and well-being of older people. The NIA is designated as the lead NIH institute for information on Alzheimer's disease. It provides information on age-related cognitive change and neurodegenerative disease, including participation in clinical studies, specifically on its Alzheimer's website.
  • Reference: Readhead et al. Multiscale Analysis of Independent Alzheimer’s Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human HerpesvirusPublished in the journal "Neuron". 2018 Jun. 21. Doi: 10.1016/j.neuron.2018.05.023

    Neuron (@NeuroCellPress), published by Cell Press, is a bimonthly journal that has established itself as one of the most influential and relied upon journals in the field of neuroscience and one of the premier intellectual forums of the neuroscience community. It publishes interdisciplinary articles that integrate biophysical, cellular, developmental, and molecular approaches with a systems approach to sensory, motor, and higher-order cognitive functions. Visit: To receive Cell Press media alerts, contact
  • Cell Press
  • National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.govNIH…Turning Discovery Into Health®
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Tuesday, July 10, 2018

Top ways to celebrate Rosh Hashanah with those who have dementia

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

5779  marks the beginning of another year. 5.9 million Americans have dementia. A good number of them are Jewish. What can you do to make someone with dementia feel good this Rosh Hashanah?

How celebrating this holy day helps uplift their spirit and yours

Here are some suggestions

Pray with them.

Most folks with dementia have strong ties to their religion. Even those with advanced dementia may spontaneously recite portions of a prayer service that was part of their past.
The problem may be to find a service that is appropriate. The traditional service is long and crowded.
Here are a few suggestions
*Go at the beginning or end of the service. That is when the least amount of congregants is in attendance.
*Contact some assisted living or nursing homes in the area. Many of them have short simple services highlighting the important prayers. This is a win, win situation. You can see what a place is like, and most often, activity directors love having visitors attend group activities. It makes all involved feel good. If this is not possible, have a short service at home. If you explain the situation to the Rabbi, he or she will let you borrow or buy a prayer book. He may even drop by for a visit. Alternatively, you can find some prayers online. Make sure to include some songs in your service or just sing the songs throughout the holiday. A good song might be: Shalom Aleichem

Carry on a family tradition

All families have something special they do during the high holidays. Of course, most families go to a synagogue. What about after that? Maybe you went to Aunt Betty’s. Aunt Betty may no longer be around, but you can recreate the atmosphere that was there. Invite one or two understanding friends to help you with this. The memories of visiting Aunt Betty will be there

Related to this is talking about past experiences on Rosh Hashanah or other holidays.

Discuss what happened at Aunt Betty’s. Regale a story about a funny experience that took place at Aunt Betty’s.
Do not ask: Do you remember?, but rather, just tell the story and let your loved one with dementia add comments. Talk about family members both past and present. You might say: "When Uncle Harry shook the table, he made us all laugh". Tell some jokes and laugh some more. Laughter is the best medicine

Eat a traditional meal or foods together

This activity can wake up the taste buds of a dementia person. Before the holiday, discuss the recipes. Talk about the different ingredients you need. Prepare a simple recipe together. Plan the meal. Ask: What should we eat first?etc.
Have him or her help set the table or fold the napkins.
You can talk about favorite family foods. Then make sure you have some of these favorites during the actual meal.

No matter what you do the goal is to make your loved one with dementia, feel good. Do not be a stickler for the rules. Reward good tries. If you feel a need to go to a traditional service, hire someone or have a friend go with you. If the service is too much for the dementia person, the friend can take him for a walk or take him home. Often congregants feel a need to take a break from the service whether they have dementia or not.

With some planning, this Rosh Hashanah, 5779, can be a good one for you and your loved one with dementia

Sunday, July 8, 2018

Best Alzheimer's drugs

Caregivers, and healthcare professionals,here is some great information

Here is a great dementia resource for caregivers and healthcare professionals,

Your residents will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two

Follow alzheimersideas on twitter

The Dementia Caregiver's Little Book of Hope [Kindle Edition]

St. Michael's Hospital: 

A new study ranks the safety and effectiveness of four Alzheimer's drugs. Ranked on concentration, memory, alertness and mood, learn what the researchers found. 

A new study ranking the safety and effectiveness of four drugs taken to enhance concentration, memory, alertness and moods, found that donepezil was most likely to effectively improve cognition in patients with Alzheimer's dementia. 

However, patients who took donepezil were more likely to experience side effects including nausea, vomiting and diarrhea than those who received a placebo, according to the study, published online in the Journal of the American Geriatrics Society.

Improving Cognition in Alzheimer's

Drugs for Early to Midstage
Brand NameGeneric Name
Remynil or Razadyne®galantamine
Drugs for Moderate to Severe Stage
Namenda® or Ebixa®memantine
In 2015, 46 million people worldwide had Alzheimer's disease, according to the study. In 2013, 146,593 people aged 65 and older in Ontario alone used cognitive enhancers, according to a 2016 Ontario Drug Policy Research report. 

"Alzheimer's dementia is the most common form of dementia in North America, and most people who have moderate to severe Alzheimer's will be on these medications," said Dr. Andrea Tricco, a scientist in the Li Ka Shing Knowledge Institute of St. Michael's Hospital and lead author of the study. "This analysis will give both patients and clinicians a full picture of how each of these drugs will likely affect their cognition, as well as their overall he

Safety & Effectiveness

Although there have been previous reviews of the safety and effectiveness of cognitive enhancers in treating Alzheimer's dementia, the authors said this was the first to rank their comparative safety and effectiveness. 

The study used network meta-analysis, an advanced statistical analysis technique, to systematically review existing evidence from 142 clinical trials of four common cognitive enhancers administered alone or in combination published between 1996 and 2015. The number of patients in each study ranged from 13 to 2,045, and the review evaluated a total of 33,889 patients.

The researchers compared the safety and effectiveness of any combination of donepezil, rivastigmine, galantamine or memantine in treating moderate to severe Alzheimer's dementia based on the results of the clinical trials that examined a number of patient outcomes, including cognition, function behaviour, global status, mortality, serious adverse events, falls, bradycardia, headache, diarrhea, vomiting and nausea. Donepezil was likely the most effective medication for Alzheimer's dementia across all effectiveness outcomes, including cognition, behavior and overall health, according to the study.

Best Course of Alzheimer's Treatment

Donepezil was also the only cognitive enhancer that reached the minimal clinically important threshold -- meaning effects on outcomes were observed clinically, as well as statistically -- on the Alzheimer's Disease Assessment cognition scale, making it the likely first choice for those patients and clinicians considering these medications, the authors said.

Although no significant risk of serious harm, falls or reduced heart rate was associated with any of the medications in the study, the data was limited on these specific outcomes.

Previous research by the authors found that cognitive enhancers do not improve cognition or function in people with mild cognitive impairment, and these patients experience significantly more nausea, diarrhea, vomiting and headaches.

The findings of the current study will help guide patients and clinicians who are making decisions about the best course of treatment for Alzheimer's dementia, said Dr. Tricco.

"The more information we are able to gather about how each of these medications can affect a patient's cognition and health, the more likely we are to be able to improve their health outcomes," she said.

  • St. Michael's Hospital:
    St. Michael’s Hospital provides compassionate care to all who enter its doors. The hospital also provides outstanding medical education to future health care professionals in more than 29 academic disciplines. Critical care and trauma, heart disease, neurosurgery, diabetes, cancer care, care of the homeless and global health are among the Hospital’s recognized areas of expertise. Through the Keenan Research Centre and the Li Ka Shing International Healthcare Education Centre, which make up the Li Ka Shing Knowledge Institute, research and education at St. Michael’s Hospital are recognized and make an impact around the world. Founded in 1892, the hospital is fully affiliated with the University of Toronto.

Friday, July 6, 2018

Too much iron could cause dementia

Caregivers, and healthcare professionals,here is some great information

Here is a great dementia resource for caregivers and healthcare professionals,

Your residents will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two

Follow alzheimersideas on twitter

The Dementia Caregiver's Little Book of Hope [Kindle Edition]

DIET: IRON accumulation within neurons can cause brain aging and dementia. A fast-aging African fish has helped researchers discover why. Find out how it works and what you should do about it. 

During aging as well as during Alzheimer’s or Parkinson’s disease, iron accumulates in the human brain. Now, researchers found that in vertebrates, a microRNA called miR-29 inhibits these deposits – possibly offering new ways to treat Alzheimer’s and Parkinson’s disease as well as strokes. Results were published in the Journal BMC Biology on February 13, 2017.

Anti-Aging Molecule in the Brain

As we get older, our brain ages. Cognitive abilities decline and the risk of developing neurodegenerative diseases like dementia, Alzheimer’s and Parkinson’s disease or having a stroke steadily increases. 

Aging in fast motion: The natural lifespan of N. furzeri is only few months (left: male of long-lived strain, aged 6 months; right: geriatric male aged 13 months). The African fish was used as aging model by researchers from Jena (Germany) and Pisa (Italy) to show that neurons are protected from iron-accumulation by an anti-aging microRNA. The results could offer a new approach for the treatment of neurodegenerative diseases. Credit: FLI/Grimm/K√§stner
A possible cause is the accumulation of iron molecules within neurons, which seems to be valid for all vertebrates. In a collaborative research project within the consortium JenAge, researchers from the Leibniz Institute on Aging – Fritz Lipmann Institute (FLI) in Jena, Germany, and the Scuola Normale Superiore (SNS) in Pisa, Italy, found that this iron accumulation is linked to a microRNA called miR-29. This little molecule has so far been known to act as a tumor suppressor, hindering the proliferation of cancer cells. 

However, clearly, miR-29 also regulates whether or not iron can be deposited in neurons. Using the African fish Nothobranchius furzeri – the shortest-living vertebrate that can be kept under laboratory conditions – the team of Alessandro Cellerino showed a large increase of iron deposits in fish where miR-29 had been suppressed, which led to premature brain aging. In contrast, healthy fish showed the more miR-29 in their neurons, the older they were. Hence, miR-29 acts as a kind of anti-aging molecule during aging, inhibiting the accumulation of iron in neurons. 

Iron: Head Start on Treating Alzheimer's?

„We strongly believe that our results are relevant for humans as well“, says Alessandro Cellerino, Professor of Physiology at SNS in Pisa and guest scientist at the FLI, who is one of the study’s leaders. In fact, the link between an increased iron accumulation and neurodegenerative diseases or strokes in humans has been known for some time; there are also results showing a reduced concentration of miR-29 in these diseases. However, it is totally new that miR-29 acts as molecular switch that inhibits iron accumulation. “These results are surprising – and very promising, because the development of miR-29-based pharmaceuticals for cancer therapy is already ongoing. This may offer a head start for the development of new therapies for Parkinson’s or Alzheimer’s disease and for the treatment of strokes as well”, Cellerino adds.

First Biomedical Discovery in New Fish Model Has Great Potential

African killifish Nothobranchius furzeri has only recently been introduced as animal model in aging research. It was the deciphering of the fish’s genome in late 2015 by the Leibniz Institute on Aging (FLI) that laid the foundation for genetic studies in this fast-aging vertebrate. “The investment of ten years, which it took us and our collaborators to decipher the genome, now starts to pay off”, explains Prof. K. Lenhard Rudolph, who is the FLI’s Scientific Director. And Mario Baumgart, a Postdoc at the FLI that was involved in the study, adds: “There’s no other vertebrate showing such a rapid aging as this little fish. It is like aging in fast motion. Moreover, 90% of human genes can be found in the fish as well, making almost all knowledge gained from N. furzeri transferable to humans.” This is why the results about the molecular switch miR-29, which were published on February 13, 2017 in the journal BMC Biology are so promising and mean a further step towards the treatment of neurodegenerative diseases.

Should I Worry?

Older people (male or female) are not prone to accumulating excess iron from a balanced healthy diet, moderate supplementation or alcohol consumption. This age group can potentially have toxic levels of iron in their organs and glands, if they abuse alcohol, consuming excessively of nicotine products (to stop smoking), on hormone replacement therapy, have B12 deficiencies, or are receiving repeated blood transfusion. 

Although iron is an essential element for healthy life, too much iron can overwhelm the body’s natural storage capability leading to oxidative stress, tissue damage, and early aging. Iron is particularly dangerous and can catalyze these processes even in small amounts (less than a few extra grams) when mixed with other risk factors such as obesity, family history of diabetes or heart disease, inadequate consumption of antioxidants (fruits and vegetables), hormone replacement therapy, unhealthy cholesterol levels, smoking and regular alcohol consumption and for women who no longer menstruate. 

Damage from Too Much Iron

Cell and tissue damage caused by iron can either initiate and/or contribute to the following causes of that can shorten lifespan or cause sudden death:
  • Cirrhosis of the liver
  • Cardiovascular diseases
  • Cancer (particularly cancers of the liver and colon)
  • Type II diabetes
  • Septicemia (excessive iron nourishes dangerous microbe colonization)
  • Early onset neurodegenerative diseases (Alzheimer’s and Parkinson’s diseases, among others)
Individual symptoms and degree of expression will vary between people (as will the amounts of stored iron). Excessive body iron accumulation can also lead to depression, loss of muscle mass and strength, enlargement and impairment of liver and spleen, loss of body hair, hypothyroidism, loss of libido (sexual interest) and function, with noticeable changes (darkening) of skin color, chronic fatigue and joint pain (especially in the first two knuckles of the hand referred to as “iron fist”.) Too much iron should be suspect in the presence of any of these symptoms. In women, the greatest risk for and indicator of suspect iron overload is when the monthly period stops for whatever reason: taking birth control pills, hysterectomy or menopause. With the monthly blood loss from a period iron is also lost, keeping excess iron under control. 

Fortunately for most, iron metabolism is tightly regulated by their genes. Those lucky ones are similar to people who seem to be able to eat as much as they want and not get fat. Some people can consume plenty of iron-packed red meat and even imbibe in some potentially unhealthy habits, and yet not be further harmed by the invisible threat of adding too much iron to that potentially unhealthy mix. That’s because their metabolisms don’t permit absorption of any more iron than what’s needed for the body to function properly, which includes about one extra gram stored in reserve. 

For older people with genetic hemochromatosis who also have a tendency or condition causing blood loss, the extra bit of stored iron may protect them from iron deficiency and anemia.

Diseases or conditions that can produce too much iron in the elderly include:

  • Menopause (females)
  • Genetic: hemochromatosis (HHC) or iron overload; for whites: type I (classic) hemochromatosis caused by mutations of HFE; four rarer non-HFE related disease include type 2 (A and B) hemochromatosis (juvenile hemochromatosis onset before age 30), type 3 hemochromatosis (transferrin receptor 2 hemochromatosis), type 4 (A and B) hemochromatosis (ferroportin disease), and a(hypo) ceruloplasminemia
  • Genetic iron loading for non-whites: not fully known but suspect is for mutations of genes that regulate hepcidin, transferrin receptor 2 or the ferroportin gene; (Note: these mutations may also occur in white females as modifiers of HFE).
  • Genetic or acquired chronic hemolytic anemia (mechanical heart valve, blood cell disorders, enzyme deficiencies and rare cases autoimmune disease) Acquired sideroblastic anemia
  • Acquired iron overload from blood transfusion, excessive alcohol consumption, excessive use of iron supplements, hormone replacement or chronic use of nicotine products (to stop smoking)
  • Detection (iron tests)
  • Diet
  • Therapy

  • Ripa R, Dolfi L, Terrigno M, Pandolfini L, Savino A, Arcucci V, Groth M, Terzibasi Tozzini E, Baumgart M, Cellerino A. MicroRNA miR-29 controls a compensatory response to limit neuronal iron accumulation during adult life and aging. BMC Biology 2017, 15:9, DOI: 10.1186/s12915-017-0354-x.

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