Friday, November 30, 2012

Top Appropriate Holiday Gifts For Those With Dementia



Caregivers and healthcare professionals, here is some great information

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


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


PRlog

Christmas,Chanukah and alike are the perfect chance to give gifts that are not only enjoyable but also are beneficial to persons with Alzheimer’s disease or a related dementia. These presents keep on giving long after the holiday season is gone

Over 5.4 million Americans are living with dementia. Is one of them someone you know or work with? Get him/her or anyone with Alzheimer's disease a gift that will keep on giving long after the holiday is gone.

First on the list of gifts is a book by Susan Berg called Adorable Photographs of Our Baby -- Meaningful, Mind-Stimulating Activities and More for the Memory Challenged, Their Loved Ones and Involved Professionals, This book features baby photographs that seniors with dementia love. This book shares a plethora of ideas and resources for you.

Another gift dementia persons will fancy is a holiday classic musical such as: “White Christmas” or “Holiday Inn”,

For those who are Jewish, we have, Debbie Friedman's "Miracles and Wonders: A Hanukkah Musical" and “A Taste of Chanukah”

Next is a sing a long CD or audio cassette of their favorite love songs. There is a series of these called, Old Time Favorites by Nancy Pitkin. Especially for Christmas, Mitch Miller’s sing a long gang has a CD and video for a dementia person’s holiday pleasure.

“Chanukah Favorites”, by award-winning Jewish performer, Judy Caplan Ginsburgh, is a great CD for Jewish people with dementia

You may want to get a sing a long video where your loved one can see and hear performers singing songs they love and are about love. A good one is, Sing-Along with Phil Bernardi: Songs We Know and Love

Here is another idea. Give a friend with dementia some hand lotion. Any kind will do. Just be aware of any allergies or pain issues he/she might have. If he/she can tolerate it, those with a pleasant scent work well. Give him/her a relaxing hand massage talking about how good the hand massage feels, how much you love this person, and a holiday experience you both share from the past.

If you cannot afford or do not have time to get these gifts, give the gift of....read all of Top Appropriate Holiday Gifts For Those With Dementia

Wednesday, November 28, 2012

Key protein interactions involved in neurodegenerative disease revealed Read more at: http://medicalxpress.com/news/2012-11-key-protein-interactions-involved-neurodegenerative.html#jCp


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


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

Medical Xpress

Medical research Scientists from the Florida campus of The Scripps Research Institute (TSRI) have defined the molecular structure of an enzyme as it interacts with several proteins involved in outcomes that can influence neurodegenerative disease and insulin resistance. The enzymes in question, which play a critical role in nerve cell (neuron) survival, are among the most prized targets for drugs to treat brain disorders such as Parkinson's disease, Alzheimer's disease and amyotrophic lateral sclerosis (ALS)


.
The study was published online ahead of print on November 8, 2012, by the journal Structure. The new study reveals the structure of a class of enzymes called c-jun-N-terminal kinases (JNK) when bound to three peptides from different protein families; JNK is an important contributor to stress-induced apoptosis (cell death), and several studies in animal models have shown that JNK inhibition protects against neurodegeneration. "Our findings have long-range implications for drug discovery," said TSRI Professor Philip LoGrasso, who, along with TSRI Associate Professor Kendall Nettles, led the study. "Knowing the structure of JNK bound to these proteins will allow us to make novel substrate coresponsible for creating and solving the crystal structures of the three peptides (JIP1, SAB, and ATF-2) with JNK3 using a technique called x-ray crystallography, while Nettles handled much of the data analysis. All three peptides have important effects, LoGrasso said, inducing two distinct inhibitory mechanisms—one where the peptide caused the activation loop to bind directly in the ATP pocket, and another with allosteric control (th
at is, using a location on the protein other than the active site). Because JNK signaling needs to be tightly controlled, even small changes in it can alter a cell's fate. "Solving the crystal structures of these three bound peptides gives us a clearer idea of how we can block each of these mechanisms related to cell death and survival," LoGrasso said. "You have to know their structure to know how to deal with them." 

More information: "Structural Mechanisms of Allostery and Autoinhibition in JNK Family Kinases," December 5, 2012 print edition of Structure. Journal reference: Structure Provided by Scripps Research Institute 

Saturday, November 24, 2012

Remarkable recent discoveries in Alzheimer’s disease


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

Examiner


Medscape Medical News reported on the latest published research in Alzheimer’s disease on November 7, 2012 indicating individuals carrying a mutant gene for Alzheimer’s disease demonstrate markers 20 years before onset of memory changes. In addition to markers in the cerebral spinal fluid, the individuals show structural changes in the brain other than the amyloid plaques and tangles commonly found in patients with the disease.
Dr. Eric M. Reiman, the first author on this recent study, published his results in Lancet Neurology on November 6, 2012. His research group from the Banner Alzheimer’s Institute in Phoenix, Arizona studied about 5000 people who carry the gene mutation that produces Alzheimer’s disease as early as age 45 years in Colombia.
Reiman and colleagues compared carriers of the gene with non-carriers and found structural differences in area of the brain called the hippocampus as well as less grey matter in some parietal lobes in individuals with the Alzheimer’s gene mutation. The parietal lobe resides at the top of the head after the frontal lobe and before the occipital lobe at the back of the head. The researchers used magnetic resonance imaging to uncover the changes in the parietal lobe. These changes occurred 20 years before the onset of memory loss. By knowing these alterations exist early, researchers can study treatments and measure for differences at these sites.
According to the Center for Disease Control and Prevention, Alzheimer’s disease causes the most common form of dementia that produces loss of thought control, memory and language. The disease usually affects men and women over the age of 60 years. The cause of Alzheimer’s disease remains presently unknown. Most scientists think several factors such as genetic, environmental and lifestyle contribute to the development of the disease. The discovery of changes in the parietal lobe and hippocampus add significantly to progress in the research.
The National Institute on Aging describes the importance of clinical research for uncovering causes, treatment modalities and disease prevention in Alzheimer’s disease. Patients or families interested in becoming involved in research trials can go the Clinical Trials.gov website for more information. The research trial website lists trials available in all 50 states and 181 countries.

Thursday, November 22, 2012

Rogue researcher offers new hope for sufferers of Alzheimer's disease


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

EmaxHealth

Approximately 36 million people worldwide suffer from Alzheimer's disease or dementia. Although many researchers are of the opinion that the buildup of amyloid plaques in the brain is the underlying cause of Alzheimer’s disease, Claude Wischik, MD, PhD has long backed a minority view regarding its cause. He feels that the condition is due to a protein in the brain called tau. The company he co-founded 10 years ago, TauRx Pharmaceuticals Ltd., has developed an experimental Alzheimer’s medication that it will begin testing in the coming weeks in two large clinical trials.
Dr. Wischik has been studying Alzheimer’s disease for decade. When he was a young PhD student at Cambridge University in the 1980s, he began collecting brains. It was a daunting task because few organ banks kept entire brains. In his search for an Alzheimer’s cure, he needed to examine brain tissue from Alzheimer’s patients soon after death. That required obtaining family approvals and enlisting mortuary technicians to extract the brains. In a little over a decade, Dr. Wischik collected more than 300 brains. While collecting his specimens, he embraced a concept that, if he is right, could fundamentally transform Alzheimer’s research and raise new hopes for individuals suffering from Alzheimer’s disease or dementia.

Tuesday, November 20, 2012

New Approach Could Transform Alzheimer’s Treatment


Caregivers, and healthcare professionals, here is some great information

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


-Healthline

-by Suzanne Boothby

The Gist

Canadian researchers using computer-aided drug design have discovered a technique that could lead to new treatment options for those with Alzheimer's disease (AD).
Dalhousie University scientists successfully identified molecules that can prevent the accumulation of both beta-amyloid and tau—two proteins thought to cause the disease and disrupt patients’ ability to think and remember.
The biochemistry of Alzheimer’s is not well understood, but current drugs only work to mask its symptoms. This breakthrough, published in the Canadian Journal of Chemistry, could reveal ways to treat the underlying causes of AD and delay the cell damage it causes.

The Expert Take

The authors of the study are excited about their findings, and say their work could aid in the development of disease-modifying drugs for AD.
“Alzheimer's is a devastating disease for which no truly disease-modifying drugs are available,” said study co-author Dr. Donald Weaver, a clinical neurologist at Capital Health, Canada Research Chair in Clinical Neuroscience, and the DMRF Irene MacDonald Sobey Chair in Curative Approaches to Alzheimer's Disease. “Our approach is completely novel. We explore how the human body attempts to protect itself from Alzheimer's, and then we exploit this to develop an entirely new approach to therapeutics.”

Source and Method

The researchers conducted their study “in silico,” or using a computer. This phrase was coined more than 20 years ago, and is similar to other terms like “in vivo” or “in vitro.” This technique has the potential to speed the rate of discovery by reducing time spent doing lab work and clinical trials.

The Takeaway 

Alzheimer’s disease is the most common form of dementia and one of the biggest health challenges worldwide. The World Health Organization estimates global cases of dementia to double in the next 20 years, and in Canada, rates are expected to more than double. The cost of care will increase from $15 billion annually to $153 billion annually, according to the Alzheimer's Society.
This new research identifies ways to work with the body’s natural defenses to treat AD, and could make a difference for many patients and their families.

Other Research

A new study by scientists at the University of Bristol is looking at a compound first examined in the treatment of prostate cancer that could potentially delay or reverse the progression of Alzheimer’s disease.

Friday, November 16, 2012

Tips for Healthy Dementia Dining This Thanksgiving


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


Healthnews-stat.com

How to Eat Right, Keep Calm and Enjoy Thanksgiving with Someone Who Has Alzheimer's Disease or a Related Dementia

According to the National Institute of Mental Health(NIMH) over five million Americans are living with Alzheimer's disease or a related dementia. Countless others are impacted by their illness. Studies have shown that eating right staves off dementia and slows the decline of someone who already has Alzheimer's disease or another type of dementia.

What can you do as a friend, loved one, or health care professional, to make Thanksgiving enjoyable and healthy.

The first thing is to keep it simple. Do not make elaborate dishes that take lots of time. There are plenty of easy healthy recipes out there. Using South Beach Diet, Zone Diet or Weight Watchers recipes is a good place to start. You can modify the recipes according to the dementia persons' likes and dislikes.

Another tip is to involve persons with Alzheimer's disease or a related dementia. Ask them about their preferences. If they say that they do not know, help them by telling them about things you like. Say, for example, I like squash. How about you? Then talk about ways to make squash. In this way, you can discuss every item you want to have for Thanksgiving.
Have them help you prepare the food. Give dementia persons simple tasks to do. Of course, you need to know their strengths and weaknesses to choose an appropriate chore. Make sure the assignment is failure free. In other words, there is no right or wrong way to do it. While you are preparing the food, reminisce about past Thanksgivings. Do not ask: Do you remember when...? Rather say That was so much fun when we...

Have a good belly laugh while talking about the good old days. Remember, research indicates that laughter does make someone feel better.

Fill your home with pleasant soothing aromas. Making a soup before or after Thanksgiving is a good way to do this. Cook the soup on a low flame all day long to let those heavenly smells fill the air.

Do not have too many guests at the meal. Make sure to keep it low key.

You may want to have two Thanksgiving meals. One for you and one for them. The one for them need not be on Thanksgiving Day. Pick a day that you and the dementia person can spend the day together enjoying all the happiness has to offer.

Now that you have read about the tips for healthy dementia dining, go have a great day
The book Adorable Photographs of Our Baby makes a great holiday gift for someone with dementia

One Small Gene Mutation Leads to One Giant Leap for Alzheimer’s Research


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

Cornell Daily Sun

As the sixth leading cause of death in the United States, Alzheimer’s affects approximately five million adults and is estimated to cost the country $200 billion this year in terms of direct medical fees and other costs associated with caregivers and therapies. Since the first records of the disease by Alois Alzheimer in 1906, Alzheimer’s disease (AD) has become increasingly prevalent in our worldwide population, and scientists have been struggling for decades in efforts to figure out the causation of the disease and, most importantly, how to treat it. Having worked in laboratories that dedicate their work to studying neurodegenerative diseases, I’ve realized that there is an immense amount of technology, effort and time that has been put into finding just one more small piece to this puzzle — even a breakthrough in discovering the involvement of a protein in a disease, or how a specific mutation can contribute to its exacerbation, is an encouragement in the scientific field. 
There are two essential cortical biomarkers of AD — plaques, which are formed of beta-amyloid protein deposits, and tangles, comprised of the tau protein that builds up inside of cells. Current therapies have been targeting the aggregation of these proteins in hopes of detangling the deposits, as plaques and tangles contribute to massive cell and nerve death that lead to rapid cognitive decline, an inevitable symptom of AD.
The mechanism of protein accumulation is important to understand for researchers to determine the cause of buildup. Beta-amyloid (Aβ) plaque fragments are a result of a cleavage reaction of the amyloid precursor protein (APP), a membrane protein that is found in neuronal synapses. Through post-translational modifications, APP can be separated into many different sections based on proteases and their specific cleavage sites. Normally, the α-secretase protease cleaves APP in the non-amyloidogenic pathway and the protein is rendered functional for other cellular tasks. However, when β-secretase comes across APP and severs the protein at another site, it leaves open the sequence correlated to γ-secretase, the third enzyme that can come in and cleave APP. The result of these two cleavages is Aβ.
Concerted efforts have been made to block the β- and γ-secretase cleavage sites, and pharmaceutical companies are currently testing drugs for their efficacy in slowing down the rate of AD progression. However, researchers have questioned this direction, citing that these trials have been inconclusive or failed to control Aβ formation.
What is particularly fascinating about this pathway is that perhaps our genetics unknowingly held part of the answer all along. In a recent finding published in Nature by a research team from DeCode Genetics based in Iceland, a rare gene mutation on APP was found to be protective against AD. This is the first mutation of its kind to be neuroprotective, as many other mutations of APP have exacerbated the AD phenotype. Whole genome sequencing of approximately 1800 Icelanders resulted in the discovery of this variant and researchers proved that it decreased the formation of Aβ and protein aggregation by 40 percent. The single point mutation was present in slightly less than one percent of the Icelanders and statistical analysis shows that carriers of the variant were about twice as likely to reach the age of 85 than non-carriers. In addition, cognitive function of carriers in the age range of 80-100 was vastly improved in comparison to their counterparts.
As exciting as this finding is, we must keep in mind that only a small subset of Icelanders carries the protective variant and that the study should be extended to other populations for a broader analysis. Whole genome sequencing is also a relatively expensive effort that is not just a simple blood test at the doctor’s office, and you would need to conduct a specific test at a laboratory or genetics company to tell if you have the mutation. Another interesting fact is that carriers of the gene mutation also reap its protective advantages — though this scientific discovery has proven that researchers are on the right track for targeting APP and preventing Aβ formation in gene therapies, perhaps preventing APP cleavage entirely is unnecessary and only a partial reduction is needed for a therapeutic benefit.
There will always be caveats and exceptions to any scientific discovery, but the overall enthusiasm for this new insight has been greatly encouraging to the research community. With the increase of resources, technology and dedication to biomedical research in the past decade, I am positive that we will be able to step forward in our advancements to understand and develop therapies for those affected by neurodegenerative diseases.
Debbie Tseng is a second year Ph.D. candidate at Weill Cornell Medical College. She may be reached atdgt2001@med.cornell.edu. dementia views dementia resource


Wednesday, November 14, 2012

Thanksgiving Activities For Those With Dementia

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

You 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 Alzheimers1 on twitter

How to Eat Right, Keep Calm and Enjoy Thanksgiving with Someone Who Has Alzheimer's Disease or a Related Dementia How to Eat Right, Keep Calm and Enjoy Thanksgiving with Someone Who Has Alzheimer's Disease or a Related Dementia

According to the National Institute of Mental Health(NIMH) over five million Americans are living with Alzheimer's disease or a related dementia. Countless others are impacted by their illness. Studies have shown that eating right staves off dementia and slows the decline of someone who already has Alzheimer's disease or another type of dementia.

What can you do as a friend, loved one, or health care professional, to make Thanksgiving enjoyable and healthy.

The first thing is to keep it simple. Do not make elaborate dishes that take lots of time. There are plenty of easy healthy recipes out there. Using South Beach Diet, Zone Diet or Weight Watchers recipes is a good place to start. You can modify the recipes according to the dementia persons' likes and dislikes.

Another tip is to involve persons with Alzheimer's disease or a related dementia. Ask them about their preferences. If they say that they do not know, help them by telling them about things you like. Say, for example, I like squash. How about you? Then talk about ways to make squash. In this way, you can discuss every item you want to have for Thanksgiving.

Have them help you prepare the food. Give dementia persons simple tasks to do. Of course, you need to know their strengths and weaknesses to choose an appropriate chore. Make sure the assignment is failure free. In other words, there is no right or wrong way to do it. While you are preparing the food, reminisce about past Thanksgivings. Do not ask: Do you remember when...? Rather say That was so much fun when we...

Have a good belly laugh while talking about the good old days. Remember, research indicates that laughter does make someone feel better.

Fill your home with pleasant soothing aromas. Making a soup before or after Thanksgiving is a good way to do this. Cook the soup on a low flame all day long to let those heavenly smells fill the air.

Do not have too many guests at the meal. Make sure to keep it low key.

You may want to have two Thanksgiving meals. One for you and one for them. The one for them need not be on Thanksgiving Day. Pick a day that you and the dementia person can spend the day together enjoying all the happiness has to offer.

Now that you have read about the tips for healthy dementia dining, go have a great day

The book Adorable Photographs of Our Baby makes a great holiday gift for someone with dementia

Monday, November 12, 2012

Israeli Scientists Nearing Blood Test for Alzheimer's


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

Israeli scientists are getting closer to developing a blood test to detect the asymptomatic, early stages of Alzheimer's disease.

By Hana Levi Julian, MSW, LCSW-R

Israeli scientists are getting closer to developing a blood test to detect the asymptomatic, earlystages of Alzheimer's disease.
Researchers at Tel Aviv University say the earliest clues to the disease are found in metabolic processes which can already been seen in the brain.
Shiri Stempler, a PhD candidate at TAU's Sackler Faculty of Medicine has been working with Professors Eytan Ruppin and Lior Wolf at the university's Blavatnik School of Computer Science to develop predictor models that use metabolic information to pinpoint progression of the disease.
The models were 90 percent accurate in predicting the stage of the disease, according to findings published in the journal Neurobiology of Aging.
In their study, the researchers used data collected from the hippocampus region of the brain, which controls memory and learning – the area which is damaged as Alzheimer's disease progresses.
Based on the number of metabolic genes found in the neurons and surrounding tissue, they built a predictive model which relates abnormalities in these genes to the progression of the disease.
Stempler noted that in Alzheimer's patients, they found that out of almost 1500 genes, the researchers found 50 genes that were most predictive of the disease, and were either over and under expressed – meaning there were either too many or too few.
The study is the first step towards identifying biomarkers that may ensure better detection and analysis of the disease at an early stage, said the scientists, all with a simple blood test.
"We hope that by studying metabolism, and the alterations to metabolism that occur in the very early stages of the disease, we can find new therapeutic strategies,” Stempler said.

Next the researchers will try to identify biomarkers in the blood that are associated with these metabolic changes, which may lead to detection of the disease, and its progression, with an easy, non-invasive blood test.

Saturday, November 10, 2012

Blood test predicts progression of Alzheimer's

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

Medical Xpress

A new study from Tel Aviv University suggests that early clues about the progression of the disease can be found in the metabolism of the brain, making it possible to detect and diagnose Alzheimer's at an early stage with a simple blood test.
When it comes to Alzheimer's disease, scientists usually—and understandably—look to the brain as their first center of attention. Now researchers at Tel Aviv University say that early clues regarding the progression of the disease can be found in the brain's metabolism. In very early stages of the disease, before any symptoms appear, metabolic processes are already beginning to change in the brain, says PhD candidate Shiri Stempler of TAU's Sackler Faculty of Medicine. Working with Profs. Eytan Ruppin and Lior Wolf of TAU's Blavatnik School of Computer Science, Stempler has developed predictor models that use metabolic information to pinpoint the progression of Alzheimer's. These models were 90 percent accurate in predicting the stage of the disease. Published in the journal Neurobiology of Aging, the research is the first step towards identifying biomarkers that may ensure better detection and analysis of the disease at an early stage, all with a simple blood test. It could also lead to novel therapies. "We hope that by studying metabolism, and the alterations to metabolism that occur in the very early stages of the disease, we can find new therapeutic strategies," adds Stempler. Interrupting a regulated process Metabolism describes a set of chemical reactions in cells which sustain life by controlling processes such as growth and reproduction. It is also responsible for providing energy to the body. To delve deeper into the connection between metabolism, brain functioning, and Alzheimer's disease, the researchers used data collected from the hippocampus region of the brain. Controlling memory and learning, this region of the brain is damaged as Alzheimer's progresses. Based on the number of metabolic genes found in the neurons and surrounding tissue, they built a predictive model which relates abnormalities in these genes to the progression of the disease. Out of almost 1500 genes, the researchers were able to select 50 genes that were the most predictive of Alzheimer's, says Stempler, noting that in Alzheimer's patients these genes are either over or under expressed, meaning that there are either too many or too few. Ads by Google 3 Early Signs of Dementia - Doctor: Know These 3 Warning Signs You're About to Suffer Dementia - www.newsmax.com Alzheimer's Directory - Alzheimer's Care for Every Need. Free Consult with Local Advisors. - Find.APlaceForMom.com When they compared the findings from these 50 genes among Alzheimer's patients, healthy patients, and primates (including chimpanzees and rhesus monkeys), the researchers discovered that in all but the Alzheimer's group, the number of the specific genes was tightly limited, with little difference in their number between individuals among each of the species, she explains. This implies that these genes are significant to normal brain functioning, and their strict regulation in healthy patients is compromised by Alzheimer's disease. Exploring new pathways Whether metabolic changes are a cause of the disease or merely a symptom remains a topic for future study. But the discovery of this connection is encouraging. "The correlation between metabolic gene expression and cognitive score in Alzheimer's patients is even higher than the correlation we see in medical literature between beta amyloid plaques – found in deposits in the brains of Alzheimer's patients – and cognitive score, pointing to a strong association between cognitive decline and an altered metabolism," Stempler says. Next the researchers will try to identify biomarkers in the blood that are associated with these metabolic changes. They may lead to detection and information about the disease's progression with an easy and non-invasive blood test. And as their work advances, Stempler hopes to develop therapeutic strategies that are based around these alterations in the metabolic network to help Alzheimer's patients, such as medications that can re-introduce strict regulation over gene expression. They believe that the research is a promising direction for Alzheimer's research. 

Journal reference: Neurobiology of Aging Provided by Tel Aviv University 

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