High blood sugar and dementia

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Group Health Research Institute.

17 out of 17 levels of people's sugar showed a direct connection between sugar & dementia. See the results and read researcher's conclusions. 

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A joint Group Health-University of Washington (UW) study in the New England Journal of Medicine has found that higher blood sugar levels are associated with higher dementia risk, even among people who do not have diabetes. 

Blood sugar levels averaged over a five-year period were associated with rising risks for developing dementia, in this report about more than 2,000 Group Health patients age 65 and older in the Adult Changes in Thought (ACT) study.

For example, in people without diabetes, risk for dementia was 18 percent higher for people with an average glucose level of 115 milligrams per deciliter compared to those with an average glucose level of 100 mg/dl. And in people with diabetes, whose blood sugar levels are generally higher, dementia risk was 40 percent higher for people with an average glucose level of 190 mg/dl compared to those with an average glucose level of 160 mg/dl.

"The most interesting finding was that every incrementally higher glucose level was associated with a higher risk of dementia in people who did not have diabetes," said first author Paul K. Crane, MD, MPH, an associate professor of medicine at the UW School of Medicine, adjunct associate professor of health services at the UW School of Public Health, and affiliate investigator at Group Health Research Institute. "There was no threshold value for lower glucose values where risk leveled off."

"One major strength of this research is that it is based on the ACT study, a longitudinal cohort study, where we follow people for many years as they lead their lives," said senior author Eric B. Larson, MD, MPH, a senior investigator at Group Health Research Institute who also has appointments at the UW Schools of Medicine and Public Health. "We combine information from people's research visits every other year with data from their visits to Group Health providers whenever they receive care. And this gave us an average of 17 blood sugar measurements per person: very rich data."

These measurements included blood glucose (some fasting, some not) and glycated hemoglobin (also known as HbA1c). Blood sugar levels rise and fall in peaks and valleys throughout each day, but glycated hemoglobin doesn't vary as much over short intervals.

Combining glucose and glycated hemoglobin measures into a composite measure required special statistical techniques, which Drs. Crane and Larson's co-authors Rod Walker, MS, a biostatistician, and Rebecca Hubbard, PhD, an associate investigator, both from Group Health Research Institute, had developed. (Dr. Hubbard is also an affiliate assistant professor of biostatistics at the UW School of Public Health.) These sophisticated statistical models required specialized data on the relationships between glycated hemoglobin and glucose levels, and they used data generated by co-author David M. Nathan, MD, a professor of medicine at Harvard Medical School and director of the Diabetes Center at Massachusetts General Hospital.

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• Sugar & Alzheimer's
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So should people try to eat less sugar -- or foods with a lower "glycemic index"? Not necessarily, Dr. Crane said: "Your body turns your food into glucose, so your blood sugar levels depend not only on what you eat but also on your individual metabolism: how your body handles your food." But he does suggest that taking walks couldn't hurt: The ACT study has previously linked physical activity to later onset and reduced risk of dementia, including Alzheimer's disease.

Furthermore, Dr. Crane emphasized that these results come from an observational study: "What we found was that people with higher levels of glucose had a higher risk of dementia, on average, than did people with lower levels of glucose," he said. "While that is interesting and important, we have no data to suggest that people who make changes to lower their glucose improve their dementia risk. Those data would have to come from future studies with different study designs."

Source:

Group Health Research Institute.

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Journal Reference:

1. Paul K. Crane, Rod Walker, Rebecca A. Hubbard, Ge Li, David M. Nathan, Hui Zheng, Sebastien Haneuse, Suzanne Craft, Thomas J. Montine, Steven E. Kahn, Wayne McCormick, Susan M. McCurry, James D. Bowen, Eric B. Larson. Glucose Levels and Risk of Dementia. New England Journal of Medicine, 2013; 369 (6): 540 DOI: 10.1056/NEJMoa1215740

November is Alzheimer's Awareness Month

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The Alzheimer's Association was founded in 1980. It has been the leader in making the fight against Alzheimer’s disease a national priority, Every November this organization makes an extra effort to enlighten the general public about Alzheimer's disease by having National Alzheimer’s Disease Awareness Month.
See President Obama's proclamation of National Alzheimer's Disease Awareness Month

President Ronald Reagan helped to launch a national campaign against Alzheimer’s disease in 1983 after he designated a National Alzheimer’s Disease Week in 1982. He called members of the Alzheimer's Association to the White House for the signing of a proclamation declaring National Alzheimer’s Disease Month.

The founder of the Alzheimer’s Association was Jerome Stone. He led a group of family caregivers, Association volunteers and staff in the effort to bring attention to the cause on Capitol Hill. That advocacy effort continues even stronger today with Association public policy staff and volunteers leading the call for increased government funding for critical Alzheimer research and support programs. Anyone can become an Alzheimer's disease advocate.

November is National Alzheimer's Disease Awareness Month and National Family Caregivers Month
According to the Alzheimer’s Association 2017
Alzheimer’s Disease Facts and Figures report, there are more than 5.3 million people are living with Alzheimer’s and over 10 million family caregivers. This November, during National Alzheimer’s Disease Awareness Month and National Family Caregivers Month, the Alzheimer’s Association

What are you doing to find out all you can about this mind robbing disease and related dementias?
Visit this blog often to find out the latest news.
Here is what the president had to say
A Proclamation by the President of the United States of America
During National Alzheimer's Disease Awareness Month, we recognize the dignity and courage of the men and women living with Alzheimer's disease. We also honor the devoted family members and caretakers who bring them love and comfort, and we underscore our dedication to finding a cure for this tragic disease
...read the whole proclamation from 2011
Become an Alzheimer's advocate

LED flickering lights reduce placques in Alzheimer's

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

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MIT News

Using LED lights flickering at a specific frequency, MIT researchers have shown that they can substantially reduce the beta amyloid plaques seen in Alzheimer’s disease, in the visual cortex of mice. 

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This treatment appears to work by inducing brain waves known as gamma oscillations, which the researchers discovered help the brain suppress beta amyloid production and invigorate cells responsible for destroying the plaques.

Further research will be needed to determine if a similar approach could help Alzheimer’s patients, says Li-Huei Tsai, the Picower Professor of Neuroscience, director of MIT’s Picower Institute for Learning and Memory, and senior author of the study, which appears in the online edition of Nature.

Researchers in Li-Huei Tsai's laboratory at the Picower Institute for Learning and Memory have shown that disrupted gamma waves in the brains of mice with Alzheimer’s disease can be corrected by a unique non-invasive technique using flickering light.


“It’s a big ‘if,’ because so many things have been shown to work in mice, only to fail in humans,” Tsai says. “But if humans behave similarly to mice in response to this treatment, I would say the potential is just enormous, because it’s so noninvasive, and it’s so accessible.”

Tsai and Ed Boyden, an associate professor of biological engineering and brain and cognitive sciences at the MIT Media Lab and the McGovern Institute for Brain Research, who is also an author of the Nature paper, have started a company called Cognito Therapeutics to pursue tests in humans. The paper’s lead authors are graduate student Hannah Iaccarino and Media Lab research affiliate Annabelle Singer.

“This important announcement may herald a breakthrough in the understanding and treatment of Alzheimer's disease, a terrible affliction affecting millions of people and their families around the world,” says Michael Sipser, dean of MIT’s School of Science. “Our MIT scientists have opened the door to an entirely new direction of research on this brain disorder and the mechanisms that may cause or prevent it. I find it extremely exciting.”

Brain wave stimulation

Alzheimer’s disease, which affects more than 5 million people in the United States, is characterized by beta amyloid plaques that are suspected to be harmful to brain cells and to interfere with normal brain function. Previous studies have hinted that Alzheimer’s patients also have impaired gamma oscillations. These brain waves, which range from 25 to 80 hertz (cycles per second), are believed to contribute to normal brain functions such as attention, perception, and memory.

In a study of mice that were genetically programmed to develop Alzheimer’s but did not yet show any plaque accumulation or behavioral symptoms, Tsai and her colleagues found impaired gamma oscillations during patterns of activity that are essential for learning and memory while running a maze.

Next, the researchers stimulated gamma oscillations at 40 hertz in a brain region called the hippocampus, which is critical in memory formation and retrieval. These initial studies relied on a technique known as optogenetics, co-pioneered by Boyden, which allows scientists to control the activity of genetically modified neurons by shining light on them. Using this approach, the researchers stimulated certain brain cells known as interneurons, which then synchronize the gamma activity of excitatory neurons.

After an hour of stimulation at 40 hertz, the researchers found a 40 to 50 percent reduction in the levels of beta amyloid proteins in the hippocampus. Stimulation at other frequencies, ranging from 20 to 80 hertz, did not produce this decline.

Tsai and colleagues then began to wonder if less-invasive techniques might achieve the same effect. Tsai and Emery Brown, the Edward Hood Taplin Professor of Medical Engineering and Computational Neuroscience, a member of the Picower Institute, and an author of the paper, came up with the idea of using an external stimulus — in this case, light — to drive gamma oscillations in the brain. The researchers built a simple device consisting of a strip of LEDs that can be programmed to flicker at different frequencies.

Using this device, the researchers found that an hour of exposure to light flickering at 40 hertz enhanced gamma oscillations and reduced beta amyloid levels by half in the visual cortex of mice in the very early stages of Alzheimer’s. However, the proteins returned to their original levels within 24 hours.

The researchers then investigated whether a longer course of treatment could reduce amyloid plaques in mice with more advanced accumulation of amyloid plaques. After treating the mice for an hour a day for seven days, both plaques and free-floating amyloid were markedly reduced. The researchers are now trying to determine how long these effects last.

Furthermore, the researchers found that gamma rhythms also reduced another hallmark of Alzheimer’s disease: the abnormally modified Tau protein, which can form tangles in the brain.

“What this study does, in a very carefully designed and well-executed way, is show that gamma oscillations, which we have known for a long time are linked to cognitive function, play a critical role in the capacity of the brain to clean up deposits,” says Alvaro Pascual-Leone, a professor of neurology at Harvard Medical School who was not involved in the research. “That’s remarkable and surprising, and it opens up the exciting prospect of possible translation to application in humans.”

Tsai’s lab is now studying whether light can drive gamma oscillations in brain regions beyond the visual cortex, and preliminary data suggest that this is possible. They are also investigating whether the reduction in amyloid plaques has any effects on the behavioral symptoms of their Alzheimer’s mouse models, and whether this technique could affect other neurological disorders that involve impaired gamma oscillations.

Two Modes of Action

The researchers also performed studies to try to figure out how gamma oscillations exert their effects. They found that after gamma stimulation, the process for beta amyloid generation is less active. Gamma oscillations also improved the brain’s ability to clear out beta amyloid proteins, which is normally the job of immune cells known as microglia.

“They take up toxic materials and cell debris, clean up the environment, and keep neurons healthy,” Tsai says.

In Alzheimer’s patients, microglia cells become very inflammatory and secrete toxic chemicals that make other brain cells more sick. However, when gamma oscillations were boosted in mice, their microglia underwent morphological changes and became more active in clearing away the beta amyloid proteins.

“The bottom line is, enhancing gamma oscillations in the brain can do at least two things to reduced amyloid load. One is to reduce beta amyloid production from neurons. And second is to enhance the clearance of amyloids by microglia,” Tsai says.

The researchers also sequenced messenger RNA from the brains of the treated mice and found that hundreds of genes were over- or underexpressed, and they are now investigating the possible impact of those variations on Alzheimer’s disease. 

MORE INFORMATION:

• The research was funded by the JPB Foundation, the Cameron Hayden Lord Foundation, a Barbara J. Weedon Fellowship, the New York Stem Cell Foundation Robertson Award, the National Institutes of Health, the Belfer Neurodegeneration Consortium, and the Halis Family Foundation.

Blood pressure helps 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]

Georgetown University Medical Center

Top researchers show the generic drug candesartan (brand name: ATACAND^®) may not only slow progression of Alzheimer’s, but also prevent or delay its development. See how. 

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WASHINGTON  — In laboratory neuronal cultures, an FDA-approved drug used to treat high blood pressure reduced cell damage often linked to Alzheimer’s disease, say researchers at Georgetown University Medical Center (GUMC) and the National Institutes of Health.

They say their work, published online in the journal Alzheimer's Research and Therapy, provides information supporting the potential effect of the generic drug candesartan (brand name: ATACAND^®) — as well as other Angiotensin receptor blockers (ARBs) for the early treatment of Alzheimer’s disease.

“Our findings make sense in many ways,” says the study’s senior author Juan M. Saavedra, MD, from GUMC’s Department of Pharmacology and Physiology.  “Hypertension reduces blood flow throughout the body and brain and is a risk factor of Alzheimer’s disease. Previous epidemiological studies found that Alzheimer’s progression is delayed in hypertensive patients treated with ARBs.”

Using neuronal cultures, the researchers explored the action of candesartan on the neurotoxic effects of exposure to excessive glutamate, a demonstrated injury factor in the early stages of Alzheimer’s disease.

The scientists found that candesartan prevented glutamate-induced neuronal death. They conducted in-depth gene analyses of the laboratory results, demonstrating that candesartan prevented neuronal inflammation and many other pathological processes, including alterations in amyloid metabolism, a hallmark of Alzheimer’s disease.

The study’s first author, Abdel G. Elkahloun, PhD, from the Comparative Genomics and Cancer Genetics Branch of the National Human Genome Research Institute, then compared gene expression in the neuronal cultures with published gene databases of autopsy samples from Alzheimer’s disease patients. “The correlations were impressive — the expression of 471 genes that were altered by excess glutamate in our cultures were also altered in brain autopsy samples from patients who suffered from Alzheimer’s disease. Candesartan normalized expression of these genes in our cultures,” Elkahloun says.

“We hypothesize that candesartan, or other members of the ARB group, may not only slow progression of Alzheimer’s but also prevent or delay its development,” Saavedra says.

The researchers say this work has immediate translational value, supporting testing candesartan, or other ARBs, in controlled clinical studies on patients at early stages of Alzheimer’s disease. 

Statins for dementia

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

Statins certainly seem to lower the risk of Alzheimer's. On the other hand, they can sometimes cause temporary memory loss, which does go away if one stops the statins. Find out what you need to know to strike the right balance. 

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As with any medication, the more you know about statins, the more ability you have to help your doctor give you the best treatment possible.

New York times

THE GOOD:
High dose statins prevent dementia 

High doses of statins prevent dementia in older people, according to research presented at the ESC Congress by Dr. Tin-Tse Lin from Taiwan. The study of nearly 58,000 patients found that high potency statins had the strongest protective effects against dementia.

Dr. Lin said: “Statins are widely used in the older population to reduce the risk of cardiovascular disease. But recent reports of statin-associated cognitive impairment have led the US Food and Drug Administration (FDA) to list statin-induced cognitive changes, especially for the older population, in its safety communications.”

He added: “Previous studies had considered statin therapy to exert a beneficial effect on dementia. But few large-scale studies have focused on the impact of statins on new-onset, non-vascular dementia in the geriatric population.”

Accordingly, the current study examined whether statin use was associated with new diagnoses of dementia. The researchers used a random sample of 1 million patients covered by Taiwan’s National Health Insurance. From this they identified 57,669 patients aged >65 years who had no history of dementia in 1997 and 1998. The analysis included pre-senile and senile dementia but excluded vascular dementia.

There were 5,516 new diagnoses of dementia during approximately 4.5 years of follow-up. The remaining 52,153 patients aged >65 formed the control group. Subjects were divided into tertiles according to their mean daily equivalent1 dosage and total (across the entire follow up period) equivalent dosage.

The adjusted hazard ratios (HRs) for dementia were significantly inversely associated with increased daily or total equivalent statin dosage. The HRs for the three tertiles of mean equivalent daily dosage (lowest to highest) were 0.622, 0.697 and 0.419 vs control (p<0 .001="" 0.332="" 0.632="" 0.773="" age="" and="" cardiovascular="" control="" different="" dosage="" effect="" equivalent="" for="" gender="" highest="" hrs="" in="" lowest="" of="" p="" protective="" remained="" risk="" span="" statins="" subgroups.="" tertiles="" the="" three="" to="" total="" trend="" vs="" were="">

THE BAD:
Statin-Associated Memory Loss

Doctors found that some patients to whom they precribed statins ended up reporting memory loss assoicated with the drug. 

It certainly did not happen to everyone. In the study, "Statin-associated memory loss: analysis of 60 case reports and review of the literature", patients reporting such memory loss were identified and observed. Other studies followed, including one in 2010 that reported 600 such cases linked to Lipitor.

Although there was a clear association, no one has been able to prove a cause-and-effect relationship. That is why doctors are careful to check for other reasons behind memory loss before they start cutting back the statins. Heart disease, age and even Alzheimer's can be to blame.

Dementia-expert Dr. P. Murali Doraiswamy offers the following advice.

"Clearly, if lowering the dose made the problem better, then that suggests the statin was the cause. However, reducing the dose of a statin can raise risk for heart disease and stroke in some situations. I don’t recommend people stop or change dose of statins on their own, but to work through their doctors. This may also sometimes involve educating your doctors about the new risks associated with statins."

Dr. Lin said: “The adjusted risks for dementia were significantly inversely associated with increased total or daily equivalent statin dosage. Patients who received the highest total equivalent doses of statins had a 3-fold decrease in the risk of developing dementia. Similar results were found with the daily equivalent statin dosage.”

He added: “It was the potency of the statins rather than their solubility (lipophilic or hydrophilic) which was a major determinant in reducing dementia. High potency statins such as atorvastatin and rosuvastatin showed a significant inverse association with developing dementia in a dose-response manner. Higher doses of high potency statins gave the strongest protective effects against dementia.” 

Dr. Lin continued: “The results were consistent when analysing daily doses of different kinds of statins. Almost all the statins (except lovastatin) decreased the risk for new onset dementia when taken at higher daily doses. A high mean daily dosage of lovastatin was positively associated with the development of dementia, possibly because lovastatin is a lipophilic statin while the anti-inflammatory cholesterol lowering effect of lovastatin is not comparable to that of atorvastatin and simvastatin.”

Dr. Lin concluded: “To the best of our knowledge, this was the first large-scale, nation-wide study which examined the effect of different statins on new onset dementia (except vascular dementia) in an elderly population. We found that high doses of statins, particularly high potency statins, prevent dementia.”

The European Society of CardiologyThe European Society of Cardiology (ESC) represents more than 80 000 cardiology professionals across Europe and the Mediterranean. Its mission is to reduce the burden of cardiovascular disease in Europe.

MORE INFORMATION:

About ESC CongressThe ESC Congress is currently the world’s premier conference on the science, management and prevention of cardiovascular disease.  The spotlight of this year's event is "The Heart Interacting with Systemic Organs".  ESC Congress takes place from 31 August to 4 September at the RAI centre in Amsterdam, Netherlands. More information: ESC Congress.

References
More information on the ESC Press Conference page: Statins for all forever?

Calm disturbing dementia behavior without 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

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

University of Michigan Health System

ANN ARBOR, Mich. — Doctors write millions of prescriptions a year for drugs to calm the behavior of people with Alzheimer’s disease and other types of dementia. But non-drug approaches actually work better, and carry far fewer risks, experts conclude in a new report. 

The new DICE model - for
Describe, Investigate, Evaluate, and Create -
seeks to reduce psychotropic medication use in dementia patients.

In fact, non-drug approaches should be the first choice for treating dementia patients’ common symptoms such as irritability, agitation, depression, anxiety, sleep problems, aggression, apathy and delusions, say the researchers in a paper just published by the British Medical Journal.

The best evidence among non-drug approaches is for those that focus on training caregivers — whether they are spouses, adult children or staff in nursing homes and assisted living facilities — to make behavioral and environmental interventions.

The researchers, from the University of Michigan Medical School and Johns Hopkins University, reviewed two decades’ worth of research to reach their conclusions about drugs like antipsychotics and antidepressants, and non-drug approaches that help caregivers address behavioral issues in dementia patients.

They lay out their findings along with a framework that doctors and caregivers can use to make the most of what’s already known. Called DICE for Describe, Investigate, Evaluate, and Create, the framework tailors approaches to each person with dementia, and as symptoms change.

“The evidence for non-pharmaceutical approaches to the behavior problems often seen in dementia is better than the evidence for antipsychotics, and far better than for other classes of medication,” says first author Helen C. Kales, M.D., head of the U-M Program for Positive Aging at the University of Michigan Health System and investigator at the VA Center for Clinical Management Research . “The issue and the challenge is that our health care system has not incentivized training in alternatives to drug use, and there is little to no reimbursement for caregiver-based methods.”

Coincidentally, a new U.S. Government Accountability Office report published the same day as the BMJ paper addresses the issue of overuse of antipsychotic medication for the behavior problems often seen in dementia.  It finds that one-third of older adults with dementia who had long-term nursing home stays in 2012 were prescribed an antipsychotic medication -- and that about 14 percent of those outside nursing homes were prescribed an antipsychotic that same year.

The GAO calls on the federal government to work to reduce use of these drugs further than it’s already doing, by addressing use in dementia patients outside nursing homes.

Kales, however, cautions that penalizing doctors for prescribing antipsychotic drugs to these patients could backfire, if caregiver-based non-drug approaches aren’t encouraged.

She and her colleagues from Johns Hopkins, Laura N. Gitlin PhD and Constantine Lyketsos MD, note in their paper that “there needs to be a shift of resources from paying for psychoactive drugs and emergency room and hospital stays to adopting a more proactive approach.”

But they also write, “drugs still have their place, especially for the management of acute situations where the safety of the person with dementia or family caregiver may be at risk.” For instance, antidepressants make sense for dementia patients with severe depression, and antipsychotic drugs should be used when patients have psychosis or aggression that could lead them to harm themselves or others. But these uses should be closely monitored and ended as soon as possible,

The authors lay out five non-pharmacologic categories to start with based on their review of the medical evidence. These approaches have been shown to help reduce behavior issues:

• Providing education for the caregiver
• Enhancing effective communication between the caregiver and the person with dementia
• Creating meaningful activities for the person with dementia
• Simplifying tasks and establishing structured routines
• Ensuring safety and simplifying and enhancing the environment around the patient, whether in the home or the nursing/assisted living setting

They also note that many “hidden” medical issues in dementia patients – such as urinary tract infection and other infections, constipation, dehydration and pain – can lead to behavioral issues, as can drug interactions. So physicians should look to assess and address these wherever possible.

Kales, Gitlin and Lyketsos  are working with the U-M Center for Health Communications Research to launch a National Institute of Nursing Research-sponsored clinical trial this spring that will test the DICE approach through a computer based tool for caregivers called the WeCareAdvisor. The tool will help families identify tips and resources in a single computer interface to address behavioral symptoms.  The tips are designed to prevent or mitigate possible triggers for common behavioral symptoms such as pacing, repetitive questioning, restlessness, or shadowing.

"Behavior-based strategies may take longer than prescriptions. But if you teach people the principles behind DICE, the approach becomes more natural and part of one’s routine. It can be very empowering for caregivers or nursing home staff.” -- Helen Kales, M.D.

For instance, de-cluttering the environment, using music or simple activities that help to engage a person with dementia , or using a calm voice instead of being confrontational, could help greatly to reduce behavioral symptoms, Kales says. And making sure that caregivers get breaks from their responsibilities and take care of themselves, especially in the home, can help them avoid burnout and taking their frustration out on patients.

“Behavior-based strategies may take longer than prescriptions,” acknowledges Kales, a member of the U-M Institute for Healthcare Policy and Innovation. “But if you teach people the principles behind DICE, the approach becomes more natural and part of one’s routine. It can be very empowering for caregivers or nursing home staff.”

More research on both new drug options and the best ways to assess and address behavioral symptoms is needed, the authors conclude. But in the meantime, the evidence to date comes down in favor of non-drug approaches in most cases.

THE COMPONENTS OF THE DICE APPROACH ARE:

• D: Describe - Asking the caregiver, and the person with dementia if possible, to describe the “who, what, when and where” of situations where problem behaviors occur and the physical and social context for them. Caregivers could take notes about the situations that led to behavior issues, to share with health professionals during visits.

• I: Investigate – Having the health provider look into all the aspects of the person’s health, dementia symptoms, current medications and sleep habits, that might be combining with physical, social and caregiver-related factors to produce the behavior.

• C: Create – Working together, the patient’s caregiver and health providers develop a plan to prevent and respond to behavioral issues in the person with dementia, including everything from enhancing the patient’s activities and environment, to educating and supporting the caregiver.

• E: Evaluate – Giving the provider responsibility for assessing how well the plan is being followed and how it’s working, or what might need to be changed.

More information

Reference: BMJ 2015; 350 doi: http://dx.doi.org/10.1136/bmj.h369 (Published 02 March 2015)

Funding: National Institutes of Health, NR014200, Johns Hopkins Alzheimer’s Disease Research Center (P50AG005146).

Previous publication - the DICE model: Journal of the American Geriatrics Society, April 2014. Paper

Drug to prevent Alzheimer's

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]

Neuroscience News

Source: University of Kentucky.

Researchers have known for decades that the hallmark plaques and tangles in the brain associated with Alzheimer’s develop long before people experience memory loss. Ai-Ling Lin, an assistant professor at Sanders-Brown, hopes to demonstrate that low doses of Rapamycin, a drug commonly used as an immunosuppressant for organ transplant recipients, can restore brain function before the disease changes in the brain affect a person’s memory.

“We know that Rapamycin signals blood vessels to dilate, which increases cerebral blood flow and helps regulate the physical and chemical processes that support effective cell function – also known as metabolic homeostasis,” Lin said. “We hope our research will demonstrate that Rapamycin prompts tangible benefit by preventing the cognitive decline associated with Alzheimer’s disease.”

Her study is unique in that it will also assess whether a relatively new imaging concept called multimodal MRI (mMRI) is effective in measuring the efficacy of other potential treatments. mMRI uses traditional MRI plus another form of imaging (CT scan or PET scan, for example) to provide complementary information.

“We have two eyes for a reason. You can function with just one, but eyesight is improved when both eyes work well,” Lin explained. “mMRI follows the same concept: multiple layers of data increase accuracy.”

“If I can demonstrate that mMRI is an effective surrogate for the types of testing we currently have at our disposal, we have a new avenue to explore potential treatments on a faster and more straightforward track.”

Lin will be studying the drug in mice with the APOE4 gene, which is associated with an increased risk of AD. She will validate mMRI results with biological and behavioral tests to confirm mMRI’s accuracy.

Lin will be studying the drug in mice with the APOE4 gene, which is associated with an increased risk of AD. She will validate mMRI results with biological and behavioral tests to confirm mMRI’s accuracy. NeuroscienceNews.com image is in the public domain.

Her work will be funded by a five-year, $2.88 million grant from the National Institutes of Health.

It will be a while before Rapamycin as a therapeutic target for Alzheimer’s will be ready for human clinical trials, but the concept of mMRI as a surrogate for other testing methods has potential for speedy adoption, as the mMRI methods are readily available to be used in humans. “Being able to test a drug and also a means of assessing other drugs in the future is truly exciting,” Lin said.

Linda Van Eldik, director of the Sanders-Brown Center on Aging, says that this latest grant is another important step in Sanders-Brown’s race against Alzheimer’s.

“As many as one in five people carry the Alzheimer’s gene APOE4, so the idea that a readily-available drug already demonstrated to be safe in humans might prevent what is arguably the most devastating and expensive disease in modern history is exciting,” said Van Eldik. “On top of that, Ai-Ling’s work might also speed the ability to test other treatments. It’s a win-win for science and for the people it serves.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source: Laura Dawahare – University of Kentucky
Image Source: NeuroscienceNews.com image is in the public domain.
Video Source: Video credited to University of Kentucky.