7 Brain Benefits of Turmeric Derivative for Dementia Prevention

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

The Salk team expanded upon their previous development of a drug candidate, called J147, which takes a different tack by targeting Alzheimer's major risk factor--old age. In the new work, the team showed that the drug candidate worked well in a mouse model of aging not typically used in Alzheimer's research. When these mice were treated with J147, they had better memory and cognition, healthier blood vessels in the brain and other improved physiological features, 

"Initially, the impetus was to test this drug in a novel animal model that was more similar to 99 percent of Alzheimer's cases," says Antonio Currais, the lead author and a member of Professor David Schubert's Cellular Neurobiology Laboratory at Salk. "We did not predict we'd see this sort of anti-aging effect, but J147 made old mice look like they were young, based upon a number of physiological parameters."

Alzheimer's disease is a progressive brain disorder, recently ranked as the third leading cause of death in the United States and affecting more than five million Americans. It is also the most common cause of dementia in older adults, according to the National Institutes of Health.

"While most drugs developed in the past 20 years target the amyloid plaque deposits in the brain (which are a hallmark of the disease), none have proven effective in the clinic," says Schubert, senior author of the study.

Expanding the Fight to More Common Dementias

Several years ago, Schubert and his colleagues began to approach the treatment of the disease from a new angle. Rather than target amyloid, the lab decided to zero in on the major risk factor for the disease--old age. Using cell-based screens against old age-associated brain toxicities, they synthesized J147.

Previously, the team found that J147 could prevent and even reverse memory loss and Alzheimer's pathology in mice that have a version of the inherited form of Alzheimer's, the most commonly used mouse model. However, this form of the disease comprises only about 1 percent of Alzheimer's cases. For everyone else, old age is the primary risk factor, says Schubert. The team wanted to explore the effects of the drug candidate on a breed of mice that age rapidly and experience a version of dementia that more closely resembles the age-related human disorder.

Young Mice, Old Mice and J147-fed Mice

In this latest work, the researchers used a comprehensive set of assays to measure the expression of all genes in the brain, as well as over 500 small molecules involved with metabolism in the brains and blood of three groups of the rapidly aging mice. The three groups of rapidly aging mice included one set that was young, one set that was old and one set that was old but fed J147 as they aged.

7 Benefits

The old mice fed J147 saw the following benefits:

1. They performed better on memory and other tests for cognition
2. They displayed more robust motor movements.
3. They had fewer pathological signs of Alzheimer's in their brains.
4. J147 prevented the leakage of blood from the microvessels in the brains of old mice. "Damaged blood vessels are a common feature of aging in general, and in Alzheimer's, it is frequently much worse," says Currais.
   
   Importantly, because of the large amount of data collected on the three groups of mice, it was possible to demonstrate that many aspects of gene expression and metabolism in the old mice fed J147 were very similar to those of the young animals. These included:
5. markers for increased energy metabolism,
6. reduced brain inflammation and
7. reduced levels of oxidized fatty acids in the brain.

Human Clinical Trials

Currais and Schubert note that while these studies represent a new and exciting approach to Alzheimer's drug discovery and animal testing in the context of aging, the only way to demonstrate the clinical relevance of the work is to move J147 into human clinical trials for Alzheimer's disease.

"If proven safe and effective for Alzheimer's, the apparent anti-aging effect of J147 would be a welcome benefit," adds Schubert. The team aims to begin human trials next year.

Related Article:

Curry Derivative J147 Beats Aricept for Alzheimer's

MORE INFORMATION:

• Other authors on the paper include Oswald Quehenberger of the University of California, San Diego; and Joshua Goldberg, Catherine Farrokhi, Max Chang, Marguerite Prior, Richard Dargusch, Daniel Daugherty and Pamela Maher of the Salk Institute.
• This study was supported by the Salk Institute Pioneer Fund Postdoctoral Scholar Award and the Salk Nomis Fellowship Award, fellowships from the Hewitt Foundation and Bundy Foundation, and grants from the Burns Foundation and NIH.

SOURCE:

• Salk Institute

Marijuana & Vascular Dementia

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The American College of Cardiology

As marijuana legalization spreads, new research is improving our understanding of side effects. Heart cells have cannabis receptors relevant to vascular squeezing ability. Learn about marijuana's link to vascular dementia. 

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WASHINGTON - Using marijuana raises the vascular risks of stroke and heart failure, major risk factors leading to vascular dementia. Even after accounting for demographic factors, other health conditions and lifestyle risk factors such as smoking and alcohol use, the data is compelling, according to research being presented at the American College of Cardiology’s 66th Annual Scientific Session.

Vascular Health

Coming at a time when marijuana, medically known as cannabis, is on track to become legal for medical or recreational use in more than half of U.S. states, this study sheds new light on how the drug affects vascular health. While previous marijuana research has focused mostly on pulmonary and psychiatric complications, the new study is one of only a handful to investigate cardiovascular outcomes. 

“Like all other drugs, whether they’re prescribed or not prescribed, we want to know the effects and side effects of this drug,” said Aditi Kalla, MD, Cardiology Fellow at the Einstein Medical Center in Philadelphia and the study’s lead author. “It’s important for physicians to know these effects so we can better educate patients, such as those who are inquiring about the safety of cannabis or even asking for a prescription for cannabis.”

Nationwide Inpatient Sample

The study drew data from the Nationwide Inpatient Sample, which includes the health records of patients admitted at more than 1,000 hospitals comprising about 20 percent of U.S. medical centers. Researchers extracted records from young and middle-aged patients—age 18-55 years—who were discharged from hospitals in 2009 and 2010, when marijuana use was illegal in most states. 

Marijuana use was diagnosed in about 1.5 percent (316,000) of more than 20 million health records included in the analysis. Comparing cardiovascular disease rates in these patients to disease rates in patients not reporting marijuana use, researchers found marijuana use was associated with a significantly increased risk for cardiovascular events such as stroke, heart failure, coronary artery disease and sudden cardiac death.

Marijuana - Independent Association

Marijuana use was also linked with a variety of factors known to increase cardiovascular risk, such as obesity, high blood pressure, smoking and alcohol use. After researchers adjusted the analysis to account for these factors, marijuana use was independently associated with a 26 percent increase in the risk of stroke and a 10 percent increase in the risk of developing heart failure. 

“Even when we corrected for known risk factors, we still found a higher rate of both stroke and heart failure in these patients, so that leads us to believe that there is something else going on besides just obesity or diet-related cardiovascular side effects,” Kalla said. “More research will be needed to understand the pathophysiology behind this effect.”

Heart Cells Have Canabis Receptors

Research in cell cultures shows that heart muscle cells have cannabis receptors relevant to contractility, or squeezing ability, suggesting that those receptors might be one mechanism through which marijuana use could affect the cardiovascular system. It is possible that other compounds could be developed to counteract that mechanism and reduce cardiovascular risk, Kalla said. 

Because the study was based on hospital discharge records, the findings may not be reflective of the general population. The study was also limited by the researchers’ inability to account for quantity or frequency of marijuana use, purpose of use (recreational or medical), or delivery mechanism (smoking or ingestion).

Further Insights

Kalla suggested that the growing trend toward legalization of marijuana could mean that patients and doctors will become more comfortable speaking openly about marijuana use, which could allow for better data collection and further insights into the drug’s effects and side effects. 

SOURCE:

• The American College of Cardiology
  The American College of Cardiology is a 52,000-member medical society that is the professional home for the entire cardiovascular care team. The mission of the College is to transform cardiovascular care and to improve heart health. The ACC leads in the formation of health policy, standards and guidelines. The College operates national registries to measure and improve care, offers cardiovascular accreditation to hospitals and institutions, provides professional medical education, disseminates cardiovascular research and bestows credentials upon cardiovascular specialists who meet stringent qualifications.

Detecting Alzheimer's disease earlier

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Eurekalert

LOUISVILLE, Ky. - Unique graphic characters called Greebles may prove to be valuable tools in detecting signs of Alzheimer's disease decades before symptoms become apparent.

In an article published online last week in Journal of Alzheimer's Disease, Emily Mason, Ph.D., a postdoctoral associate in the Department of Neurological Surgery at the University of Louisville, reported research showing that cognitively normal people who have a genetic predisposition for Alzheimer's disease (AD) have more difficulty distinguishing among novel figures called Greebles than individuals without genetic predisposition.

Alzheimer's disease (AD) is a progressive, irreversible neurodegenerative disease characterized by declining memory, cognition and behavior. AD is the most prevalent form of dementia, affecting an estimated 5.5 million individuals in the United States and accounting for 60 to 80 percent of dementia cases. The ability to detect the disease earlier may allow researchers to develop treatments to combat the disease.

"Right now, by the time we can detect the disease, it would be very difficult to restore function because so much damage has been done to the brain," Mason said. "We want to be able to look at really early, really subtle changes that are going on in the brain. One way we can do that is with cognitive testing that is directed at a very specific area of the brain."

AD is characterized by the presence of beta amyloid plaques and tau neurofibrillary tangles in the brain. Tau tangles predictably develop first in the perirhinal and entorhinal cortices of the brain, areas that play a role in visual recognition and memory. Mason and her colleagues developed cognitive tests designed to detect subtle deficiencies in these cognitive functions. They hoped to determine whether changes in these functions would indicate the presence of tau tangles before they could be detected through imaging or general cognitive testing.

Working in her previous position at Vanderbilt University, Mason identified test subjects age 40-60 who were considered at-risk for AD due to having at least one biological parent diagnosed with the disease. She also tested a control group of individuals in the same age range whose immediate family history did not include AD.

The subjects completed a series of "odd-man-out" tasks in which they were shown sets of four images depicting real-world objects, human faces, scenes and Greebles in which one image was slightly different than the other three. The subjects were asked to identify the image that was different.

The at-risk and control groups performed at similar levels for the objects, faces and scenes. For the Greebles, however, the at-risk group scored lower in their ability to identify differences in the images. Individuals in the at-risk group correctly identified the distinct Greeble 78 percent of the time, whereas the control group correctly identified the odd Greeble 87 percent of the time.

"Most people have never seen a Greeble and Greebles are highly similar, so they are by far the toughest objects to differentiate," Mason said. "What we found is that using this task, we were able to find a significant difference between the at-risk group and the control group. Both groups did get better with practice, but the at-risk group lagged behind the control group throughout the process."

Mason would like to see further research to determine whether the individuals who performed poorly on the test actually developed AD in the future.

"The best thing we could do is have people take this test in their 40s and 50s, and track them for the next 10 or 20 years to see who eventually develops the disease and who doesn't," Mason said.

In recent years, a great deal of research has focused on identifying early biomarkers of Alzheimer's disease. However, not everyone who has an individual biomarker ultimately develops the disease. Brandon Ally, Ph.D., assistant professor of neurological surgery at UofL and senior author of the publication, said the tests with Greebles can provide a cost-effective way to identify individuals who may be in the early stages of AD, as well as a tool for following those individuals over time.

"We are not proposing that the identification of novel objects such as Greebles is a definitive marker of the disease, but when paired with some of the novel biomarkers and a solid clinical history, it may improve our diagnostic acumen in early high-risk individuals," Ally said. "As prevention methods, vaccines or disease modifying drugs become available, markers like novel object detection may help to identify the high priority candidates."

Robert P. Friedland, M.D., professor and Mason and Mary Rudd Endowed Chair in Neurology at UofL, has studied clinical and biological issues in Alzheimer's disease and related disorders for 35 years. He believes that early detection will enhance the ability of patients and physicians to employ lifestyle and therapeutic interventions.

"This work shows that the effects of Alzheimer's disease on cognition can be measured decades before the onset of dementia," Friedland said. "The fact that the disease takes so long to develop provides us with an opportunity to slow its progression through attention to the many factors that are linked to the disease, such as a sedentary lifestyle, a high fat diet, obesity, head injury, smoking, and a lack of mental and social engagement."

###

The article, "Family history of Alzheimer's disease is associated with impaired perceptual discrimination of novel objects," will appear in the Journal of Alzheimer's Disease, Volume 57, Issue 2.

ANSWER: Greeble No. 4 is different.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

Dementia-Quadrupling Donepezil

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Alzheimer's and Dementia Weekly
Donepezil (Aricept) boosts memory & thinking in Alzheimer's. More donepezil means more boost - along with intensified side-effects. A new trial shows how donepezil can be safely boosted when combined with solifenacin. Find out more.

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IRVINE, California -- Donepezil helps Alzheimer's and other types of dementia. Doctors often minimize its use because it can have a variety of side-effects. New research shows that by adding solifenacin to each pill of donepezil, a patient could potentially boost the dosage by as much as 400% without added side-effects.

Here's a simplified explanation of how it works.

Early-to-Midstage Alzheimer's
Brand Name	Generic Name
Aricept®	donepezil
Exelon®	rivastigmine
Remynil or Razadyne®	galantamine
Drugs for Moderate-to-Severe Stage
Namenda® or Ebixa®	memantine

1. Acetylecholine is used by the brain to send messages from cell to cell.
2. If there is not enough acetylecholine in the brain, memory and thinking start to fail.
3. Alzheimer's often experiences dangerous drops in acetylcholine.
4. Donepezil helps boost the level of acetylcholine throughout the body.
5. This can help an Alzheimer's brain get back to normal. However, it can also overload other systems in the body, causing nausea, weight-loss and other side-effects.
6. The brain is separated from the rest of the body by the "blood-brain barrier".
7. A pill of donepezil travels from the stomach to the entire body. It passes through the blood-brain barrier, boosting acetylcholine in the brain.
8. Solifenacin is another drug that blocks donepezil. However, it CANNOT pass through the blood-brain barrier.
9. Therefore, it seems that solifenacin cannot get to the brain and as a result, cannot block donepezil in the brain.
10. At the same time, solifenacin can block donepezil everywhere else in the body, stopping side-effects like nausea in the stomach.
11. The result is no nausea or other side-effects in the body. The patient just gets the good effect in the brain.

For now, researchers call this combination of donepezil-plus-solifenacin by the name CPC-201. The new combination will mean that the brain can get the benefits of a lot more donepezil with fewer side-effects.


Chase Pharmaceuticals Corporation (Chase) announced its results from a Phase 2 study of CPC-201.

400%

The CPC-201 Phase 2 results, presented by Thomas Chase, MD, chief scientific officer and co-founder of Chase, and the former Scientific Director and head of the Experimental Therapeutics Branch for the National Institute of Neurological Disorders and Stroke, confirmed that solifenacin attenuated donepezil adverse events, enabling the tolerable administration of doses of donepezil to as much as 400 percent of the current standard treatment of donepezil. Secondary endpoints provided signals of enhanced efficacy, as would be predicted from increased tolerable dosing of donepezil. The data were presented during an oral session at the 2016 Alzheimer’s Association Conference (AAIC) in Toronto, Canada (Abstract a12446).

The primary endpoint of this Phase 2 single-blind, crossover trial was to safely increase the tolerated dose of donepezil from 10 mg/day up to as much as 40 mg/day. This trial consisted of 41 moderate (MMSE 10-20) Alzheimer’s type subjects who were being successfully treated with 10 mg/day of donepezil. The anticholinergic solifenacin was first titrated to 15 mg/day and then donepezil escalated to each subject’s maximum tolerated dose or to the protocol limit of 40 mg/day. Subjects then continued for a three-month maintenance period. All subjects were able to tolerably maintain above the currently approved doses of donepezil and 85 percent of subjects reached and tolerated the maximum allowable donepezil dose of 40 mg/day. Moreover, in the maintenance phase of the trial, subjects experienced significantly less dose-limiting side effects than those that would be predicted for 10 mg/day of donepezil. 

A Real Difference

Although this Phase 2 study was not designed nor powered to provide meaningful estimates of anti-dementia efficacy, both the ADAS-Cog and the CGI-I scales in the study yielded positive signals of enhanced efficacy. 

During the dose maintenance phase, at a median donepezil dose of 40 mg/day, total gastrointestinal adverse events were greatly attenuated and about 80 percent below those predicted from trials of previously approved doses of 10 mg/day of donepezil. As would be expected with a cholinergic blocker that does not cross the blood-brain barrier, solifenacin had no effect on cognitive function and there were no drug-related serious adverse events (SAE) or clinically significant cardiovascular or laboratory abnormalities. There were no drug related drop­outs and no new AEs or evidence of solifenacin toxicity.

“Pre-clinical studies have repeatedly shown that there is a strong dose/efficacy relationship associated with AChEIs. Further, PET scan studies in humans show that at the typical dose of 10 mg/day of donepezil, the central enzymatic inhibition is no greater than about 30 percent, substantially lower than that which would be expected from optimal dosing. Yet, historically, it has not been possible to tolerably increase the dose of donepezil to meaningfully higher levels,” said Douglas Ingram, chief executive officer of Chase. “We believe we have the means to finally unlock the true potential of optimally dosed AChEIs. Moreover, we are employing an efficient development and regulatory pathway and plan to commence a superiority trial versus the current gold-standard treatment for Alzheimer’s, 10 mg/day of donepezil. If successful in Phase 3, CPC-201 could be the new standard for the symptomatic treatment of Alzheimer's disease and benefit millions of suffering patients.”

What Do Aricept, Exelon & Razadyne Do?

Teepa Snow
MEDICATION VIDEO
See Teepa Snow talk about the top medications for Alzheimer's & dementia. In plain English, she explores what they do and how they work. Get clarity on Aricept, Exelon and Razadyne (generic donepezil, rivastigmine and galantamine). 

Technical Talk

“We believe that adverse events have long limited AChEI dosing to suboptimal levels, in turn limiting the efficacy of donepezil and other AChEIs,” said Thomas Chase, M.D. “Our Phase 2 findings, together with those from our earlier Phase 1 studies, robustly support our hypothesis that the co-formulation of a peripheral anticholinergic with donepezil enables the safe and tolerable administration of multiples of the current standard of care doses of AChEI such as donepezil.”

The mean change in ADAS-Cog over the course of the study showed improvement versus subject baseline and, adjusted for underlying disease progression using a multi-study meta-analysis, subjects showed a mean (± SEM) benefit of 2.45 points over 10 mg/day donepezil or 5.4 ± .84 points compared to predicted untreated disease progression. Combined Clinical Global Impression (CGI-I) scores from investigators and caregivers at 26 weeks averaged 3.1 ± .20 points, thus improving by .94 ± .20 points (p < .001; n = 16). The responder rate (as measured by those who either did not worsen or improved over the course of the study) was over 90 percent.

MORE INFORMATION:

About CPC-201
Chase’s lead candidate, CPC-201, is a patent-protected combination of donepezil (an AChEI), one of the few pharmaceuticals proven to improve cognition in Alzheimer’s patients, and solifenacin, a peripherally acting cholinergic blocker.

SOURCE:

About Chase
Chase Pharmaceuticals Corporation is a clinical-stage biopharmaceutical company focused on the development and commercialization of improved treatments for neurodegenerative disorders. Chase’s development program, if successful, will profoundly improve the symptomatic treatment of Alzheimer's disease. The company was co-founded by Thomas Chase, MD, the former Scientific Director and head of the Experimental Therapeutics Branch for the National Institute of Neurological Disorders and Stroke and Kathleen Clarence-Smith, MD, PhD, the former head of CNS development at each of Sanofi, Hoffmann-La Roche and Otsuka. Chase is led by its chief executive officer and president, Douglas Ingram, formerly the president of Allergan, Inc.

Chase has closed over $24 million in funding to date, with approximately $22 million through a Series B financing led by New Rhein Healthcare Investors, LLC and including, among others, Edmond de Rothschild Investment Partners, Cipla Ventures and Brain Trust Accelerator Fund.

EDITED BY:
Peter Berger

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I

Rosemary Emulates Aricept & Donepezil

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Alzheimer's and dementia weekly

Aricept^® (generic: donepezil) treats Alzheimer's by blocking AChE. Rosemary does that naturally. Learn about rosemary's dementia-fighting benefits from USDA Dr. J. Duke.

"Rosemary contains more than a dozen antioxidants and a half-dozen compounds reported to prevent the breakdown of acetylcholine. It's fabulous that the classical herb of remembrance has so many compounds that might help people suffering from Alzheimer's."

These are the words of Dr. James Duke, former U.S. Department of Agriculture (USDA) Chief of Medicinal Plant Research. 

Dr. Duke is one of the world's leading authorities on medicinal plants. He helped build the USDA database that demonstrates how rosemary may slow the progress of Alzheimer's.

Techtalk

How Aricept^® and Rosemary Help

The brain depends on a neurotransmitter called acetylcholine, or ACh for short. The brain keeps making fresh batches. In order to keep the brain from getting flooded with it, there is an "esterase" that breaks it down after use. Think of the esterase as the garbage truck, carting away extra acetylcholine. In Alzheimer's, there is a shortage of acetylcholine, so we want to inhibit (or block) the esterase (the garbage collector), so that more acetylcholine stays in the brain. To do that, a person needs to consume an acetylcholine esterase inhibitor, such as Aricept^® or rosemary.

His strong advocacy of rosemary has to do with a chemical called acetylcholine. Anyone who has lived with Alzheimer's in the past decade has heard of the drug Aricept^®, sold generically as donepezil. It is the #1 drug therapy for Alzheimer's.

Aricept^® is a medicine that does one thing: it prevents the breakdown of acetylcholine.

So does rosemary.

Dr. Duke said that when he learned of the new medications that fought Alzheimer's by inhibiting the breakdown of acetylcholine, "I probed my U.S. Department of Agriculture (USDA) database for herbs with phytochemical constituents that were also reported to prevent the breakdown of ACh (acetylcholine).

"Even though I myself had been the source of the overwhelming proportion of the data in the database for more than a decade, I was surprised at the output. The database yielded about a half dozen anti-AChE (acetylcholine esterase) compounds, with Rosmarinus officinalis (rosemary) the proud winner in terms of their numbers and potencies." 

Dr. Duke's Big Bet

Back in 1994, Dr. James Duke publicly bet his hair that rosemary shampoo would do as well as over-the-counter medication in helping the symptoms of Alzheimer's.

Why?

"Because," he said, "aromatic phytochemicals are absorbed transdermally through the pores in the scalp just as elsewhere on hairy areas of the body, so it would be a very good bet indeed that some of the volatile aromatic phytochemicals in rosemary shampoo would make their way into the circulation and thence to the brain."

Probing the USDA phytochemical database once again on Labor Day 2007, he found that rosemary has now been reported to contain nearly a dozen aromatic compounds potentially active against AChE (acetylcholine esterase). 

Dr. Duke shares more about that memory from three years ago. "On that same day I heard, at least thrice, a commercial broadcast on NBC telling listeners that Aricept^®(donepezil HCl), the most heavily promoted of synthetic anti-Alzheimer's drugs, probably modifies a neurotransmitter involved in Alzheimer's. But Aricept^® consists only of a single AChE inhibitor, and it's synthetic and unnatural; rosemary contains nearly a dozen!!" 

Extra Bonus

In addition to its benefits to memory and cognition, herbs like rosemary also contain thousands of phytochemicals that have other positive effects on health. In addition, aromatic herbs like rosemary will also produce an attractive aroma in the otherwise depressing environment that Alzheimer's can often induce. 

Dr. Duke's Takeaway

Dr. James Duke sums up with the following advice: "All of this leads me to conclude that rosemary shampoo, rosemary tea (and aromatic mint teas), and rosemary in skin lotions and in bath water are safe and pleasant ways to reduce the risk of Alzheimer's disease. And cholinergic foods… chased down with an anti-AChE herbal tea… would be my suggestion for retarding dementia."

Rosemary of Yore

• Sir Thomas Moore (1478-1535) wrote, "As for rosemary, I let it run all over my garden walls, not only because my bees love it but because it is the herb sacred to remembrance..."
• In ancient Greece, students wore sprigs of rosemary in their hair to fortify the brain and refresh the memory. In Greek mythology, Minerva, the goddess of knowledge, is associated with rosemary. Also part of Greek mythology were the nine daughters of Mnemosyne, or memory, who are often depicted as holding sprigs of rosemary.
• Rosemary has been used as a symbol for remembrance (during weddings, war commemorations and funerals) in Europe and Australia.
• Mourners would throw it into graves as a symbol of remembrance for the dead.
• In William Shakespeare's Hamlet, Ophelia chides Hamlet, saying, "There's rosemary, that's for remembrance; pray, love, remember." (Hamlet, iv. 5.)
• In 1607, Roger Hackett, one doctor of divinity of the time, said of rosemary that, "It helpeth the brain, strengtheneth the memorie and is very medicinable for the head."
• Rabbi Doctor Moses Maimonides, often deemed the greatest Talmudic scholar since Moses at Sinai, taught 800 years ago that tea made of rosemary leaves soothes the nerves, sharpens brain function and memory, and helps induce sleep.

Fighting dementia and insulin resistance

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Alzheimer's and dementia weekly

• EurekAlert
• 
  

New research shows memory and executive function are particularly vulnerable to the effects of insulin resistance. Learn how diet, exercise and watching your weight will prevent insulin-resistance, and as a result, protect your brain. 

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A new Tel Aviv University study published in the Journal of Alzheimer's Disease finds that insulin resistance, caused in part by obesity and physical inactivity, is also linked to a more rapid decline in cognitive performance. According to the research, both diabetic and non-diabetic subjects with insulin resistance experienced accelerated cognitive decline in executive function and memory. 

The study was led jointly by Prof. David Tanne and Prof. Uri Goldbourt and conducted by Dr. Miri Lutski, all of TAU's Sackler School of Medicine. 

"These are exciting findings because they may help to identify a group of individuals at increased risk of cognitive decline and dementia in older age," says Prof. Tanne. "We know that insulin resistance can be prevented and treated by lifestyle changes and certain insulin-sensitizing drugs. Exercising, maintaining a balanced and healthy diet, and watching your weight will help you prevent insulin resistance and, as a result, protect your brain as you get older."

A two-decade study

Insulin resistance is a condition in which cells fail to respond normally to the hormone insulin. The resistance prevents muscle, fat, and liver cells from easily absorbing glucose. 

As a result, the body requires higher levels of insulin to usher glucose into its cells. Without sufficient insulin, excess glucose builds up in the bloodstream, leading to prediabetes, diabetes, and other serious health disorders. 

The scientists followed a group of nearly 500 patients with existing cardiovascular disease for more than two decades. They first assessed the patients' baseline insulin resistance using the homeostasis model assessment (HOMA), calculated using fasting blood glucose and fasting insulin levels. Cognitive functions were assessed with a computerized battery of tests that examined memory, executive function, visual spatial processing, and attention. The follow-up assessments were conducted 15 years after the start of the study, then again five years after that. 

The study found that individuals who placed in the top quarter of the HOMA index were at an increased risk for poor cognitive performance and accelerated cognitive decline compared to those in the remaining three-quarters of the HOMA index. Adjusting for established cardiovascular risk factors and potentially confounding factors did not diminish these associations. 

"This study lends support for more research to test the cognitive benefits of interventions such as exercise, diet, and medications that improve insulin resistance in order to prevent dementia," says Prof. Tanne. The team is currently studying the vascular and non-vascular mechanisms by which insulin resistance may affect cognition. 

SOURCE:

• EurekAlert

Overuse of antipsychotropic meda affect those with Alzheimer's disease

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neuroscience news

Research lead is related to the use of psychotropic medications in Alzheimer’s patients. I should note that strong cautions have already been issued with respect to the use of these medications in the elderly (e.g. https://www.mind.uci.edu/alzheimers-disease/articles-of-interest/medications-to-avoid-for-patients/). As a practical matter, however, at present agitated and aggressive behaviors are considered a common symptom of advanced Alzheimer’s and therefore the use of these drugs as chemical restraints is common even by the most conservative physicians. Furthermore, as the medical profession is very diverse many physicians have not updated their practice and are far from cautious in prescribing these medications to the elderly. Indeed, chemical restraints are the norm in nursing home practice, so it is my belief that psychotropic medications are ubiquitous in nursing homes.

A family member is an active medical professional (a physician assistant who works as a front-line health care provider in a family practice office in rural America), so I have some insight into how a conservative medical practitioner will behave. I have observed two things: first, when a symptom is in the list of potential symptoms for a disease that has been diagnosed in the patient, there is a strong presumption that the symptom is caused by the disease. Second, when a symptom is a side effect of a medication (particularly one prescribed by another doctor), there is a presumption that the need for the medication outweighs the side effect.

A combination of close familiarity with my mother’s symptoms/behavior on and off a variety of drugs and my knowledge of the ubiquitous bank gaming of regulatory controls in financial markets leads me to wonder whether the drug companies aren’t playing the same kind of game. In particular the addition of “behavioral and psychological symptoms of dementia” (BPSD) to the criteria for the diagnosis of late-stage Alzheimer’s is as far as I can tell of very recent vintage. (I believe they were introduced with the DSM-5 in 2013.) BPSD are symptoms treated by psychotropic medications. These same medications are also commonly used to treat mild sleep and anxiety disorders in the general population.

The problem with all the psychotropic medications is that they are used to treat the same behaviors that they can also cause as side effects, including irritability, anxiety, “disinhibition” which maps into a willingness to hit out at or behave abusively to others, aggressiveness, and self-harm. In sufficiently high doses, however, the patient is heavily sedated and they are very effective chemical restraints.

My suspicion is that the introduction of BPSD into the definition of common symptoms of Alzheimer’s has developed as a result of the ubiquitous use of psychotropic medications in this population. That is, as far as I can tell the studies that have found BPSD to be common in Alzheimer’s are population-based studies that did not control for the use of medications that have as side effects BPS behaviors. Successfully bringing BPSD into the clinical definition of Alzheimer’s is hugely profitable for the drug companies that now have physician’s biases – to attribute symptoms to the disease that has already been diagnosed, rather than to the drug that may cause it as a side effect – working on their side.

In short, what I would really like to see is a careful statistician’s review of the studies that find that BPSD are common symptoms of Alzheimer’s and an analysis of whether sufficient controls for the use of medicines that have as side effects the same symptoms have been implemented. (With psychotropic medications, the length of use is an important factor because they build up in the system. Thus long-term use has different effects from short-term use. Long-term prescriptions are not a good proxy for long-term use, since refill/renewal of shorter term prescriptions is common practice.)