Archives for June 2016

Pat Summitt Showed Just How Wrong Alzheimer’s Stereotypes Are

(Time) The disease takes many terrible forms.

In the fell clutch of circumstance
I have not winced nor cried aloud.
Under the bludgeonings of chance
My head is bloody, but unbowed.

—William Ernest Henley, “Invictus”

There are great parallels between William Henley’s Victorian poem “Invictus” and consummate coach Pat Summitt, who succumbed to Alzheimer’s after a battle beyond the clash of even the greatest basketball games. Wrote Henley in his seminal 1888 poem about the throes of unthinkable struggle,

“I am the master of my fate; I am the captain of my soul.”

Summitt indeed was captain of her soul, with a legacy that far exceeds her record 1,098 wins and eight national championships as coach of the Lady Volunteers at University of Tennessee. Always the mentor and teacher, even when her memory and mind failed her, she led quietly.

“There’s not going to be any pity party, and I’ll make sure of that,” she told the Knoxville News Sentinel in 2011 after announcing her Early Onset Alzheimer’s diagnosis.

“Obviously, I realize I may have some limitations with this condition since there will be some good days and some bad days.”

Though cut from my freshman high school basketball team, I know something of Summitt’s struggle. I was diagnosed with Early Onset Alzheimer’s in 2009 after experiencing the horrific symptoms of short-term memory loss, inability to recognize individuals and places I’ve known all my life, difficulty completing simple tasks, terrible judgment, confusion with time and place, intense withdrawal and challenges with problem-solving and spatial relationships. The diagnosis came two weeks after I was diagnosed with prostate cancer, which in consult with my doctors and family, I am not treating. It is my exit strategy.

You can’t remove a brain.

I carry the marker gene for Alzheimer’s. It runs on both sides of my family. My maternal grandfather and my mother died of Alzheimer’s in bruising prizefights like Summitt’s; my paternal uncle died of Alzheimer’s about two years ago; and before my father’s death, he was diagnosed with dementia.

A death in slow motion, Alzheimer’s can take twenty to twenty-five years to run its serpentine course. It’s like having a sliver of your brain shaved away every day. Some with the disease are taken earlier. Like a snowflake, no two patterns are identical, which confounds researchers in finding a cure.

So those with the disease march on, like Pat, feeling intensely alone. Beyond the shadows of others, they quietly fend off the debilitating symptoms, the loss of self-esteem, the taboo of losing what is most precious to us.

The stereotype of Alzheimer’s is not factual—an end stage for 85-year-olds in a nursing home. As the great Bugs Bunny once observed (adopting a line from the writer Elbert Hubbard), “Like the man said: don’t take life too seriously. No one gets out of it alive.” Until we understand collectively that Alzheimer’s strikes people in the prime of life—individuals at first glance who seem just like you—there will be no critical mass to demand a cure for this disease that is poised to annihilate the Baby Boomer generation and generations to come. It’s been said that in 25 years there will be two kinds of people—those with Alzheimer’s and those caring for someone with Alzheimer’s. Pat Summitt did not want, nor do I want, your pity. Please understand this could be your story some day.

I’ll never forget sitting in the neurologist office outside Boston, side-by-side with my wife Mary Catherine, listening to the diagnosis. I felt as though I was slipping into Louis Carroll’s Alice in Wonderland, where “nothing would be what it is, because everything would be what it isn’t.”

What “would be” was devastating. I felt the tears running down the sides of my face. My eyes didn’t blink. I reached for my wife’s hand and asked: “What about the kids?” I felt so isolated. Yet, I was overcome with sadness for my wife. This wasn’t fair to her. And I couldn’t fix it.

Dammit, I couldn’t fix it!

I focus every day on living with Alzheimer’s. The death part—thank you, Bugs—comes later. What was once familiar is now fleeting. Today, I have little short-term memory, a progression of blanks, analogous to someone shutting off a light in my brain. Close to 60 percent of what I take in can now be gone in 30 seconds. It is dispiriting to lose a thought in a second. There are 86,400 seconds a day—to stand exposed, and yet stand one’s ground, to begin to grasp in fundamental, naked terms who one really is, the good, the bad, and the ugly.

The ugly is unnerving. I often fly into inexorable rage and hurl the phone across the room, a perfect strike to the sink, when I can’t remember how to dial. I smash the lawn sprinkler against an oak tree in the backyard because I don’t recall how it works. My skin melts in a second-degree burn when I push open with a bare hand the flaming-hot glass door to the family room wood stove to stoke the fire. And I cry privately, the tears of a little boy, because I fear I’m alone, nobody cares, and the innings are starting to fade.

And then there are the terrifying days of hallucinations and delusions, caused by changes in the brain, common in Alzheimer’s and dementia patients—false impressions of objects, events and sensory perceptions like smell, taste or imagined voices. The hallucinations are the most troubling, as they were for my mother: those spider-like creatures that crawl regularly, some in sprays of blood, along the ceiling at different times of day, sometimes in a platoon, that turn at 90-degree angles, then inch a third of the way down the wall before floating toward me. I brush them away, almost in amusement, knowing for now they are not real, yet still fearful of their representation of my cognitive decline. On a recent morning, I hallucinated a bird in my bedroom circling above me in ever-tighter orbits. Then precipitously the bird dove to my chest in a suicide mission. I screamed in horror.

In Alzheimer’s, I’ve learned, the brain’s ability to process shrinks. Literally. As the brain shrinks, it instinctively makes decisions on what functions to power and what functions to power down to preserve fuel. Years ago, I thought I was Clark Kent, an award-winning investigative reporter. I even wore at times in amusement a trademark blue T-shirt with the iconic Superman shield under my Brooks Brothers dress shirt. But these days, I feel more like a baffled Jimmy Olsen, the fictional fledgling photojournalist from the Daily Planet. Or on days of muddle, more like Mr. Magoo, the wispy cartoon character created in 1949 who couldn’t see straight, exacerbated by his stubbornness to acknowledge a problem. Or like Mr. Potato Head, with the wacky pushpins and all. Or like a codfish landed on a steamy Cape Cod dock. A fish rots from the head down.

Perhaps Ernest Hemingway said it best when he observed, “The world breaks everyone, and afterward, some are strong at the broken places.”

Pat Summitt, unbowed, was strong in the broken places. She fought with gut instincts in faith, hope and humor.

In death, as in life, she will always be our coach.


Can Alzheimer’s Be Stopped?

( Alzheimer’s disease strikes at the core of what makes us human: our capacity to think, to love, and to remember. The disease ravages the minds of over 40 million victims worldwide, and it is one of the greatest medical mysteries of our time.

Join investigators as they gather clues and attempt to reconstruct the molecular chain of events that ultimately leads to dementia, and follow key researchers in the field who have helped to develop the leading theories of the disease.

Along the way, meet individuals from all walks of life who will reveal what it’s like to struggle with Alzheimer’s. Among them, members of a unique Colombian family who have learned that their genetic predisposition all but guarantees early onset Alzheimer’s.

Yet there may be hope. Join these courageous patients participating in clinical trials, and then go behind the scenes of the major drug trials to see how researchers target and test therapies that may slow and even prevent Alzheimer’s.

Watch the full program here. It aired April 13, 2016 on PBS.



Website © 1996–2016 WGBH Educational Foundation


New Link Found Between Diabetes, Alzheimer’s Disease

(Diabetologia via ScienceDaily) Drugs used to treat diabetes could also be used to treat Alzheimer’s disease, and vice versa, according to new research from the University of Aberdeen.

This is also the first study of its kind to show that Alzheimer’s disease can lead to diabetes, as opposed to diabetes occurring first as was previously thought.

The study reports that Alzheimer’s Disease and type 2 diabetes are so closely related that drugs currently used to control glucose levels in diabetes may also alleviate the symptoms and progression of Alzheimer’s disease.

The paper, published in the journal Diabetologia (the journal of the European Association for the Study of Diabetes), found for the first time that dementia-related complications within the brain can also lead to changes in glucose handling and ultimately diabetes. This is contrary to what was previously thought — that diabetes begins with a malfunction in the pancreas or a high fat, high sugar diet.

The research was led by Professor Bettina Platt who formed a unique collaboration between her Alzheimer’s research team and the diabetes research team led by Professor Mirela Delibegovic. The teams were keen to investigate why the two diseases are so commonly found together in elderly patients.

The researchers developed a model of Alzheimer’s disease and were surprised to find that increased levels of a gene involved in the production of toxic proteins in the brain not only led to Alzheimer’s -like symptoms, but also to the development of diabetic complications.

Professor Platt said of her research:

“Many people are unaware of the relationship between diabetes and Alzheimer’s disease, but the fact is that around 80% of people with Alzheimer’s disease also have some form of diabetes or disturbed glucose metabolism. This is hugely relevant as Alzheimer’s is in the vast majority of cases not inherited, and lifestyle factors and comorbidities must therefore be to blame.

“Our research teams are particularly interested in the impact of lifestyle related factors in dementia and by collaborating with experts in diabetes and metabolism, we have been able to investigate the nature of the link in great detail.

“Until now, we always assumed that obese people get type 2 diabetes and then are more likely to get dementia — we now show that actually it also works the other way around.

“Additionally, it was previously believed that diabetes starts in the periphery, i.e. the pancreas and liver, often due to consumption of an unhealthy diet, but here we show that dysregulation in the brain can equally lead to development of very severe diabetes — so again showing that diabetes doesn’t necessarily have to start with your body getting fat — it can start with changes in the brain.

“This study provides a new therapeutic angle into Alzheimer’s disease and we now think that some of the compounds that are used for obesity and diabetic deregulation might potentially be beneficial for Alzheimer’s patients as well.

The good news is that there are a number of new drugs available right now which we are testing to see if they would reverse both Alzheimer’s and diabetes symptoms.

We will also be able to study whether new treatments developed for Alzheimer’s can improve both, the diabetic and cognitive symptoms.”


Story Source:

The above post is reprinted from materials provided by Diabetologia. Note: Materials may be edited for content and length.

Journal Reference:

Kaja Plucińska, Ruta Dekeryte, David Koss, Kirsty Shearer, Nimesh Mody, Phillip D. Whitfield, Mary K. Doherty, Marco Mingarelli, Andy Welch, Gernot Riedel, Mirela Delibegovic, Bettina Platt. Neuronal human BACE1 knockin induces systemic diabetes in mice. Diabetologia, 2016; 59 (7): 1513 DOI: 10.1007/s00125-016-3960-1

Copyright 2016 ScienceDaily or by third parties, where indicated.


Reversal of Memory Loss from Alzheimer’s Disease in Ten Patients

(Buck Institute for Research on Aging) Small trial from the Buck Institute and UCLA succeeds using systems approach to memory disorders.

Results from quantitative MRI and neuropsychological testing show unprecedented improvements in ten patients with early Alzheimer’s disease (AD) or its precursors following treatment with a programmatic and personalized therapy.  Results from an approach dubbed metabolic enhancement for neurodegeneration are now available online in the journal Aging.

The study, which comes jointly from the Buck Institute for Research on Aging and the UCLA Easton Laboratories for Neurodegenerative Disease Research is the first to objectively show that memory loss in patients can be reversed, and improvement sustained, using a complex, 36-point therapeutic personalized program that involves comprehensive changes in diet, brain stimulation, exercise, optimization of sleep, specific pharmaceuticals and vitamins, and multiple additional steps that affect brain chemistry.

“All of these patients had either well-defined mild cognitive impairment (MCI), subjective cognitive impairment (SCI) or had been diagnosed with Azheimer’s disease before beginning the program,”

said author Dale Bredesen, MD, a professor at the Buck Institute and professor at the Easton Laboratories for Neurodegenerative Disease Research at UCLA, who noted that patients who had had to discontinue work were able to return to work and those struggling at their jobs were able to improve their performance.

“Follow up testing showed some of the patients going from abnormal to normal.”

One of the more striking cases involved a 66-year old professional man whose neuropsychological testing was compatible with a diagnosis of MCI and whose PET scan showed reduced glucose utilization indicative of AD. An MRI showed hippocampal volume at only the 17th percentile for his age. After 10 months on the protocol a follow-up MRI showed a dramatic increase of his hippocampal volume to the 75th percentile, with an associated absolute increase in volume of nearly 12 percent.

In another instance, a 69-year old professional man and entrepreneur, who was in the process of shutting down his business, went on the protocol after 11 years of progressive memory loss. After six months, his wife, co-workers and he noted improvement in memory. A life-long ability to add columns of numbers rapidly in his head returned and he reported an ability to remember his schedule and recognize faces at work. After 22 months on the protocol he returned for follow-up quantitative neuropsychological testing; results showed marked improvements in all categories with his long-term recall increasing from the 3rd to 84th percentile. He is expanding his business.

Another patient, a 49-year old woman who noted progressive difficulty with word finding and facial recognition went on the protocol after undergoing quantitative neuropsychological testing at a major university. She had been told she was in the early stages of cognitive decline and was therefore ineligible for an Alzheimer’s prevention program. After several months on the protocol she noted a clear improvement in recall, reading, navigating, vocabulary, mental clarity and facial recognition. Her foreign language ability had returned. Nine months after beginning the program she did a repeat of the neuropsychological testing at the same university site. She no longer showed evidence of cognitive decline.

All but one of the ten patients included in the study are at genetic risk for AD, carrying at least one copy of the APOE4 allele. Five of the patients carry two copies of APOE4 which gives them a 10-12 fold increased risk of developing AD.

“We’re entering a new era,” said Bredesen.

“The old advice was to avoid testing for APOE because there was nothing that could be done about it. Now we’re recommending that people find out their genetic status as early as possible so they can go on prevention.”

Sixty-five percent of the Alzheimer’s cases in this country involve APOE4; with seven million people carrying two copies of the ApoE4 allele.

Bredesen’ s systems-based approach to reverse memory loss follows the abject failure of monotherapies designed to treat AD and the success of combination therapies to treat other chronic illnesses such as cardiovascular disease, cancer and HIV. Bredesen says decades of biomedical research, both in his and other labs, have revealed that an extensive network of molecular interactions is involved in AD pathogenesis, suggesting that a broader-based therapeutic approach may be more effective.

“Imagine having a roof with 36 holes in it, and your drug patched one hole very well—the drug may have worked, a single ‘hole’ may have been fixed, but you still have 35 other leaks, and so the underlying process may not be affected much,” Bredesen said.

“We think addressing multiple targets within the molecular network may be additive, or even synergistic, and that such a combinatorial approach may enhance drug candidate performance, as well.”

While encouraged by the results of the study, Bredesen admits more needs to be done.

“The magnitude of improvement in these ten patients is unprecedented, providing additional objective evidence that this programmatic approach to cognitive decline is highly effective,” Bredesen said.

“Even though we see the far-reaching implications of this success, we also realize that this is a very small study that needs to be replicated in larger numbers at various sites.”

Plans for larger studies are underway.

Cognitive decline is often listed as the major concern of older adults. Already, Alzheimer’s disease affects approximately 5.4 million Americans and 30 million people globally. Without effective prevention and treatment, the prospects for the future are bleak. By 2050, it’s estimated that 160 million people globally will have the disease, including 13 million Americans, leading to potential bankruptcy of the Medicare system. Unlike several other chronic illnesses, Alzheimer’s disease is on the rise–recent estimates suggest that AD has become the third leading cause of death in the United States behind cardiovascular disease and cancer.

Dr. Bredesen’s book describing for a broad audience the interventions described in this paper, will be released by Penguin Random House in May 2017. Dr. Bredesen hopes to eventually transform the perception and reality of Alzheimer’s disease from a death sentence to a preventable and reversible condition.

Citation: Reversal of Cognitive Decline in Alzheimer’s Disease

Other collaborators on the study include Edwin C. Amos, Jonathan Canick, Mary Ackerley, Cyrus Raji, Milan Fiala, and Jamila Ahdidan.  Multiple entities provided support for the research which supported the study. They include the National Institutes of Health (AG16570, AG034427 and AG036975). Please see paper for the complete list.

The Buck Institute for Research on Aging is the U.S.’s first independent research organization devoted to Geroscience – focused on the connection between normal aging and chronic disease. Based in Novato, CA, The Buck is dedicated to extending “Healthspan”, the healthy years of human life and does so utilizing a unique interdisciplinary approach involving laboratories studying the mechanisms of aging and those focused on specific diseases. Buck scientists strive to discover new ways of detecting, preventing and treating age-related diseases such as Alzheimer’s and Parkinson’s, cancer, cardiovascular disease, macular degeneration, osteoporosis, diabetes and stroke.  In their collaborative research, they are supported by the most recent developments in genomics, proteomics, bioinformatics and stem cell technologies. For more information:

The Easton Laboratories for Neurodegenerative Disease Research are part of the UCLA Department of Neurology which encompasses more than 26 disease-related research programs. This includes all of the major categories of neurological diseases and methods, encompassing neurogenetics and neuroimaging as well as health services research. The 140 faculty members of the Department are distinguished scientists and clinicians who have been ranked #1 in NIH funding for 9 consecutive years beginning in 2002. The Department is dedicated to understanding the human nervous system and improving the lives of people with neurological diseases, focusing on three key areas: patient/clinical care, research, and education. For more information, see


© Buck Institute


New Alzheimer’s Disease Drug May Help People at Risk

( Alzheimer’s disease affects more than 5 million Americans — and according to the Alzheimer’s Association, every 66 seconds someone in the U.S. develops the disease. Today, there is hope for people with Alzheimer’s and those at risk: A new drug aims to stop the disease before symptoms start.

Harvard neurologist and Alzheimer’s researcher at Brigham and Women’s Hospital in Boston, Massachusetts, Dr. Reisa Sperling, is leading the new drug trial, and believes it will be a game changer.

“We’re really trying to detect Alzheimer’s disease before symptoms (start) and try to prevent people from developing the devastating memory loss,” Sperling told TODAY.

The 3 1/2-year study will monitor patients’ cognitive skills and brains to see if the drug has an impact, compared to people taking a placebo.

So how does it work? Alzheimer’s is associated with heavy protein buildup in the brain, referred to as amyloid. This buildup is linked to cognitive decline and memory loss. The new drug, solanezumab, is designed to stop the amyloid buildup in patients who experience early warning signs. It’s currently being tested in the Anti-Amyloid Treatment in Asymptomatic Alzheimer’s study (A4 study, for short).

“We want to help people live their lives with dignity and end their lives ballroom dancing, instead of in nursing homes,” Sperling said.

Research suggests that lifestyle factors can also help to boost your brain. Dr. David Perlmutter recommends steering clear of sugar and carbs, which can lead to the production of free radicals, which in turn may cause brain deterioration. Instead, he advises to follow a diet high in antioxidants, prebiotic fiber and healthy fats.

“It’s never too late to change your diet and begin some aerobic exercise,” Perlmutter told TODAY. “Research demonstrates that even in our 70s, even in our 80s, we have the ability to increase the growth of new brain cells.”

Though it’s important to note that these lifestyle changes are not a cure to the disease.

The A4 Study

The A4 Study is a landmark public-private partnership, funded by the National Institutes of Health, Eli Lilly and Company, and several philanthropic organizations. It is coordinated by the Alzheimer’s Therapeutic Research Institute, located at the University of Southern California.

See a list of study sites.

Research is taking place at 56 U.S. sites, as well as four sites in Canada and one in Australia.

You may qualify for the A4 study if you:

  • Are 65 to 85 years old
  • Have normal thinking and memory abilities
  • Have elevated levels of amyloid in the brain, as shown by a PET brain scan
  • Have a family member, friend, or other person with whom you have contact at least once a week who can answer questions about you once a year (contact may be in person or by phone)
  • Are willing and able to receive IV infusions of the investigational treatment (solanezumab) or a placebo every 4 weeks for 3 years
  • Are willing to have your health monitored using:
    • memory and thinking tests
    • electrocardiograms to look at your heart
    • PET scan to look for amyloid plaques associated with Alzheimer’s
    • MRI scans, another type of brain scan
    • blood and urine tests

People who do not qualify for the main A4 study may be asked to participate in a separate study, in which they will take memory tests every 6 months.

To find out more about A4:

View a video with Dr. Sperling:

View the video with Spanish subtitles:



By Gabrielle Frank, Today

Copyright NBCUniversal Media, LLC

The A4 Study


Undiagnosed Dementia May Be Putting Older Adults’ Safety at Risk

(MedicalNewsToday) Many older Americans may be at increased risk of engaging in potentially unsafe activities due to lack of dementia diagnosis. This is the conclusion of a new study by researchers from Johns Hopkins University School of Medicine in Baltimore, MD.

The study found that older adults who had symptoms of dementia but who had not been formally diagnosed were almost twice as likely to drive, cook, manage medication, or undertake other activities that might put them in harm’s way, compared with adults who had received a dementia diagnosis.

Lead author Dr. Halima Amjad, of the Division of Geriatric Medicine and Gerontology at Johns Hopkins, and colleagues recently published their findings in the Journal of the American Geriatrics Society.

Dementia is a term used to describe a number of diseases characterized by a decline in memory and thinking skills. Alzheimer’s disease is the most common form of dementia, accounting for around 60-80 percent of all cases.

Symptoms of dementia may vary from person to person, though problems with short-term memory – such as remembering to pay bills, keeping track of a wallet or keys, or remembering appointments – reduced concentration, and poor reasoning and judgment are common signs.

At present, there is no single test to diagnose dementia; Alzheimer’s and other forms of dementia are diagnosed based on the individual’s medical history, a physical examination, and changes in memory and everyday functioning and behavior.

Comparing Unsafe Sctivity in Fiagnosed vs. Undiagnosed Dementia

Previous studies have shown that individuals with dementia are at greater risk for safety issues when engaging in certain activities, compared with those without the condition.

However, Dr. Amjad and colleagues note that such studies have included a small number of patients and have only investigated the effect of dementia on single issues.

For this latest research, the team analyzed data of 7,609 adults aged 65 and older who were part of the National Health and Aging Trends Study (NHATS) – an ongoing Johns Hopkins study that started in 2011.

As part of this study, participants underwent regular in-person interviews, which gathered a wealth of information, including data on daily life activities, living arrangements, and well-being.

Participants also underwent regular cognitive tests and physical examinations, used to assess their health as they aged.

For the purpose of their investigation, Dr. Amjad and colleagues allocated the participants to one of four groups:

  • Adults who had received a formal diagnosis of dementia from a doctor, based on reports of such a diagnosis from themselves or a companion
  • Adults who had dementia based on cognitive test scores and interviews, but who had not been formally diagnosed by a doctor – defined as having “undiagnosed” dementia
  • Adults with possible dementia
  • Adults without dementia.

The team analyzed subjects’ engagement in any activities that could be deemed unsafe to participate in with symptoms of dementia, such as driving, caring for another person, managing finances, handling medication, and preparing hot meals.

Awareness of Functional Problems Lacking with Undiagnosed Dementia

The results of the study did present some good news. Compared with adults who had possible dementia or no dementia, those who had diagnosed or undiagnosed dementia were less likely to engage in potentially unsafe activities.

For example, only 23 percent of older adults with undiagnosed dementia engaged in driving, compared with 59 percent of those with possible dementia and 84 percent without dementia.

“That in itself is good news, though the numbers are still important from a public health and safety standpoint,” notes Dr. Amjad. “Either the patients themselves or their family members are self-regulating and doing these activities less frequently as their disease is progressing.”

However, the study results also revealed that, compared with adults who had received a formal diagnosis of dementia, those with undiagnosed dementia were much more likely to participate in unsafe activities.

For instance, they found that around 28 percent of adults with undiagnosed dementia engaged in driving, compared with almost 17 percent of those with diagnosed dementia.

Around 29 percent of adults with undiagnosed dementia were still handling their finances, compared with only 12 percent of those with diagnosed dementia.

A total of 42 percent of those with undiagnosed dementia continued to prepare hot meals, compared with just 17 percent of those with diagnosed dementia.

Furthermore, around 50 percent of adults with undiagnosed dementia were still preparing their own medication, compared with 22 percent with diagnosed dementia.

“When patients receive a formal dementia diagnosis, their families are typically aware that, at some point, their loved ones will not be able to drive or will need more help with their medicine,” explains Dr. Amjad.

“But when people are undiagnosed, families and friends may ignore or be unaware of functional problems that already exist.”

A ‘Wake-up Call’ for Doctors, Families of Older Adults

According to study co-author David Roth, Ph.D., director of the Johns Hopkins Center for Aging and Health, the findings raise some important questions about dementia diagnosis.

“First, are those with dementia receiving adequate medical care, including accurate and up-to-date diagnoses?” she asks. “Second, are diagnoses of dementia being properly communicated to patients and their families?”

Dr. Amjad adds that the results should be a “wake-up call” for doctors who care for the elderly and the families of loved ones who might be in the early stages of dementia.

“If elderly patients are having difficulty with activities, they may benefit from a physician formally screening them for dementia.

But families are really the front line in recognizing when someone shouldn’t be driving or needs more help with managing medicines. That means being watchful and aware as loved ones get older and dementia is more likely.”


MediLexicon International Ltd, Bexhill-on-Sea, UK

© 2004-2016 All rights reserved.


Understanding How Chemical Changes in the Brain Affect Alzheimer’s Disease

(University of Western Ontario) A new study from Western University is helping to explain why the long-term use of common anticholinergic drugs used to treat conditions like allergies and overactive bladder lead to an increased risk of developing dementia later in life. The findings show that long-term suppression of the neurotransmitter acetylcholine – a target for anticholinergic drugs – results in dementia-like changes in the brain.

“There have been several epidemiological studies showing that people who use these drugs for a long period of time increase their risk  of developing dementia,” said  Marco Prado, PhD, a Scientist at the Robarts Research Institute and Professor in the departments of Physiology and Pharmacology and Anatomy & Cell Biology at Western’s Schulich School of Medicine & Dentistry.

“So the question we asked is ‘why?’”

For this study, published in the journal Cerebral Cortex, the researchers used genetically modified mouse models to block acetylcholine in order to mimic the action of the drugs in the brain. Neurons that use acetylcholine are known to be affected in Alzheimer’s disease; and the researchers were able to show a causal relationship between blocking acetylcholine and Alzheimer’s-like pathology in mice.

“We hope that by understanding what is happening in the brain due to the loss of acetylcholine, we might be able to find new ways to decrease Alzheimer’s pathology,” said Prado.

Prado and his partner Dr. Vania Prado, DDS, PhD, along with PhD candidates Ben Kolisnyk and Mohammed Al-Onaizi, have shown that blocking acetylcholine-mediated signals in neurons causes a change in approximately 10 per cent of the Messenger RNAs in a region of the brain responsible for declarative memory. Messenger RNA encodes for specific amino acids which are the building blocks for proteins and several of the changes they uncovered in the brains of mutant mice are similar to those observed in Alzheimer’s disease.

“We demonstrated that in order to keep neurons healthy you need acetylcholine,” said Prado.

“So if acetylcholine actions are suppressed, brain cells respond by drastically changing their messenger RNAs and when they age, they show signs of pathology that have many of the hallmarks of Alzheimer’s disease.”

Importantly, by targeting one of the messenger RNA pathways they uncovered, the researchers improved pathology in the mutant mice.

The study, conducted at Western’s Robarts Research Institute, used human tissue samples to validate the mouse data and mouse models to show not only the physical changes in the brain, but also behavioral and memory changes. The researchers were able to show that long-term suppression of acetylcholine caused brain cells to die and as a consequence decrease memory in the aging mice.

“When the mutant mice were old, memory tasks they mastered at young age were almost impossible for them, whereas normal mice still performed well,” said Kolisnyk.

The researchers hope their findings will have an impact on reducing the burden of dementia by providing new ways to reverse the loss of acetylcholine.

The researchers were supported by CIHR, Brain Canada and NSERC and the work was done in collaboration with researchers at the UCL Institute of Neurology, The Hebrew University of Jerusalem and McMaster University.

Citation 2016/06/22/understanding-chemical-changes-brain-affect-alzheimers-disease/

© 1878 – 2016 Western University


10 Ways for Caregivers to Nurture Themselves

( En español | When caregivers are on call around the clock, they are often so selfless in their care of a loved one that they neglect to take care of themselves.

Did you know caregivers have a higher-than-normal incidence of getting sick? They can become so depleted that they cannot maintain the stamina to continue caring for others.

Don’t let this happen to you. Follow these 10 tips to nurture yourself physically, mentally and spiritually every day, even when you are at the bedside of another. Following these tips will help you find the health and happiness you deserve. And when you take care of yourself, you can care for your loved one even better.

1. Eat well-balanced meals

And do so on a regular schedule. Take a daily multivitamin. Drink six to eight glasses of water a day.

2. Exercise every day

Move your body daily, even if it’s simply 15 minutes of stretching, yoga, calisthenics or walking. Use the stairs to keep your circulation going.

3. Get outdoors

Fresh air renews the body and spirit — even if you only have time for a brief outing. When possible, open a window.

4. Get your zzz’s

Strive for a minimum of seven to eight hours of consecutive sleep in a 24-hour period. Nap when your loved one naps.

5. Treat yourself

That is, get treatments for your own aches and pains before they turn into something more serious.

6. Don’t ignore your emotions

Pay attention to your own feelings and emotions, and seek counseling if needed. Vent feelings to trusted family members or friends.

7. Take time for yourself

Use relaxation or stress management methods such as meditation, visualization and yoga. Books and videos are available to guide you in these techniques.

8. Read, pray or meditate for at least 15 minutes a day

Consume daily prayer books and helpful magazines like Today’s Caregiver and Caring Today, or books such as Chicken Soup for the Caregiver’s Soul to uplift your spirits. If you’re religious, seek the counsel of a spiritual leader you trust and respect.

9. Chuckle more often

Laugh, reminisce and share stories of happy times.

10. Ask for help

Friends, family and religious groups may be eager to assist and are only waiting to be asked and directed. Doing everything yourself deprives others of an opportunity to serve.

See also: 

Nurturing your relationships

Wanna talk? Need to vent? Need advice? Chat online with other caregivers in the same situation.


AARP is a nonprofit, nonpartisan organization that helps people 50 and older improve the quality of their lives.

Copyright 2016 AARP