Alzheimer's and link to high blood sugar

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• University of Bath

SUGAR'S TIPPING POINT: Molecular links between blood sugar and Alzheimer’s were established by scientists. They show how excess blood sugar damages a vital enzyme involved with early-stage Alzheimer’s. Learn more about sugar & Alzheimer's. 

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Abnormally high blood sugar (also called glucose) levels, or hyperglycaemia, is well-known as a characteristic of diabetes and obesity, but its link to Alzheimer’s disease is less familiar. 

Diabetes patients have an increased risk of developing Alzheimer’s disease compared to healthy individuals. In Alzheimer’s disease abnormal proteins aggregate to form plaques and tangles in the brain which progressively damage the brain and lead to severe cognitive decline.

The Link

Scientists already knew that glucose and its break-down products can damage proteins in cells via a reaction called glycation but the specific molecular link between glucose and Alzheimer’s was not understood. 

But now scientists from the University of Bath Departments of Biology and Biochemistry, Chemistry and Pharmacy and Pharmacology, working with colleagues at the Wolfson Centre for Age Related Diseases, King’s College London, have unraveled that link. 

By studying brain samples from people with and without Alzheimer’s using a sensitive technique to detect glycation, the team discovered that in the early stages of Alzheimer’s glycation damages an enzyme called MIF (macrophage migration inhibitory factor) which plays a role in immune response and insulin regulation.

The Tipping Point

MIF is involved in the response of brain cells called glia to the build-up of abnormal proteins in the brain during Alzheimer’s disease, and the researchers believe that inhibition and reduction of MIF activity caused by glycation could be the ‘tipping point’ in disease progression. It appears that as Alzheimer’s progresses, glycation of these enzymes increases. 

The study is published in the journal Scientific Reports. 

Professor Jean van den Elsen, from the University of Bath Department of Biology and Biochemistry, said: “We’ve shown that this enzyme is already modified by glucose in the brains of individuals at the early stages of Alzheimer’s disease. We are now investigating if we can detect similar changes in blood.

Chronology of Alzheimer’s Progression

“Normally MIF would be part of the immune response to the build-up of abnormal proteins in the brain, and we think that because sugar damage reduces some MIF functions and completely inhibits others that this could be a tipping point that allows Alzheimer’s to develop. 

Dr. Rob Williams, also from the Department of Biology and Biochemistry, added: “Knowing this will be vital to developing a chronology of how Alzheimer’s progresses and we hope will help us identify those at risk of Alzheimer’s and lead to new treatments or ways to prevent the disease. 

Dr. Omar Kassaar, from the University of Bath, added: “Excess sugar is well known to be bad for us when it comes to diabetes and obesity, but this potential link with Alzheimer’s disease is yet another reason that we should be controlling our sugar intake in our diets.”

MORE INFORMATION:

• The study is a collaboration between Dr Rob Williams and Prof Jean van den Elsen in the Department of Biology & Biochemistry, Prof Tony James in the Department of Chemistry and Prof Stephen Ward in the Department of Pharmacy & Pharmacology.
• It was funded by the Dunhill Medical Trust. Human brain tissue for this study was provided through Brains for Dementia Research, a joint initiative between Alzheimer’s Society and Alzheimer’s Research UK in association with the Medical Research Council.

REFERENCE:

• Macrophage Migration Inhibitory Factor is subjected to glucose modification and oxidation in Alzheimer’s Disease, Omar Kassaar, Marta Pereira Morais, Suying Xu, Emily L. Adam, Rosemary C. Chamberlain, Bryony Jenkins, Tony D. James, Paul T. Francis, Stephen Ward, Robert J. Williams & Jean van den Elsen. || Scientific Reports volume 7, Article number: 42874 (23 February 2017)

SOURCE:

• University of Bath

Does rosemary improve memory?

Caregivers, and healthcare professionals,here is some great information

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

Your residents will love the Amazon Kindle Fire

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Green Pharmacy (.Jim Duke's Botanical Desk Reference)

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"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.

• 
  

SOURCE:
Green Pharmacy (Dr. Jim Duke's Botanical Desk Reference)

Dementia risk lower in fat people?

Caregivers, and healthcare professionals,here is some great information

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2 MILLION BRITONS, in the biggest study in history, astonished researchers. Obese people had 29% less dementia risk than normal-weight people. Underweight? Bigger risk. See what doctors say about these unexpected results. 

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Very obese people (BMI greater than 40 kg/m2) are 29% less likely to get dementia than people in the normal weight range. The unexpected results are according to new research published in The Lancet Diabetes & Endocrinology journal.

Largest Ever Study

The findings, which come from the largest ever study to examine the statistical association between BMI and dementia risk, also show that middle-aged obese people (BMI greater than 30 kg/m2) are nearly 30% less likely to develop dementia than people of a healthy weight, contradicting findings from some previous research, which suggested that obesity leads to an increased risk of dementia.

Researchers based at the London School of Hygiene & Tropical Medicine, and OXON Epidemiology, both in London, UK, analysed data from the Clinical Practice Research Datalink (CPRD), a large database of patient information recorded during routine general practice over nearly 20 years, representing around 9% of the UK population. 

2 Million People's Medical Records

The researchers analysed the medical records of nearly two million (1,958,191) people with an average (median) age of 55 years at the start of the study period, and an average (median) BMI of 26.5 kg/m2, just within the range usually classed as overweight.  During an average (median) of nine years follow-up, nearly fifty thousand (45,507) people were diagnosed with dementia.

People who were underweight in middle age were a third (34%) more likely to be diagnosed with dementia than those of a healthy weight, and this increased risk of dementia persisted even 15 years after the underweight was recorded.

Increase in BMI -> Decrease in Dementia

As participants’ BMI at middle age increased, the risk of dementia reduced, with very obese people (BMI greater than 40 kg/m2) 29% less likely to get dementia than people in the normal weight range.  An increase in BMI was associated with a substantial steadily decreasing risk of dementia for BMI of up to 25 kg/m² (classed as a healthy weight).  Above a BMI of 25 kg/m² (classed as overweight or obese), dementia risk decreased more gradually, and this trend continued up to a BMI of 35 kg/m² or higher.

The association between BMI and dementia risk wasn’t affected by the decade in which the participants were born, nor by their age at diagnosis. Adjusting for confounding factors known to increase the risk of dementia, such as alcohol use or smoking, made little difference to the results.

Need to Re-Think

According to study author Professor Stuart Pocock from the London School of Hygiene & Tropical Medicine, “Our results suggest that doctors, public health scientists, and policy makers need to re-think how to best identify who is at high risk of dementia.  We also need to pay attention to the causes and public health consequences of the link between underweight and increased dementia risk which our research has established.  However, our results also open up an intriguing new avenue in the search for protective factors for dementia – if we can understand why people with a high BMI have a reduced risk of dementia, it’s possible that further down the line, researchers might be able to use these insights to develop new treatments for dementia.” [2]

Protective?

“The reasons why a high BMI might be associated with a reduced risk of dementia aren’t clear, and further work is needed to understand why this might be the case,” adds Dr Nawab Qizilbash from OXON Epidemiology in London, UK and Madrid, Spain, the study’s lead author.  “If increased weight in mid-life is protective against dementia, the reasons for this inverse association are unclear at present. Many different issues related to diet, exercise, frailty, genetic factors, and weight change could play a part.” [2] 

Writing in a linked Comment, Professor Deborah Gustafson from SUNY Downstate Medical Center in New York, USA, says, “The published literature about BMI and dementia is equivocal. Some studies report a positive association between high mid-life BMI and dementia, whereas others do not… Many considerations are needed in the assessment of the epidemiology of the association between BMI and late-onset dementia, as is the case for many recorded associations involving late-life disorders. To understand the association between BMI and late-onset dementia should sober us as to the complexity of identifying risk and protective factors for dementia. The report by Qizilbash and colleagues is not the final word on this controversial topic.”

FOOTNOTES:

1. Although a BMI less than 18.5 kg/m2 is usually classed as underweight, a slightly higher threshold (20 kg/m2) was used in this study to enable comparison with earlier studies, which had taken BMI lower than 20 kg/m2 as the threshold.
2. Quotes direct from authors and cannot be found in text of Article

REFERENCE:

• http://www.thelancet.com/journals/landia/article/PIIS2213-8587(15)00033-9/abstract
  
• Full bibliographic information:BMI and risk of dementia in two million people over two decades: a retrospective cohort study. Nawab Qizilbash, John Gregson, Michelle E Johnson, Neil Pearce, Ian Douglas, Kevin Wing, Stephen J W Evans, Stuart J Pocock. Lancet Diabetes Endocrinol 2015, Published Online April 10, 2015. http://dx.doi.org/10.1016/S2213-8587(15)00033-9

SOURCE:

• Huff Post Live

Fight dementia with sleep apnea treatment

Caregivers, and healthcare professionals,here is some great information

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

Your residents will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

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

Follow alzheimersideas on twitter
The Dementia Caregiver's Little Book of Hope [Kindle Edition]

• The University of Sydney Brain and Mind Centre, OSA, 

The University of Sydney Brain and Mind Centre is connecting sleep and dementia to explore treatment and prevention. 

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Obstructive Sleep Apnoea (OSA) has been linked to brain changes seen in the early stages of dementia, University of Sydney research reveals. 

Published in The European Respiratory Journal, the study’s authors say the finding provides evidence that screening older people for obstructive sleep apnoea (OSA) and providing treatment where needed could help prevent dementia in this population

Obstructive Sleep Apnoea (OSA) is a condition in which the walls of the throat relax and narrow during sleep, which stops breathing and is known to reduce blood oxygen levels. The new study indicates that the decline in blood oxygen levels may be linked to a shrinking of the brain’s temporal lobes and a corresponding decline in memory.

50% of Dementia Risk is Modifiable

"Diagnosing and treating obstructive sleep apnoea could be an opportunity to prevent cognitive decline before it’s too late."
Professor Sharon Naismith, University of Sydney

Study leader, Professor Sharon Naismith of the University of Sydney's Brain and Mind Centre said: “Between 30 and 50 percent of dementia risk is due to modifiable factors, such as depression, high blood pressure, obesity and smoking. In recent years, researchers have recognised that various sleep disturbances are also risk factors for dementia. We wanted to look specifically at obstructive sleep apnoea and its effects on the brain and cognitive abilities.”

The researchers worked with a group of 83 people, aged between 51 and 88 years, who had visited their doctor with concerns over their memory or mood but had no OSA diagnosis. Each participant was assessed for their memory skills and symptoms of depression, and each was given an MRI scan to measure the dimensions of different areas of the brain.

Participants also attended a sleep clinic where they were monitored overnight for signs of OSA using polysomnography. This technique records brain activity, levels of oxygen in the blood, heart rate, breathing and movements.

Low Levels of Oxygen

The researchers found that patients who had low levels of oxygen in their blood while they were sleeping tended to have reduced thickness in the left and right temporal lobes of the brain. These are regions known to be important in memory typically affected in dementia.

These brain changes were also linked with participants’ poorer ability to learn new information. The researchers say this is the first time a direct link of this kind has been shown.

"There is no cure for dementia so early intervention is key. On the other hand, we do have an effective treatment for obstructive sleep apnoea."
Professor Sharon Naismith, University of Sydney

Conversely, patients with signs of OSA were also more likely to have increased thickness in other regions of the brain, which the researchers say could be signs of the brain reacting to lower levels of oxygen with swelling and inflammation.

It Can Be Treated

OSA is more common in older people and has already been linked with heart disease, stroke and cancer, but it can be treated with a continuous positive airway pressure (CPAP) device, which prevents the airway closing during sleep.

Professor Naismith added: “We chose to study this group because they are older and considered at risk of dementia. Our results suggest that we should be screening for OSA in older people. We should also be asking older patients attending sleep clinics about their memory and thinking skills—and carrying out tests where necessary.

"Treating OSA an Opportunity to Prevent Cognitive Decline"

“There is no cure for dementia so early intervention is key. On the other hand, we do have an effective treatment for OSA. This research shows that diagnosing and treating OSA could be an opportunity to prevent cognitive decline before it’s too late.”

Professor Naismith and her team are now doing research to discover whether CPAP treatment can prevent further cognitive decline and improve brain connectivity in patients with mild cognitive impairment.

PEOPLE:

• Professor Sharon Naismith is the Leonard P Ullman Chair in Psychology at the Charles Perkins Centre. She is also an NHMRC Career Development Fellow and Clinical Neuropsychologist who heads the Healthy Brain Ageing Program at the Brain and Mind Centre. Professor Naismith is co-chief investigator of the newly established Australian Dementia Network (ADNet).

SOURCE:

• The University of Sydney Brain and Mind Centre

Why Bill Gates donates big for Alzheimer's research

Caregivers, and healthcare professionals,here is some great information

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

Your residents will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

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Follow alzheimersideas on twitter
The Dementia Caregiver's Little Book of Hope [Kindle Edition]


GatesNotes - The Blog of Bill Gates

Bill Gates wrote a $100,000,000 check for Alzheimer's research. See him share his thoughts on what will it take to find a breakthrough. 

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Why I'm Digging Deep Into Alzheimer's - by Bill Gates

In every part of the world, people are living longer than they used to. Thanks to scientific advancements, fewer people die young from heart disease, cancer, and infectious diseases. It’s no longer unusual for a person to live well into their 80s and beyond. My dad will celebrate his 92nd birthday in a couple weeks, a milestone that was practically unimaginable when he was born.

This fact—that people are living longer than ever before—should always be a wonderful thing. But what happens when it’s not?

The longer you live, the more likely you are to develop a chronic condition. Your risk of getting arthritis, Parkinson’s, or another non-infectious disease that diminishes your quality of life increases with each year. But of all the disorders that plague us late in life, one stands out as a particularly big threat to society: Alzheimer’s disease.

You have a nearly 50 percent chance of developing the disease if you live into your mid-80s. In the United States, it is the only cause of death in the top 10 without any meaningful treatments that becomes more prevalent each year. That trend will likely continue as baby boomers age, which means that more families will watch their loved ones suffer from cognitive decline and slowly disappear. Despite this growing burden, scientists have yet to figure out what exactly causes Alzheimer’s or how to stop the disease from destroying the brain.

I first became interested in Alzheimer’s because of its costs—both emotional and economic—to families and healthcare systems. The financial burden of the disease is much easier to quantify. A person with Alzheimer’s or another form of dementia spends five times more every year out-of-pocket on healthcare than a senior without a neurodegenerative condition. Unlike those with many chronic diseases, people with Alzheimer’s incur long-term care costs as well as direct medical expenses. If you get the disease in your 60s or 70s, you might require expensive care for decades.

These costs represent one of the fastest growing burdens on healthcare systems in developed countries. According to the Alzheimer’s Association, Americans will spend $259 billion caring for those with Alzheimer’s and other dementias in 2017. Absent a major breakthrough, expenditures will continue to squeeze healthcare budgets in the years and decades to come. This is something that governments all over the world need to be thinking about, including in low- and middle-income countries where life expectancies are catching up to the global average and the number of people with dementia is on the rise.

The human cost of Alzheimer’s is much more difficult to put into numbers. It’s a terrible disease that devastates both those who have it and their loved ones. This is something I know a lot about, because men in my family have suffered from Alzheimer’s. I know how awful it is to watch people you love struggle as the disease robs them of their mental capacity, and there is nothing you can do about it. It feels a lot like you’re experiencing a gradual death of the person that you knew.

My family history isn’t the sole reason behind my interest in Alzheimer’s. But my personal experience has exposed me to how hopeless it feels when you or a loved one gets the disease. We’ve seen scientific innovation turn once-guaranteed killers like HIV into chronic illnesses that can be held in check with medication. I believe we can do the same (or better) with Alzheimer’s.

I’ve spent considerable time over the last year learning about the disease and the progress made to date. There’s a lot of amazing work being done in this field to delay Alzheimer’s and reduce its cognitive impact. What I’ve heard from researchers, academics, funders, and industry experts makes me hopeful that we can substantially alter the course of Alzheimer’s if we make progress in five areas:

• We need to better understand how Alzheimer’s unfolds. The brain is a complicated organ. Because it’s so difficult to study while patients are alive, we know very little about how it ages normally and how Alzheimer’s disrupts that process. Our understanding of what happens in the brain is based largely on autopsies, which show only the late stages of the disease and don’t explain many of its lingering mysteries. For example, we don’t fully understand why you are more likely to get Alzheimer’s if you’re African American or Latino than if you’re white. If we’re going to make progress, we need a better grasp on its underlying causes and biology.
• We need to detect and diagnose Alzheimer’s earlier. Since the only way to diagnose Alzheimer’s definitively is through an autopsy after death, it’s difficult to identify the disease definitively early in its progression. Cognitive tests exist but often have a high variance. If you didn’t sleep well the night before, that might skew your results. A more reliable, affordable, and accessible diagnostic—such as a blood test—would make it easier to see how Alzheimer’s progresses and track how effective new drugs are.
• We need more approaches to stopping the disease. There are many ways an Alzheimer’s drug might help prevent or slow down the disease. Most drug trials to date have targeted amyloid and tau, two proteins that cause plaques and tangles in the brain. I hope those approaches succeed, but we need to back scientists with different, less mainstream ideas in case they don’t. A more diverse drug pipeline increases our odds of discovering a breakthrough.
• We need to make it easier to get people enrolled in clinical trials. The pace of innovation is partly determined by how quickly we can do clinical trials. Since we don’t yet have a good understanding of the disease or a reliable diagnostic, it’s difficult to find qualified people early enough in the disease’s progression willing to participate. It can sometimes take years to enroll enough patients. If we could develop a process to pre-qualify participants and create efficient registries, we could start new trials more quickly.
• We need to use data better. Every time a pharmaceutical company or a research lab does a study, they gather lots of information. We should compile this data in a common form, so that we get a better sense of how the disease progresses, how that progression is determined by gender and age, and how genetics determines your likelihood of getting Alzheimer’s. This would make it easier for researchers to look for patterns and identify new pathways for treatment.

By improving in each of these areas, I think we can develop an intervention that drastically reduces the impact of Alzheimer’s. There are plenty of reasons to be optimistic about our chances: our understanding of the brain and the disease is advancing a great deal. We’re already making progress—but we need to do more.

I want to support the brilliant minds doing this work. As a first step, I’ve invested $50 million in the Dementia Discovery Fund—a private fund working to diversify the clinical pipeline and identify new targets for treatment. Most of the major pharmaceutical companies continue to pursue the amyloid and tau pathways. DDF complements their work by supporting startups as they explore less mainstream approaches to treating dementia.

I’m making this investment on my own, not through the foundation. The first Alzheimer’s treatments might not come to fruition for another decade or more, and they will be very expensive at first. Once that day comes, our foundation might look at how we can expand access in poor countries.

But before we can even begin to think about how we do that, we need lots of scientific breakthroughs. With all of the new tools and theories in development, I believe we are at a turning point in Alzheimer’s R&D. Now is the right time to accelerate that progress before the major costs hit countries that can’t afford high priced therapies and where exposure to the kind of budget implications of an Alzheimer’s epidemic could bankrupt health systems.

This is a frontier where we can dramatically improve human life. It’s a miracle that people are living so much longer, but longer life expectancies alone are not enough. People should be able to enjoy their later years—and we need a breakthrough in Alzheimer’s to fulfill that. I’m excited to join the fight and can’t wait to see what happens next.

MORE INFORMATION:

• If you want to receive updates on how I’m getting involved in the fight to stop Alzheimer’s disease, sign up to become a Gates Notes Insider.

SOURCE:

• GatesNotes - The Blog of Bill Gates

Is there a connection between Alzheimer's and eye disease

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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Follow alzheimersideas on twitter
The Dementia Caregiver's Little Book of Hope [Kindle Edition]

HealthDay News

Researchers have discovered a link between three degenerative eye diseases and Alzheimer's disease.

They say their findings could lead to new ways to identify people at high risk for Alzheimer's.

"We don't mean people with these eye conditions will get Alzheimer's disease," said lead researcher Cecilia Lee, an assistant professor of ophthalmology at the University of Washington School of Medicine.

"The main message from this study is that ophthalmologists should be more aware of the risks of developing dementia for people with these eye conditions and primary care doctors seeing patients with these eye conditions might be more careful on checking on possible dementia or memory loss," Lee explained in a university news release.

The study involved 3,877 randomly selected patients, aged 65 and older. They were tracked over the course of five years, during which time 792 were diagnosed with Alzheimer's disease.

Patients with age-related macular degeneration, diabetic retinopathy or glaucoma had a 40 to 50 percent greater risk of Alzheimer's disease than those without the eye conditions, the researchers said.

"What we found was not subtle," said Paul Crane, a professor of medicine at the university. "This study solidifies that there are mechanistic things we can learn from the brain by looking at the eye."

The study was published Aug. 8 in Alzheimer's & Dementia: The Journal of the Alzheimer's Association.

Alzheimer's is the most common form of dementia, which affects more than 46 million people worldwide. That number is expected to rise to 131.5 million by 2050, the researchers estimate.

More information

The U.S. National Institute on Aging has more about Alzheimer's disease.

SOURCE: University of Washington, news release, 

Alzheimer's: New drug trial

Caregivers, and healthcare professionals,here is some great information

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CNBC
Biogen

Skeptical Alzheimer's experts expressed surprising optimism regarding Biogen's BAN-2401 drug. Dr. Ronald Peterson is one of the world's top experts on Alzheimer's and Director of the Mayo Clinic Alzheimer Disease Research Center. See him discuss results from Biogen's positive phase-2-trial Alzheimer's treatment. 

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1. The final analysis at 18 months of the 856 patient Phase II clinical study in early Alzheimer’s disease demonstrated statistically significant slowing in clinical decline and reduction of amyloid beta accumulated in the brain
2. First late-stage study data successfully demonstrating potential disease-modifying effects on both clinical function and amyloid beta accumulation in the brain
3. New data provide compelling evidence to further support amyloid hypothesis as a therapeutic target for Alzheimer’s disease

Statistical Significance

Biogen announced positive topline results from the Phase II study with BAN2401, an anti-amyloid beta protofibril antibody, in 856 patients with early Alzheimer's disease. The study achieved statistical significance on key predefined endpoints evaluating efficacy at 18 months on slowing progression in Alzheimer’s Disease Composite Score (ADCOMS) and on reduction of amyloid accumulated in the brain as measured using amyloid-PET (positron emission tomography). 

Study 201 (ClinicalTrials.gov identifier NCT01767311) is a placebo-controlled, double-blind, parallel-group, randomized study in 856 patients with mild cognitive impairment (MCI) due to Alzheimer's disease (AD) or mild Alzheimer's dementia (collectively known as early Alzheimer’s disease) with confirmed amyloid pathology in the brain. Efficacy was evaluated at 18 months by predefined conventional statistics on ADCOMS, which combines items from the Alzheimer's Disease Assessment Scale-cognitive subscale (ADAS-Cog), the Clinical Dementia Rating Sum of Boxes (CDR-SB) scale and the Mini-Mental State Examination (MMSE) to enable sensitive detection of changes in early AD symptoms. Patients were randomized to five dose regimens, 2.5 mg/kg biweekly, 5 mg/kg monthly, 5 mg/kg biweekly, 10 mg/kg monthly and 10 mg/kg biweekly, or placebo.

Slowing Down Alzheimer's

Topline results of the final analysis of the study demonstrated a statistically significant slowing of disease progression on the key clinical endpoint (ADCOMS) after 18 months of treatment in patients receiving the highest treatment dose (10 mg/kg biweekly) as compared to placebo. Results of amyloid PET analyses at 18 months, including reduction in amyloid PET standardized uptake value ratio (SUVR) and amyloid PET image visual read of subjects converting from positive to negative for amyloid in the brain, were also statistically significant at this dose. Dose-dependent changes from baseline were observed across the PET results and the clinical endpoints.

Clinical Benefit

Further, the highest treatment dose of BAN2401 began to show statistically significant clinical benefit as measured by ADCOMS as early as 6 months including at 12 months.

BAN2401 demonstrated an acceptable tolerability profile through 18 months of study drug administration. The most common treatment emergent adverse events were infusion-related reactions and Amyloid Related Imaging Abnormalities (ARIA). Infusion related reactions were mostly mild to moderate in severity. Incidence of ARIA-E (edema) was not more than 10% in any of the treatment arms, and less than 15% in patients with APOE4 at the highest dose per the study protocol safety and reporting procedures. 

Detailed results of the study will be presented at future academic conferences.

Impressive 18-Month Results

“The 18-month results of the BAN2401 trial are impressive and provide important support for the amyloid hypothesis,” said Jeff Cummings, M.D., founding director, Cleveland Clinic Lou Ruvo Center for Brain Health. “I look forward to seeing the full data set shared with the broader Alzheimer’s community as we advance against this devastating disease.” 

“This is the first late-stage anti-amyloid antibody study to successfully achieve statistically significant results at 18 months, further validating the amyloid hypothesis,” said Lynn Kramer, M.D., Chief Clinical Officer and Chief Medical Officer, Neurology Business Group, Eisai. “We will discuss these very encouraging results with regulatory authorities to determine the best path forward. We continue to work towards the goal of delivering BAN2401 to patients and healthcare professionals as early as possible.” 

“The prospect of being able to offer meaningful disease-modifying therapies to individuals suffering from this terrible disease is both exciting and humbling,” said Alfred Sandrock, M.D., Ph.D., executive vice president and chief medical officer at Biogen. “These BAN2401 18-month data offer important insights in the investigation of potential treatment options for patients with Alzheimer’s disease and underscores that neurodegenerative diseases may not be as intractable as they once seemed.” 

As reported in December 2017, the study did not achieve its primary outcome measure which was designed to enable a potentially more rapid entry into Phase III development based on Bayesian analysis at 12 months of treatment. Upon the final analysis at 18 months using predefined conventional statistical method, the study did demonstrate a statistically significant slowing of disease progression on the key clinical endpoint (ADCOMS) after 12 months of treatment in patients receiving the highest treatment dose (10 mg/kg biweekly) as compared to placebo. 

MORE INFORMATION:

1. About BAN2401
   BAN2401 is a humanized monoclonal antibody for Alzheimer’s disease that is the result of a strategic research alliance between Eisai and BioArctic. BAN2401 selectively binds to neutralize and eliminate soluble, toxic Aβ aggregates that are thought to contribute to the neurodegenerative process in Alzheimer’s disease. As such, BAN2401 may have the potential to have an effect on disease pathology and to slow down the progression of the disease. Eisai obtained the global rights to study, develop, manufacture and market BAN2401 for the treatment of Alzheimer’s disease pursuant to an agreement concluded with BioArctic in December 2007. In March 2014, Eisai and Biogen entered into a joint development and commercialization agreement for BAN2401 and the parties amended that agreement in October 2017.
2. About ADCOMS
   Developed by Eisai, ADCOMS (AD Composite Score) combines items from the ADAS-Cog (Alzheimer’s Disease Assessment Scale-cognitive subscale), CDR-SB (Clinical Dementia Rating Sum of Boxes) and the MMSE (Mini-Mental State Examination) scales to enable a sensitive detection of changes in clinical functions of early AD symptoms and changes in memory. This Study 201 utilizes ADCOMS as its key endpoint for assessing clinical symptoms.

SOURCES:

• CNBC Television
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