Jul 242015

We asked, and you answered!  Below you will find a Q&A with Dr. David Knopman in our Alzheimer’s Association International Conference (AAIC) feature “Ask the Expert.” We asked you to share what you would ask a researcher if you had a chance, and you asked important probing questions regarding Alzheimer’s symptoms, diagnosis, treatments and advancements. Read all of the questions and answers below.

ask the expert

Raenelle asks…

Is a brain autopsy still the only way to definitively diagnose Alzheimer’s disease?

That’s a great question, one that I’m asked almost every day. It’s not true now.

One of the great advances that have been made over the last 10 years in Alzheimer’s research is the availability and use of imaging – brain scans, spinal fluid analysis – so that we can now, at least on a research basis, diagnose Alzheimer’s disease in life. From a practical point of view, that may not apply to a patient being seen in a clinic, but these results that have been accomplished in real-time have informed us about how good – or not so good – our diagnoses are when they are just based on a history from a family informant and the examination of the patient. In fact, a clinical examination based on the patient history and the exam is pretty good for diagnosing Alzheimer’s disease and dementia. It’s not perfect, however, and on the research level, we aspire to achieve a much higher level of perfection.

I want to emphasize that while understanding the cause of the cognitive impairment/dementia isn’t necessarily 100% accurate, diagnosing Mild Cognitive Impairment (MCI) or dementia can be extremely accurate.

Bill asks…

What are some of the biggest advancements in our understanding of Alzheimer’s in the past couple of years? Are we getting close to a cure?

Prior to 10 years ago, most of the work that was done in understanding the biology of Alzheimer’s disease required people to have died so that we could examine their brains under a microscope. With the advent of advanced imaging techniques  such as positron emission tomography (PET) scans, making better use of MRI scans, and using spinal fluid analyses, we are now able to plot out the course of the disease in living people before they have symptoms, as they’re developing symptoms and once their symptoms become more advanced. This has been an important piece of progress because now we can look at patients and understand what is going on in their brains in real-time.

While this hasn’t led to a cure in 2015, it has certainly advanced the game tremendously. In virtually all of the clinical trials being done with anti-amyloid therapies, amyloid imaging with PET scanning is a requirement to ensure that we know that we are treating people with the biology of Alzheimer’s disease. This requirement only came about because of the advances we’ve made in the past couple of years.

Noreen asks…

How much does genetic testing tell us? If other family members have Alzheimer’s, what are my chances of getting it?

There are three genes in which mutations are known to cause Alzheimer’s disease with a very high likelihood, but it’s important to recognize that the number of families that have a mutation in one of these three genes is extremely rare – only about 500 families globally.

On the other hand, there are genes such as APOE – the best known and most important – which are actually very common in the general population but have a much lower likelihood of causing Alzheimer’s if someone happens to have the “bad” variant.

If you have a family member with Alzheimer’s, find out who diagnosed that person and whether or not that person had an imaging or autopsy confirmation the disease. If there was no proof of diagnosis, more questions should be asked about what the underlying cause might have been. However, if there is reasonable certainty that this is a familial or genetic disease, there is testing commercially available that is highly accurate. Talk to your physician and then see a medical geneticist for definitive testing.

Sonja asks…

If it can be determined that Alzheimer’s starts around 10 years before symptoms begin, is there an opportunity to treat it before symptoms starts?

The answer, we hope, is yes.

In fact, worldwide, there are four studies trying to do that. One I am involved in, the A4 study, accepts individuals between the ages of 65 and 85 in order to perform amyloid PET imaging; if individuals have elevated levels of amyloid, they are eligible for the study. This study is funded by the National Institutes of Health (NIH) with contributions from the Alzheimer’s Association and Lilly Pharmaceuticals.

A second trial involves a very small group of people with the autosomal dominate inherited mutations that is ongoing and recruiting individuals who are asymptomatic.

An exotic study taking place in the country of Colombia focuses on a very large extended family carrying a genetic mutation that consistently causes Alzheimer’s in family members. These families have teamed up with researchers in the U.S. and Colombia to perform clinical trials using anti-amyloid drugs.

The fourth trial, the Tomorrow study, is also seeking a similar approach. This is a very exciting area; we now have the tools to complete a study in people while they are symptomatic; we simply did not have these tools a few years ago.

Gena asks…

Why is the rate of decline for some people with Alzheimer’s so much faster than others?

This is a question that we still can’t answer today as there is a lot of variability from patient to patient. By being able to look at the biology of the disease in living people through imaging and spinal fluid biomarkers, I hope that that answer will eventually be revealed to us.

Age makes a difference, and other health issues make a difference, but beyond that, there are some very important features of the disease that determine the rate that people progress at that we still don’t know.

Mark asks…

Are there promising results for any drugs currently being investigated for treating Alzheimer’s?

Yes. To be honest, the results we’ve heard at AAIC aren’t going to translate into available therapies next week or probably even next year, but what I’ve heard regarding several drugs presented is very encouraging. While there is nothing definitive at this point, we are better at conducting the trials, we’ve learned how to enroll the right patients and we do things better overall.

It is difficult to know the right dose without testing; sometimes there are failures and sometimes there are successes. It is difficult to know what the side effects will be until we test in humans. This is an arduous process of finding drugs that work for this complicated, variable and heterogeneous disease, but I believe the results presented at AAIC are promising. Though I am hopeful, I don’t want to raise expectations too high.

Gena asks…

What do you think about the use of ultrasound as a treatment for Alzheimer’s? A recent study with laboratory animals appeared to show promise.

This is not going to be suitable for humans for a long time. That said, it’s an exciting idea, and I am open to any idea that might have value. This study was done in rodents; to scale it up and begin to test it in humans is very expensive. There are questions about safety, dosage, number of treatments – and these are the kind of things that need to be done. I hope that the investigators behind this study will have a strong enough scientific rationale and find success in funding to see if this idea works. At this point, it is still very early for that particular approach.

Ian asks…

Finding a cure is the ultimate goal.  The World Dementia Council and other U.S. organizations have set a goal of accomplishing this by 2025. What are your thoughts on this goal?

Yogi Berra is quoting as saying: “It’s tough to make predictions, especially about the future,” but I am hopeful that we are continuing to make progress. More importantly, there is more funding that is going towards research. The number of promising projects that we can fund at this point may be very low, but with private and federal funding sources, we hope we can pursue many other avenues. Funding is what is going to increase the likelihood that we will find a cure by 2025.



About David Knopman, M.D.:

knopmanDr. Knopman earned his M.D. degree from the University of Minnesota (UM) Medical School, where he also completed his neurology residency. This was followed by a fellowship in behavioral neurology at Hennepin County Medical Center and UM. He was a faculty member at the University of Minnesota from 1980 to 2000. Dr. Knopman joined the Department of Neurology at the Mayo Clinic, Rochester, Minnesota, in 2000, where he is currently professor of neurology, Mayo Clinic College of Medicine, a consultant in Neurology at the Mayo Clinic, and a co-investigator in the Mayo Alzheimer’s Disease Research Center. His research and clinical interests have been in dementing illnesses. He is an author on more than 300 articles on various topics in dementia. Dr. Knopman is deputy editor of Neurology, the journal of the American Academy of Neurology (AAN). He was the senior author on the 2001 AAN Practice Parameter on the Diagnosis of Dementia and was co-chair of the National Institute of Aging-Alzheimer’s Association workgroup that drafted the revised criteria for Alzheimer’s disease dementia. Dr. Knopman joined the Alzheimer’s Association Medical and Scientific Advisory Council in 2012.

Apr 182014

When my husband Jim, who just turned 53, was first diagnosed with younger-onset Alzheimer’s disease, I wasn’t quite sure what was going on. The doctor didn’t tell us Alzheimer’s is fatal. He didn’t tell us there is no cure or that we should get our affairs in order. He didn’t tell us how long Jim might have left. He simply said, “See you back in six months.” If you are lucky, your doctor might refer you to the Alzheimer’s Association. I had to find it on my own.

We couldn’t tell anyone. Jim didn’t want to. He had a top security clearance job. He had a mother that had passed away from this very same disease. He knew more than I did. He kept up with his normal routine. He kept living as if there were a million tomorrows.

At the same time, I was starting to live as if there was no tomorrow. I grasped for anything I could that might keep Jim with me—seizing every opportunity to discuss plans and outcomes and new treatments and experiments and research. I was clutching every snippet of time, trying to create lasting memories for us and our two children (who were 5 and 8 at the time).

It was all so hard to take in. He seemed so healthy and fine 95 percent of the time. He was handsome and athletic and smart and rarely got sick. How could it be that in just a few years, he would be taken from me? From his children? From everyone who loves and cares for him?

For a few very long and stressful years, we kept this secret. Maybe the doctor is wrong. Maybe it is a tumor. Maybe it is mini strokes or a thyroid problem or high blood pressure. Couldn’t it be something as simple as lack of sleep or depression? Then Jim’s brother was diagnosed with Alzheimer’s and subsequently passed away at the very young age of 52. It became apparent to me—to us—that this does indeed run in Jim’s family.

That is when it dawned on me; our children are susceptible to this disease. This nightmare could return to our family again and again unless something is done.

Breaking Our Silence

We had long discussions about our future, our options, our finances, how to tell the kids.

Then Jim lost his job.

We had more long discussions. Jim started having more and more symptoms. Then we decided it was time: time to be part of the solution; time to join the cause; time to make sure the whole world understands what a horrible and heartbreaking story we have along with MILLIONS of others.

Three years ago this month, we joined hundreds of advocates from around the country in Washington D.C. for the annual Alzheimer’s Association Advocacy Forum.

We weren’t quite sure what to expect. I was nervous. Although we had been to D.C. numerous times, we had never tried to speak to a member of Congress before. We had never gone through security to enter a building on Capitol Hill, or walked the marble halls. We listened to the echo of our footsteps as we marched closer and closer to the offices of elected officials who can help change the future of this disease—the future that awaits our children.

I was encouraged to share our story. And so I did. And I cried. And Jim cried. Others in our group cried. It was a relief—a relief to be heard; a relief to be doing SOMETHING to make a difference; a relief to get it behind us.

But we hadn’t really gotten it behind us. Jim was still diagnosed, there still was no cure or real treatments or preventions. Which is why last year, we marched ourselves right back to D.C. again. We weren’t as nervous. We knew the routine. We were prepared.

Now, another year has gone by and there is still no cure, no treatments to slow its progression and no prevention. More federal money has been given for research, but not nearly enough (BILLIONS short) and absolutely no new programs and financial help for those of us struggling each day to pay bills and to take care of loved ones afflicted.

So, last week, Jim and I once again descended upon our elected officials to ask for help as part of the Advocacy Forum. We met with Sen. Mark Warner (D-Va.), Rep. Scott Rigell (R-Va) and asked them to support an additional $200 million dollars for Alzheimer’s research and to co-sponsor the Alzheimer’s Accountability Act.blog forum

Both of the Congressmen we met with have supported this cause in the past by signing on to co-sponsor the Hope for Alzheimer’s Act. One is a democrat and one is a republican. They are both businessmen. They understand the damage this disease is doing to our country and our Medicaid system. They understand the dire straits we will all be in if a change doesn’t happen. They both agreed to continue to support us and to be champions for Alzheimer’s families.

The Alzheimer’s Association Advocacy Forum is a great way to be part of something so much bigger than ourselves. It is a way to connect with other families from around the country who face the same struggles and the same loneliness and the same frustrations. We have made friends whom we now keep in contact with and support year round. And each year we meet new friends and are able to rally around them and show them the ropes (so to speak).

Believe it or not, there are even advocates that fly to D.C. to participate who have no connection to Alzheimer’s or other form of dementia. They may work with the elderly or be a student who hopes to become a researcher. For other advocates, the connection may not be direct—they heard a friend of a friend suffered through this disease and decided to support the cause. Each year, the awesomeness of the human race amazes me. It is sometimes hard to remember this when you watch the news or get mired in one bad luck scenario after another. But there are good people in this world who care and who are giving of themselves unselfishly to help others, even for people they don’t know and may never know.

I am proud to be part of this and I know Jim is, too.

The three days we were in D.C. were the liveliest and most energetic I have seen him in months. He was joking and talking and enjoying himself. It makes him feel like he is helping his children. He is helping humanity. He is stopping the very thing that is taking him away from everything he holds so dear.

There is power when we work together. I encourage everyone to contact their representative. Let your voice be heard. Let them know we demand a change. We demand a cure. We demand a different future where families are not suffering from Alzheimer’s disease.

About the blog author: Karen Garner, mother of two, works full time and is care partner for her husband, Jim, who is living with younger-onset Alzheimer’s. She shares her journey through her blog, Missing Jim.

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Jan 132014

In this first blog of 2014, I would like to review some of the highlights from the world of Alzheimer’s disease research in 2013, as well as the new directions that we will likely be heading in 2014.Driving on an empty road towards the setting sun 2014

Advances in Brain Imaging 

Advances in brain imaging, specifically amyloid PET scans, have led the way towards earlier identification of Alzheimer’s. Their widespread use in larger studies has made it possible to visualize the presence of beta-amyloid deposition in individuals with no symptoms.

The year began with the publication of additional data showing that amyloid deposition in the brain leads to atrophy, or shrinkage, of specific brain areas, even before patients develop memory loss. Research groups in France, Australia and the United States reported longitudinal studies of amyloid deposition in the brain, demonstrating that its presence predicts subsequent brain atrophy and cognitive decline.

Additional developments in brain imaging were made with results of Avid’s Tau tracers, both of which allow for visualization of the abnormal Tau protein that contributes to the formation of the neurofibrillary tangles of Alzheimer’s. Tau PET scans will undoubtedly become a critical tool in Alzheimer’s research during the next few years, much like amyloid imaging has been so important since the first papers were published on its use nine years ago.

Understanding Alzheimer’s in People with Down Syndrome

In the spring of 2013, the National Institutes of Health held a meeting focusing on Alzheimer’s disease among people with Down syndrome, bringing researchers together to discuss ways to develop a consortium with an aim to understand Alzheimer’s in this highly susceptible population.

– Every person with Down syndrome (DS) will develop AD pathology by age 40

– Half of the Down Syndrome population develops dementia by age 60

The Down Syndrome Biomarker Initiative (DSBI) pilot study was launched this year as a feasibility study of a planned large-scale study to discover indicators of Alzheimer’s disease in Down syndrome, with the ultimate goal of better understanding brain aging and Alzheimer’s in adults with Down syndrome.

Economic Impact of Dementia

A major publication in the New England Journal of Medicine by the RAND Corporation estimated the economic cost of dementia to the United States was approximately $203 billion in 2010. This paper garnered major attention, as it was a well conducted analysis of the economic impact of dementia. The sheer dollar amount is greater than the cost of any other disease faced by our society and is expected to rapidly increase in the next decade.

Trials and Tribulations

2013 was also the year when the long awaited results of the phase III IGIV study were presented, which were unfortunately, negative. Additionally, researchers studying the drug Bexarotene were able to replicate some, but not all of the previously reported effects of this drug on memory and beta-amyloid in mouse models of Alzheimer’s disease. Nonetheless, a placebo controlled clinical trial of Bexarotene was launched this year for the treatment of Alzheimer’s. Results are expected mid-year in 2014.

Prevention and Early Intervention

Perhaps one of the biggest events in the Alzheimer’s research world this year was the launch of the first clinical trial to prevent Alzheimer’s dementia in the general population. The trial, Anti-Amyloid in Asymptomatic Alzheimer’s Disease, or A4, is a three-year study looking at the effectiveness of a drug given to subjects who have absolutely no outward symptoms of memory loss but have positive amyloid scans of the brain. Much will be learned when this study is completed about how soon intervention can be offered in efforts to prevent Alzheimer’s disease.

G8 on Dementia

And finally, global focus on dementia was raised at this year’s G8 summit. All G8 nations made commitments to develop an international action plan for research, share information and data across the G8 countries and to provide unprecedented collaboration. The G8 plan includes open access to all publically-funded dementia research, the introduction of a new global envoy for dementia innovation, and the ambitious aim to “find a cure or disease-altering therapy by 2025.” This plan parallels the U.S. National Alzheimer’s Project Act (NAPA), with a goal of “preventing or effectively treating Alzheimer’s” by 2025.

What Is on the Horizon in 2014?

There are an unprecedented number of clinical trials now running with the aim of preventing Alzheimer’s. As data from recent studies suggest, it may only be through early intervention, before the symptomatic stage, that we can truly affect the course of AD and even consider preventing its dementia stage.

We anticipate more discoveries this upcoming year with Tau imaging, as well as the use of biomarkers in asymptomatic individuals. New data is also expected from large-scale whole-genome studies, which are revealing other Alzheimer’s susceptibility genes. We also look forward to data from some of the new mouse models created with these newly discovered mutations to understand how they contribute to the development of Alzheimer’s, and perhaps represent treatment targets.

We look forward to keeping you updated on the world of Alzheimer’s research in the upcoming year and are optimistic that there will be great developments in 2014.  Stay tuned.

Michael S. Rafii, M.D., Ph.D.

Director, Memory Disorders Clinic
Associate Medical Core Director, Alzheimer’s Disease Cooperative Study
University of California San Diego

This post originally appeared in Alzheimer’s Insights, an ADCS Blog.


Sep 252013

British scientists recently reported finding signs of the gum-disease bacterium toothbrush (P. gingivalis) in the brains of Alzheimer’s patients. The new study is being widely reported as adding to a growing body of evidence linking periodontal (gum) disease to an increased risk for Alzheimer’s disease.

However, such data needs to be considered very carefully.

In fact, what the study found was that substances on the surface of the bacterium (lipopolysaccharides) were present in the brain tissue of four out of 10 recently deceased people who had Alzheimer’s. It was found in zero out of 10 age-matched patients who did not have Alzheimer’s. The bacteria itself was not found in the brain tissue of any people.

The theory behind linking gum disease with Alzheimer’s is that the presence of gum bacteria lipopolysaccharides in the brain may cause inflammation. This in turn could trigger a biological cascade that may be linked to the brain changes associated with Alzheimer’s disease.

We already know that P. gingivalis is commonly found in chronic periodontal (gum) disease, and, if there is significant dental disease, it can enter the bloodstream through such everyday activities as eating, brushing teeth and invasive dental treatments. While in the bloodstream, the bacteria can settle on heart valves and damage them. Hence, patients with mitral valve prolapse and other heart anomalies often take an antibiotic before dental procedures to prevent the bacteria from depositing within the heart. However, no bacteria have been reported in the brains of patients with gum disease, as the brain is an immunologically, well-protected organ, more so than any other.

It is important for readers to know that these types of studies show an association between gum disease and Alzheimer’s disease, but do not prove causation. For example:

  • The number of subjects is extremely small to make a definitive conclusion, and the finding could have occurred simply by statistical chance.
  • Only four out of 10 subjects with Alzheimer’s had such changes, not 10 out of 10. If the gum disease was causative, one would expect more than just a minority of patients exhibiting the lipopolysaccharides.
  • Finally, what if very early stage dementia caused people to actually brush their teeth less often, or altered their dietary intake? They would be at risk of developing gum disease. But the gum disease would have resulted from the early dementia, not vice versa.

It is also important to note that previous studies have shown links between gum disease and other illnesses, including heart disease and certain forms of cancer; these findings are not specific to Alzheimer’s.

The study is important and should be followed up with larger sample sizes, but given the above limitations, the study does not show that “brushing teeth reduces the risk of dementia” or that “gum disease can lead to dementia.”

Thanks for reading.

Michael S. Rafii, M.D., Ph.D.

Director, Memory Disorders Clinic
Associate Medical Core Director, Alzheimer’s Disease Cooperative Study
University of California San Diego

This post originally appeared in Alzheimer’s Insights, an ADCS Blog.

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Feb 152013

During February, Black History Month, the Alzheimer’s Association sat down for a one-on-one talk with Dr. Goldie Byrd, an African-American scientist who has spent more than a decade researching the genetics of Alzheimer’s disease. Early in her career, Dr. Byrd recognized the impact of studying the nature of Alzheimer’s disease on a genomic level. Here are some of her thoughts on her observations and her motivations for continuing her research.

“I decided to focus my research on Alzheimer’s because it’s a disease of disparity, affecting some populations far more than others; its genetics aren’t well understood; and it had an impact on my family.

There’s a tremendous stigma about Alzheimer’s. People perceive it as affecting their social standing, their professional opportunities … they don’t want be associated with that kind of stigma, especially coming from a community that’s had an historical struggle to integrate.

I remember when people wouldn’t talk about cancer — it was taboo. Now people are proud to say they’re survivors. I want to create a buzz about Alzheimer’s so that people feel free to talk about it. I want more information out there and more literacy about the disease.

We need to do a better job educating people about how to care for those with Alzheimer’s — that will help with the embarrassment. And we need to provide resources to help caregivers who have an extraordinary challenge. This disease can strip a family of so many things, including their finances.

People also need to understand that the healthier we are, the healthier the brain will be. We need to increase physical activity, reduce stress, control high blood pressure and cholesterol, reduce obesity and eat a healthy diet. Often, these things are related to socioeconomics. But where we can make changes, we should. Education really is key.”

Dr. Byrd and her team were recently recognized with a $1 million grant for outreach activities. It will be used in part to support “Keeping Memories Alive” a project to bring better understanding about Alzheimer’s to all those with the disease, caregivers and policy makers.

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Know the 10 warning signs of Alzheimer’s (PDF) Caregiver stress brochure (PDF)

Jul 242012

This post originally appeared on the ChicagoNow blog, “Ask Dr. Chill: Practical Answers to the Toughest Caregiving Questions.” It is being reposted here with the author’s permission.

Alas, I was not able to attend the Alzheimer’s Association International Conference in Vancouver this month, but I did follow it closely on the organization’s website. The event attracted over 4,300 scientists, physicians and other professionals in the Alzheimer’s community who gathered to discuss findings from their most recent batches of research.

If your eyes tend to glaze over when you read news blurbs about complicated research, I don’t blame you. The sheer amount of news these days certainly can induce medical information overload.

As an antidote, I offer my Cliff Notes version of the Alzheimer’s Association International Conference:

  • A couple of risk factors emerged, including  late-life binge drinking, changes in gait (walking patterns) and sleep changes(Note: A risk factor implies a correlation between the factor and eventual onset of the disease — it does not imply causality. Just because something is associated with something else does not mean that one causes the other.)
  • Several treatments showed promise, including experimental drug EVP-6124, intravenous immunoglobulin, medical food Souvenaid, dietary supplement citicoline, and home-based care coordination. (Note: Treatment studies focus on treating the symptoms of Alzheimer’s after the disease process is already underway. There is no evidence that any of these treatments are useful for prevention.)
  • But on the upside, four different studies indicated that targeted exercise training could reduce the risk of developing dementia among older adults who were either cognitively healthy or only had mild cognitive impairment. (Get moving, folks!)
  • Diagnostic advances now allow researchers to better identify people with Alzheimer’s when they are still presymptomatic. That’s right  early brain changes and subtle cognitive problems can now be detected so that a diagnosis of “preclinical” or “presymptomatic” Alzheimer’s disease can be made. Granted, this type of diagnostic accuracy is seen mostly in research settings and has yet to become evident in general medical practice. But what this means is that researchers can now test new drugs among presymptomatic individuals to see if the progression to symptomatic Alzheimer’s can actually be prevented.

As I scoured the event’s press releases, I felt a combination of hope, pride and sadness wash over me. My hope emerges from the incredible strides taken by the Alzheimer’s community that have revealed more about the disease in the past 20 to 30 years than we learned during most of the 20thcentury (Alzheimer’s was first identified in 1906). My pride is rooted in the many years I worked for the organization and my first-hand knowledge of its dedication to ultimately finding an end to this wretched disease.

I didn’t want to feel sadness, but it’s best not to suppress such honest parts of the human experience. My sadness stemmed from my long journey with this disease  both professionally and personally  which has taught me that any measure of hope must be balanced with a healthy dose of realism.

Note that the conference highlighted causes, treatments and prevention  but not cures. We’re simply not there yet. We’re closer to a cure than ever before, but using that emotionally-laden word more than sparingly is still premature. I applaud the organization for always putting out balanced, accurate reports with no spin or pretense.

So be hopeful, but be realistic, too. And remember that the greatest barrier to the development of better treatments is the shortage of participants in Alzheimer’s clinical trials. If you want to add a dose of activism to your mixture of hope and realism, check out the Alzheimer’s Association’s TrialMatch program and find out whether there’s a clinical trial near you.

About Guest Blog Author Carrie Steckl, Ph.D.

Carrie Steckl, Ph.D. is a freelance writer specializing in caregiving, psychology, and aging. Her blog, “Ask Dr. Chill,” provides practical answers to the toughest caregiving questions.


Jul 152011

The use of positron emission tomography (PET) imaging to diagnose Alzheimer’s disease (AD) appears to be closer to becoming a clinical tool, based on results from two articles published online in the Archives of Neurology.

In one study, Adam S. Fleisher, M.D., from Banner Alzheimer’s Institute in Phoenix, and colleagues, evaluated PET imaging using the tracer florbetapir F 18. The study population included 68 individuals with probable Alzheimer’s disease, 60 individuals with mild cognitive impairment, and 82 healthy individuals who served as controls. PET scanning was used to monitor activity of the agent being studied. Dr. Fleisher and colleagues found differences in the brain uptake of florbetapir F 18, between the three groups, and in the detection of amyloid plaque; the differences may be large enough to help distinguish between the conditions, and between impaired versus unimpaired brains.

In another study, David A. Wolk, M.D., from the Penn Memory Center in Philadelphia, and colleagues, evaluated use of a tracer called fluorine 18-labeled flutemetamol for imaging the brain. The study involved conducting PET scans on seven patients who were given the tracer. All had previously undergone a biopsy for normal pressure hydrocephalus, a progressive condition that includes dementia and can be difficult to distinguish from Alzheimer’s disease. Researchers found correspondence between readings of the PET scans and evidence of amyloid lesions the plaque associated with Alzheimer’s disease (provided by microscopic evaluation of the biopsied tissue).

    The greatest use of such scans may ultimately be to help rule out Alzheimer’s disease, instead of rule it in. That is, in the physician’s office, having a negative scan (meaning no detectable amyloid buildup in the brain) may be helpful to clinicians in ruling out Alzheimer’s disease as the cause of the memory and thinking changes a person is experiencing. However, a positive scan (showing that there is amyloid buildup in the brain) has limited utility at this point.

    Having amyloid buildup does not mean for certain that one has Alzheimer’s dementia, especially in a patient who may not have symptoms. About 30 percent of elderly people have plaque, but not Alzheimer’s dementia. It is believed that having a positive amyloid scan may reflect the early stages of Alzheimer’s disease (prior to the dementia phase) and increase one’s risk of developing Alzheimer’s dementia in the future.

    1. D. A. Wolk, I. D. Grachev, C. Buckley, H. Kazi, M. S. Grady, J. Q. Trojanowski, R. H. Hamilton, P. Sherwin, R. McLain, S. E. Arnold. Association Between In Vivo Fluorine 18-Labeled Flutemetamol Amyloid Positron Emission Tomography Imaging and In Vivo Cerebral Cortical Histopathology. Archives of Neurology, 2011

    2. A. S. Fleisher, K. Chen, X. Liu, A. Roontiva, P. Thiyyagura, N. Ayutyanont, A. D. Joshi, C. M. Clark, M. A. Mintun, M. J. Pontecorvo, P. M. Doraiswamy, K. A. Johnson, D. M. Skovronsky, E. M. Reiman. Using Positron Emission Tomography and Florbetapir F 18 to Image Cortical Amyloid in Patients With Mild Cognitive Impairment or Dementia Due to Alzheimer Disease. Archives of Neurology, 2011.

    Michael S. Rafii, M.D., Ph.D.

    Director, Memory Disorders Clinic
    Associate Medical Core Director, Alzheimer’s Disease Cooperative Study
    University of California San Diego

    This post originally appeared in Alzheimer’s Insights, an ADCS Blog.

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    May 052011

    Congress has created a new Peer-Reviewed Alzheimer’s Research program at the Department of Defense.  The program was included in the federal spending bill signed by the president on April 15, 2011.  While countless programs received funding reductions, including a $260 million cut for the National Institutes of Health, the Alzheimer’s community secured a significant victory for Alzheimer’s research in the finalized spending bill.

    The Peer-Reviewed Alzheimer’s Research program created by Congress at the Department of Defense has been funded at $15 million for its inaugural year.  This newly created program will fund innovative and outcome-oriented research that is relevant to both the Alzheimer’s community and the military.  It will provide a vital source of new funding for Alzheimer’s researchers.

    The Alzheimer’s Association worked closely with Congress on the inclusion of this provision in the bill and looks forward to working with the Department of Defense to accelerate the development of treatments that would prevent, cure, or slow the progression of Alzheimer’s disease.  Read our full statement here.

    Oct 182010

    Dear Readers,

    Many of our patients and their physicians are aware that physical inactivity and obesity are at epidemic proportions in the United States, which has resulted in an increased prevalence of chronic diseases. Relatively few, however, realize that both these conditions may be associated with poor memory function.

    Let’s consider the issue of obesity. Over the years, obesity has truly become a woman’s issue. Sixty five million of the 72 million American adults who are considered obese or overweight are women. In addition African American and Hispanic women are much more likely to be obese than white women. So what does being obese or overweight have to do with cognition in women?

    Well, recent findings from the Women’s Health Initiative, suggest that the more an older woman weighs, the poorer her memory will be. In this study, a total of 8,745 cognitively normal, post-menopausal women ages 65 to 79 underwent baseline cognitive testing as part of their routine evaluation. This study used the Modified MMSE examination ( a 100 point memory test) as the measure of cognitive function. The 3MSE has been widely used in large population based studies as a cognitive tool and has demonstrated good consistency, reliability, sensitivity and specificity for detecting cognitive impairment and dementia. For all women, both waist and hip measurements in addition to body mass index ( BMI) calculations were obtained. All the women were classified into BMI categories that corresponded to the standard World Health Organization classifications for normal weight, underweight, overweight and obesity.

    The majority of women in this sample ( 86.6% white) were classified as overweight or obese ( 70%). For every one-point increase in a woman’s BMI, her memory score dropped by one point.( p<0.001). These findings were adjusted for age and educational level and remained unchanged after controlling for common chronic conditions such as diabetes, heart disease and stroke.

    When the analyses included waist-hip ratio, BMI and 3MSE, the 3MSE scores for women with low waist-hip ratio decreased as the BMI category increased, although this relationship reversed for women with the highest waist-hip ratios. The 3MSE score increased (i.e. better cognition) with increasing BMI in the highest waist-hip ratio category. These results suggest that women who have a “pear shaped” body type (fat deposited around the hips) have poorer cognitive function compared to “apple shaped” body type women (fat deposited around the waist).

    One explanation for these findings is that the production of endogenous estrogen (i.e. “natural” estrogen produced by the body) by abdominal adipocytes ( fat cells) may play a protective role for cognitive function and may be less detrimental than fat in other areas. Further research in this area, and whether any notable differences in the strength and nature of these associations across diverse ethnic groups, will need to be explored.

    Check out the articles and links below to learn more:

    Thanks for reading.

    Neelum T. Aggarwal, M.D.
    Steering Committee Member, ADCS
    This post originally appeared in Alzheimer’s Insights, an ADCS Blog.

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