The 8 Common Causes of Dementia

Contributed by: Dennis Fortier, President, Medical Care Corporation
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I hear and read confusing comments about dementia on a daily basis. Most commonly, I find that people fail to distinguish between diseases and medical conditions that impair thinking and the advanced state of impairment that we call "dementia".

Perhaps this excellent summary from HealthBridge of dementing medical disorders will help clarify the issue. I found the list to be accurate and the supporting details well documented. I encourage you to click through and read the summary but if you want to know the eight conditions on the list, I've noted them here:

1. Alzheimer's disease
2. Vascular Dementia
3. Mixed Dementia
4. Dementia with Lewy Bodies
5. Parkinson's Disease
6. Frontotemporal Dementia
7. Creutzfeldt-Jakob Disease
8. Normal Pressure Hydrocephalus

Diagnosing the Cause of Memory Loss

Contributed by: Dennis Fortier, President, Medical Care Corporation
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Having memory loss or cognitive impairment does not mean that you have Alzheimer's Disease (AD). This important message is developed more completely at PreventAD.com, an informational website geared toward preventing Alzheimer's disease by educating the public on how to best delay its onset and progression.

Through a standard medical evaluation and diagnostic protocol, physicians often find that depression, a metabolic disorder, or other medications are impairing a patient's memory. By following published guidelines and ruling out other causes of memory loss, physicians can diagnose AD with better than 90% accuracy at an early stage of the progression.

Diagnosing Alzheimer's Disease early and accurately is crucial because for every month that treatment is delayed, there is irreversible loss of function. Current treatment of mildly-to-moderately demented AD persons with FDA-approved medication can delay AD progression meaningfully in some patients; the earlier treatment is started the more effectively the progression of AD is blocked, and the longer it is delayed.

Below are suggested steps to get the right diagnosis:

1. Find the Right Physician
2. Get Tested Professionally
3. Collect Patient and Family History
4. Identify Treatable Medical Conditions
5. Brain Imaging Studies
6. Final Diagnosis

Based on the history, examination, laboratory and brain imaging results, a properly trained physician can diagnose the cause of your condition with 90% accuracy or higher using NINDS-ADRDS criteria. Typically it takes a few weeks to complete a diagnostic evaluation of ADRD.

NIH State of the Science Conference

Contributed by: Dennis Fortier, President, Medical Care Corporation


As I write often, the purpose of this blog is to help readers discriminate between press about solid science and press with a hidden or contorted agenda. Of course, every source has some bias so it is best to read broadly, cultivate your ability to discern, and make your own decisions about the state of the science.

One particularly good source of well-vetted, scientific summary is the National Institute of Health. Among the many ways they contribute to objective scientific inquiry is their "State of the Science" conferences. On April 26-28 they will convene such a conference on "Preventing Alzheimer's Disease and Cognitive Decline".

The purpose of the conference is to evaluate the available scientific information on Alzheimer’s disease (AD) and develop a statement that advances understanding of the issue under consideration and will be useful to health professionals and the public.

Discussion topics will include:
  • What factors are associated with the reduction of risk of AD?
  • What factors are associated with the reduction of risk of cognitive decline in older adults?
  • What are the relationships between the factors that affect AD and the factors that affect cognitive decline?
  • What are the therapeutic and adverse effects of interventions to delay the onset of AD?
  • What are the therapeutic and adverse effects of interventions to improve or maintain cognitive ability, or preserve cognitive function? Are there different outcomes in identifiable subgroups?
  • If recommendations for interventions cannot be made currently, what studies need to be done that could provide the quality and strength of evidence necessary to make such recommendations to individuals?
These conferences are free to attend, allow the public as well as professionals with an opportunity to contribute, and culminate with an objective summary about the state of the science in the particular field. If you know someone with an interest, please pass this on to ensure they are aware of the opportunity to participate. Even if attendance is not practical, let's all be aware of the forthcoming consensus report that the conference will generate and make available.

Tests to Identify Alzheimer's Disease



















Contributed by: Dennis Fortier, President, Medical Care Corporation

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This post starts with a disclosing reminder that I work for Medical Care Corporation, a company focused on developing assessment technologies aimed at helping physicians evaluate patients with memory concerns. As such, I pay close attention to developments in the cognitive testing space.

Two New Tests
I have noticed several news items recently on two interesting new instruments: the Five-Word Test (5WT) and the Computer Self Test (CST). A study on the 5WT was presented in Thessaloniki, Greece at the 25th Annual Conference on Alzheimer's Disease (ADI). Research on the accuracy of the CST was published in the Journal of Alzheimer's Disease.

These stories are news worthy because Alzheimer's disease is routinely diagnosed at a very late stage of progression when treatment is fairly ineffective. As such, earlier intervention is currently our best opportunity to improve treatment efficacy. Developing brief and accurate assessment technologies for use in primary care settings could facilitate a great advance in standards of care for aging patients with memory concerns.

Daunting Challenge: Ensuring Clinical Utility
The biggest hurdle is, to make medical, economic and logistical sense, a tool for clinical use must satisfy some daunting criteria that seem to work against one another.

For example, the tool must be highly accurate if used in assisting medical decisions but must also be very brief since primary care physicians are limited in the time they can spend with each patient. The best way to improve accuracy is to add items to a test battery but doing so increases the time requirement for administration which is problematic.

Additionally, the tool must be simple enough to facilitate easy adoption but sophisticated enough to qualify for reimbursement by major insurance payers. This is another challenging trade-off. As we all know, most physician's practices are small businesses and cannot absorb the costs of additional procedures, particularly those that require specialized knowledge and staff training, if they are not paid to conduct these new procedures. All told, developing a clinically effective tool is a tricky and elusive proposition.

Detecting "Dementia" is Too Late
The 5WT and the CST seem to outperform common instruments like the Mini Mental State Exam (MMSA) and the Montreal Cognitive Assessment. Both of these common tests have a purpose but neither has been shown useful in detecting pre-dementia stages of memory loss. Therefore, outperforming them does not necessarily imply clinical utility in detecting subtle memory loss. In fact, the research on the 5WT and the CST was designed to verify accuracy in identifying "dementia".

As we have written here often, dementia is a descriptive term for a fairly severe degree of impairment (a demented person has lost such a degree of mental function that they can no longer care for themselves). Considering this, a tool for identifying dementia does not enable earlier intervention against Alzheimer's disease as, in fact, it is in the dementia stage that primary care physicians are currently intervening. As most physicians will tell you, once a patient is demented, no test is required to determine that something is wrong.

Detecting Mild Cognitive Impairment
To improve standards of care, we need tools that separate healthy aging from more subtle stages of memory loss so that physicians can diagnose an earlier stage problem and treat it before it progresses and causes irreparable damage. According to the peer-reviewed medical literature, the most accurate assessment technology suitable for clinical use is the MCI Screen. It is brief, simple, and accurate in detecting the earliest stages of subtle cognitive decline. And perhaps most importantly, it is reimbursed by Medicare and all major payers.

Why is AD More Prevalent Among Minorities?

Contributed by: Dennis Fortier, President, Medical Care Corporation
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With yesterday's release of the Alzheimer's Association's report (2010 Alzheimer's Disease Facts and Figures), one aspect of the report has been greatly emphasized in the press over the past day and a half. I refer to the report's stark conclusion that African-Americans and Hispanics are being especially hard hit.

In fact, according to the report, older African-Americans are about twice as likely as older Whites to have Alzheimer's disease and older Hispanics are about one and a half times as likely. The most obvious conclusion that readers may jump towards is that some genetic difference predisposes risk differently across the human races. However, there is a much better explanation described in more detail by U.S. News and World Report.

Many risk factors play a role in determining the likelihood of any given individual getting Alzheimer's disease. Some of the more well-established risk factors, such as high blood pressure, diabetes, and stroke, are known to be more prevalent in certain populations. There is certainly a correlation between the higher incidence of these risk factors among African-Americans and Hispanics and the incidence of Alzheimer's disease in those populations.

The good news is that these risk factors can be controlled through medical intervention. Theoretically, this should allow us to also reduce the prevalence of Alzheimer's disease in those populations.

Public Alzheimer's Discussion

Contributed by: Dennis Fortier, President, Medical Care Corporation
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A great online forum for discussing Alzheimer's disease was conducted today through Twitter. Mayo Clinic's lead expert in the area, Dr. Ronald Petersen, joined the National Alzheimer's Association and USA Today in responding to questions from the public.

Given yesterday's release of the National Alzheimer's Associations report (2010 Alzheimer's Disease Facts and Figures) about the disease, I had expected many questions about specific prevalence statistics, differences across minority groups, and rising cots of managing the disease. Instead, the questions tended toward the more personal and more locally relevant.

While the national discussion about Alzheimer's and Dementia is becoming louder and more intense, it is generally based on aggregated data that have been evaluated from afar in a scientific and impersonal manner. I found today's dialogue, which you may review here, to be refreshingly intimate.

I am hopeful that such discussions will flourish and that such public access to the central players in this field will catalyze a growing base of activism. Great job by the Mayo Clinic, the National Alzheimer's Association, and the USA Today.

Could Alzheimer's be Caused by Infection?

Contributed by: Dennis Fortier, President, Medical Care Corporation
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Beta amyloid is certainly a central component in Alzheimer's pathology. No one refutes that it is toxic to brain cells and that an accumulation of amyloid plaques is a hallmark indicator of Alzheimer's disease.

The amyloid hypothesis suggests heavy amyloid deposition in the brain is the underlying cause of this disease and we have discussed it here on many occasions (read past posts on the amyloid hypothesis here).

Having said that, there is no consensus and no well-validated explanation of why beta amyloid accumulates in some brains and not others. Nor is there a definitive understanding of why some people have lots of amyloid deposition but remain cognitively sharp.

Because an increased production of beta amyloid is a known reaction to head trauma and stroke, some have hypothesized that it plays a neuro-protective role and its presence is an indication of the brain attempting to repair itself from some other harm. Accordingly, beta amyloid could be viewed as part of a solution to some other problem.

Scientists at Massachusetts General’s Institute for Neurodegenerative Disease suggest that the other problem might be microbial infection. Their research, published in the journal PLos One, showed that brain tissue with lots of beta amyloid taken from Alzheimer's patients inhibited growth of several infectious organisms whereas brain tissue taken from healthy adults did not. This suggests that increased production of beta amyloid might be a natural defense mechanism when certain infections are present in the central nervous system.

If such an "infection hypothesis" is confirmed as the underlying cause of Alzheimer's, it would support the notion that amyloid toxicity is what degenerates the brain in Alzheimer's patients but would suggest a different treatment approach. That is, rather than removing the amyloid, a better approach would be to remove the infection that is stimulating amyloid production.

At that point, the challenge would be to find treatments that can cross the blood/brain barrier and fight infection in the brain.

FDA Drug Approval Process

Contributed by: Dennis Fortier, President, Medical Care Corporation
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With today's news about the failure of the Dimebon trial, it may be a good time for a refresher on the FDA drug approval process. Last April, this succinct summary was posted by Dr. Michael Rafii.

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Dimebon Fails Phase III Trial

Contributed by: Dennis Fortier, President, Medical Care Corporation
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The best candidate for a new Alzheimer's treatment has taken a step backwards with the failure of Dimebon to show a benefit in the CONNECTION study. While it is not surprising for a drug to fail a trial, especially in the Alzheimer's space where the disease is poorly understood, there was a sense of optimism around Dimebon that I hadn't sensed in some of the other recent trials.

In this study, 598 adults with mild to moderate AD were given either Dimebon or a placebo for a six-month period and effect on cognitive function was evaluated. Unfortunately, the drug group did not out-perform the placebo group.

The drug sponsors (Pfizer and Medivation) are conducting other trials for Dimebon including one in later stage patients and another in conjunction with Aricept. There is some hope that the drug could be approved with narrower indications based on success in one of these other studies.

Nonetheless, this result was a disappointment and bodes poorly for the immediate future of AD treatment.

Can a Purposeful Life Stave off Alzheimer's?

Contributed by: Dennis Fortier, President, Medical Care Corporation
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Headlines stating that a purposeful life can stave off Alzheimer's disease are all over the media this week. The frenzy has been sparked by a study out of Rush University Medical Center and published in Archives of General Psychiatry.

In the study of 951 older people without dementia, respondents were asked to indicate how much they agreed or disagreed with statements about their happiness and sense of purpose in life. After an average follow-up of about four years, researchers noted that those respondents who indicated more purposeful lives were less likely to be diagnosed with Alzheimer's and had slower rates of cognitive decline.

The potential to overstate this conclusion becomes obvious if we reverse the headline. Rather than asking "Can a purposeful life stave off Alzheimer's?" we could ask "Does Alzheimer's prevent a purposeful life?" Given the long incubation period of the disease, during which the brain is degrading without visible symptoms, it is plausible to draw the opposite conclusion. That is, perhaps the presence of undetected, early-stage Alzheimer's disease prevents people from pursuing full and "purposeful" lives.

The data in this study are equally supportive of each conclusion but one perspective yields better headlines.

I think most of the stories about this study, including this one in the US News & World Report, are presented fairly. However, the headlines I have seen have been generally misleading in terms of how they imply a causal relationship between a purpose-driven lifestyle and a resulting benefit in cognitive health.