Posts Tagged ‘Amyloid’

Is It Smart to Be Tested for Dementia?

December 21, 2013

This blog post is derived from an article1 in the Health and Science section of the Washington Post. First of all, it is difficult to distinguish early dementia from mild cognitive impairment. These are those minor memory impairments we experience as we age. About one in five people older than 75 have such blips, and most cases never progress to dementia or Alzheimer’s. I would argue further that what are experienced as mild memory impairments might not even indicate mild cognitive impairment. We experience memory failures throughout our lives, but as we age we tend to attribute these failures as cognitive impairments that we fear will lead to dementia.

Moreover, some memory lapses that might seem to be like dementia might really be something else. Danish researchers reviewed the records of almost 900 patients thought to have dementia and found that 41% of them were in error. Alcohol abuse and depression were the most common reasons for the misdiagnoses.

Small strokes that damage the arteries in the brain can cause a type of memory loss known as vascular dementia which is not Alzheimer’s. Currently, an autopsy is the only definitive test of Alzheimer’s where the telltale amyloid plaques and neurofibrillary tangels are found. However, it should be realized that autopsies have been done and found these telltale indicators in individuals who never had any of the symptoms of Alzheimer’s or dementia while they were alive.

Recent tests using brain scanning can be misleading. If, after reading this blog post, you remain worried, the first step should be to see a gerontologist or neurologist specializing in dementia. The claim is that when a full evaluation is done by somebody who knows how to do it, the accuracy of the diagnosis is supposed to be in the range of 90%.

Absent these full evaluations done by specialists, routine screening tests can be quite misleading. Even with the best screening tests, about 20% of those who turn up positive for dementia don’t actually have it. Another 30% of the people who screen positive for dementia actually have only mild cognitive impairment, which won’t progress or cause them serious problems.

Moreover, there is even some question whether early diagnosis improves outcomes. It should be acknowledged that there is no cure or preventive vaccine for Alzheimer’s. All that drugs can do is to slow the progression of the disease. Here is where I part company with the experts. What is the point of prolonging the progression of the disease? To my mind, this is simply a matter of prolonging the suffering. Our medical system is not designed to give us the best medical care, but rather the most expensive medical care. There is a strong willingness to prolong suffering so doctors and drug companies can take advantage of their last opportunity to cash in!

Moreover, little is said about the concept of a cognitive reserve. The explanation for those who have the brain damage indicative of Alzheimer’s, but not the symptoms, have built of a cognitive reserve. This healthymemory blog is filled with posts and ideas on how to build a healthy memory and a cognitive reserve.

1Christie Aschwanden (2013). Just remember this: It may not be smart to get yourself tested for dementia. The Washington Post, December 17, E5.

© Douglas Griffith and, 2013. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Douglas Griffith and with appropriate and specific direction to the original content.


Comments on an Article Titled Now is The Time for Young People to Face Alzheimer’s

September 18, 2013

First of all, let me state that I am in strong agreement with the title of the article. The author includes both personal experiences and statistics in the article. It begins with the story of the grandfather who has succumbed to Alzheimer’s and needs to be taken care of by the author and her mother. He requires around-the-clock care. Her grandfather is not alone as are over 5 million Americans suffering with this incurable and life-altering disease. “Symptoms usually develop slowly and get worse over time, becoming severe enough to interfere with daily tasks. Those with Alzheimer’s lose the ability to do things that were once routine. As the disease progresses, patients forget their loved ones’ faces, where they live and much more.

The stress of this disease, though, largely falls on the patient’s caregiver. An elderly adult caring for a loved one with Alzheimer’s has a 60 percent chance of dying before the patient, and this past June, my family saw this firsthand. My grandma Margaret died suddenly of an aneurism after caring for her husband of 60 years. Her death left our family lamenting the stress she lived with in her final years.

Stepping into my grandmother’s shoes has been a difficult experience for my mom and me. Trying to get through normal grief is hard enough, but simultaneously caring for my grandpa challenged us on many emotional levels. Slowly but surely, time eases the pain of grieving a loved one, but there remains a hole in our heart that will never be healed.

As a 19-year-old helping to take care of an 81-year-old with Alzheimer’s, I began to reflect on how this disease will affect future lives. As of now, someone develops Alzheimer’s every 68 seconds. That’s scary enough, but by 2050 people could develop the disease every 33 seconds.

The segment of the population over age 65 is also expected to double by 2030. While the number of older folks increases, the rate of those with Alzheimer’s will also increase. Millennials like myself need to acknowledge the fact that we will become the manifestations of these horrifying statistics. The five million Americans currently with Alzheimer’s are only a third of the 15 million projected to have the disease in 2050. I’m terrified to think what life will look like for the elderly when I turn 65 in 2058, and others in my generation should share that fear.

Young people tend to have an invincibility complex, through which the health issues of the elderly are the farthest thing from their minds. With such a serious health threat to our society, millennials simply cannot afford to only think about me me me. The problem of Alzheimer’s in America grows greater by the year, and we cannot wait until 2050 to start and look for solutions.

While I help with my grandpa’s care, I hope my family’s story will help others reflect on the devastating future of Alzheimer’s. Though the statistics don’t look bright, I remain optimistic my fellow millennials will try and think more about our collective health.”1

What is conspicuously missing from this articles is what millennials can do about Alzheimer’s. And that is what the healthymemory blog is about. See previous healthymemory blog posts, “The Myth of Alzheimer’s”, and “Sigmund Freud and Alzheimer’s Disease.” The individual who discovered Alzheimer’s disease, Alois Alzheimer, had serious doubts as to whether he had discovered a disease. And there are serious doubts as to whether there will be drugs developed that can either cure of provide an immunity to a disease. Current drugs slow the progression, and, in my view, prolong the suffering.

To this point, drugs have been primarily targeting the amyloid plaque and the neurofibrillary tangles that have been found in autopsies done on sufferers of Alzheimer’s. At one time, and this is perhaps still the case, this was regarded as the only definitive diagnosis of the disease. But these same plaques and tangles have been found in autopsies of people who exhibited none of the symptoms of Alzheimer’s . The explanation for this is that these individuals have developed a cognitive reserve that protected them from exhibited the symptoms.

So what should millennials do about Alzheimer’s? The same things that everyone else should do. Maintain physical and dental health and consume a healthy diet. Engage in mental activities that build cognitive reserve. Included here are mnemonic techniques, meditation, and mindfulness. Also use technology to extend your knowledge and to communicate with others. Maintaining and growing social relationships throughout one’s life is important. But “friending” on Facebook should not be regarded as building healthy relationships. And finally, read the healthymemoryblog.

1From the article.

© Douglas Griffith and, 2013. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Douglas Griffith and with appropriate and specific direction to the original content.

Passing 67

May 8, 2013

What is most remarkable of reaching my 67th birthday is that I don’t feel like I’m 67. I remember when I was a child looking at my grandparents and thinking how old they look. Now that I am at my grandparents’ age, I feel the same as I did when I was young. Perhaps I am walking a tad slower. The mileage I put on my bicycle has decreased significantly, but I think this is more a matter of choice and my wanting to pursue other activities than it is a decline in my physical condition. I am fairly confident that if I put the emphasis on bicycling I could not only meet, but perhaps exceed my previous mileage. I am still working full time. Research has shown that retirement can lead to significant cognitive decline. There is a significant correlation between the mean retirement age of a country and the average age for the onset of dementia. My work keeps me cognitively active and socially engaged, two activities important to brain and memory health.

My Mom lived to be 99 and passed away six months short of her 100th birthday. Unfortunately, for the last years of her life, she was plagued by dementia. Her advice to me was not to live as long as she did. Personally, I have no interest in living after my cognitive faculties have degraded. This healthymemory blog is one indication of my desire to extend my passion for memory health to others. The immediately preceding healthymemory blog post, “How Our Mind and Brain Work” goes into some detail for building a cognitive reserve that can ward off dementia. It should be remembered that there are individuals, both living and dead, who have the signature indicators of Alzheimer’s, neurofibrillary tangles and amyloid plaques, who never evidence the behavioral symptoms of Alzheimer’s. It is believe that these individuals had built up cognitive reserves. Stine-Morrow’s Dumbledore Hypothesis is that there is a tendency to rely upon old ways of thinking as we age and to, effectively, cognitively coast as we age. I should act that proper diet, exercise, and being socially engaged, are also important, and there are healthymemory blog posts on these topics.

There are also blog posts on “Passing 65,” and “Passing 66”, if you want to see my perspective over the years.

© Douglas Griffith and, 2013. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Douglas Griffith and with appropriate and specific direction to the original content.

An Update on the Prospect of a Cure for Alzheimer’s

April 17, 2013

A recent article provides an update on the prospect of a cure for Alzheimer’s.1 Here are some quotes from the article, attributed to neuropsychologist Peter J. Snyder, “There’s not going to be a single magic bullet… This isn’t a disease, but a syndrome with multiple etiologies.” Long time readers of the healthymemory blog might remember that Alzheimer himself was doubtful that this was a disease. His employment situation motivated him to make that argument (see the healthymemory blog post, “Sigmoid Freud and Alzheimer’s Disease”).

Previous healthymemory blog posts have made the point that autopsies of individuals who had never shown signs of Alzheimer’s were found to have substantial buildups of amyloid plaque and neurofibrillary tangles. That led me to conclude that the amyloid plaque and neurofibrillary tangles might be a necessary, but not a sufficient cause of Alzheimer’s. However, recent imaging studies have shown that about 30 percent of healthy adults who never develop Alzheimer’s have fairly substantial plaque buildups. A less common occurrence is people who have classic symptoms of Alzheimer’s but no amyloid in the brain. Consequently I have come to the conclusion that amyloid plaque and neurofibrillary tangles are neither a necessary nor a sufficient condition for Alzheimer’s.

It is important to note that large portion of the research on Alzheimer’s was targeted at this amyloid plaque and neurofibrillary tangles. This is an indication of how far off the mark this research has been. The conclusion reached by Snyder is that a cure for Alzheimer’s is not within reach. However, he argues that “If we can slow the progression by just five years, we can cut the cost of Alzheimer’s to society by 2050 by almost 50 percent. It’s an attainable goal.’

I would like to see the logic and the computations regarding this last statement. Won’t slowing the progression increase the duration of the disease and hence the costs? For myself, I have no interest in a treatment that will prolong the disease, prolong my agony.

There is the new Brain Research through Advancing Innovative Technologies (BRAIN). I am wildly enthusiastic about this project, and I am confident that much will be learned. However, I fear that it has been oversold with respect to cures for brain diseases and brain injuries. I hope I am wrong, but I am afraid that I am not.

And for you Baby Boomers , a cure is unlikely. Start building your cognitive reserve by following recommendation in the healthymemory blog and in similar publications. If you have not already, start building a healthy memory and a cognitive reserve (if you don’t know what a cognitive reserve is enter “cognitive reserve” into the search block of the healthymemory blog).

1Voelker, R. (2013) The pre-Alzheimer’s Brain. Monitor on Psychology, March, 46-49.

© Douglas Griffith and, 2013. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Douglas Griffith and with appropriate and specific direction to the original content.

Early Testing For Alzheimer’s

March 20, 2013

Alzheimer’s disease often progresses slowly. In the early stages some level of mild cognitive impairment is experienced, but life proceeds as normal. Not everyone who experiences this mild cognitive impairment will progress into Alzheimer’s. They have a twelve percent chance of developing it each year. Some will never develop dementia or will develop it from causes other than Alzheimer’s disease.1

Substantial effort has gone into developing tests to identify those with mild cognitive impairment who will progress into Alzheimer’s. This is difficult as a definite diagnosis awaits finding the amyloid plaques and neurofibril tangles. Positron emission tomography (PET) scans have been done to search for amyloid plaques in the brain that may begin to appear before symptoms manifest themselves. Research has found that healthy people with these plaques in their brains are more likely to develop Alzheimer’s related dementia later in life. However, it should be remembered that although these plaques and tangles might be a necessary condition for Alzheimer’s, they are not a sufficient condition. They have been found in autopsies of people who never exhibited any symptoms. The notion is that they had a cognitive reserve that protected them from this damage.

Tests can employ PET scans and/or Magnetic Resonance Imaging (MRI) scans along with analyses of brain fluid. I have seen no data regarding the accuracy of these tests with respect to hits (correct diagnosis) versus false alarms (incorrectly diagnosing progression into Alzheimer’s). Moreover, none of the current tests can help determine whether a person with early signs will progress quickly to dementia or continue to live normally for years.2

MRI’s have been successful in treating a condition that is frequently been misdiagnosed as Alzheimer’s (See the healthymemory blog post, “A Treatable Condition Misdiagnosed as Alzheimer’s). The condition is Normal Pressure Hydrocephalus and occurs when the cerebrospinal fluid that surrounds the brain is not re-absorped. It is estimated that 5% of the people diagnosed with dementia have this condition. Unlike Alzheimer’s, this condition can be corrected.

It is somewhat ironic that early testing for Alzheimer’s can be beneficial for the diagnoses of conditions other than Alzheimer’s. Currently Alzheimer’s cannot be cured. Drugs can slow the progression of the disease, but one should consider, is this simply prolonging the agony of the sufferer? When there are opportunities for participating in a test of a new treatment, one can volunteer in the spirit of contributing to science and the development of a possible cure, but realizing that there will likely be adverse events and the likelihood of a personal cure is quite low.

There is some evidence that people can actually reduce their risk of dementia by quitting smoking, living a heart-healthy lifestyle, and treating any diabetes or hypertension that might be present. The healthymemory blog would add being both cognitively and physically active; to continue to grow cognitively, and to build and maintain social relationships. Most healthymemory blog posts address these topics. I would hope that they all make, at least, some small contribution to cognitive growth.

1Wolfe, S.M. (ed) (2013) Early Testing for Alzheimer’s. Public Citizen Health Letter, February, Vol 29, No. 2. 4-5.

© Douglas Griffith and, 2012. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Douglas Griffith and with appropriate and specific direction to the original content.


Memory in Old Age: Different from Memory in the Young?

November 18, 2012

This blog post was motivated by an article in Scientific American Mind, “Memory in Old Age: Not a Lost Cause.”1 The article notes that older people retain their vocabulary, their knowledge about the world, how to perform routine tasks, but become worse at recalling recent events, short-term memory, and prospective memory (remembering to do things). While all this is correct, it is also the case that memory failures in older people are attributed to their age. They are referred to as senior moments and are sometime taken as warnings of incipient Alzheimer’s Disease. It should be remembered that memory failures are common at all ages and that while there is some decline in memory, not all memory failures in the elderly are attributable to aging.

The article provides techniques for remedying and mitigating these losses. They describe a variety of mnemonic techniques, which has its own category of posts in this blog, and external aids, which are referred to in this blog as transactive memory. These techniques are thoroughly covered in the Healthymemory Blog. You can also do a search on Prospective Memory. Of special relevance is the Healthymemory Blog post, “Prospective Memory and Technology.” The Scientific American Mind article also mentions the importance of physical and cognitive activity, recommendations you will also find in the Healthymemory Blog. The beneficial effects of nature, meditation, and social engagement were omitted from the Mind article, but are topics found in the Healthymemory Blog.

What strikes me is that these techniques benefit everyone, not just elderly. We should not wait until we reach old age, start becoming sensitized to our memory failures, fearful of Alzheimer’s Disease and dementia, before using these techniques and improving our memories and cognitive performance. These techniques should be introduced, as appropriate, beginning at home and in pre-school, throughout our formal education, and be part of a process of lifetime learning.

Most everyone has become knowledgeable and fearful of the amyloid plaques and neurofibrillary tangles of Alzheimer’s. A final diagnosis of Alzheimer’s awaits an autopsy confirming the presence of these plaques and tangles. What is not well known is that their have been autopsies of cadavers whose brains had these amyloid plaques and neurofibrillary tangles, but who had not exhibited any of the symptoms of Alzheimer’s while they were living. The explanation for this finding is that these people had built up a cognitive reserve that enabled them to overcome these physical manifestations of Alzheimer’s. So whatever your age, if you have not started yet, START BUILDING YOUR COGNITIVE RESERVE!

1Arkowitz, H. , & Lilienfeld, S.O., (2012). Memory in Old Age: Not a Lost Cause, Scientific American Mind, November/December, 72-73.

© Douglas Griffith and, 2012. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Douglas Griffith and with appropriate and specific direction to the original content.

New Approaches to Alzheimer’s Disease

October 17, 2012

Between 1998 and 2011, 101 experimental treatments for Alzheimer’s were scrapped. Only three drugs made it to market, and they do not cure Alzheimer’s, they merely slow it down. Treatments that target the obvious hallmarks of Alzheimer’s disease are the sticky plaques that clog up people’s brains. Two of the largest trials of treatments to attack these plaques failed. So it appears that other approaches are needed that focus on other earlier events. The immediately preceding post outlined one of these new approaches. Another article1 described new trials that are focusing on protecting synapses. Synapses are the gaps across which neurons communicate.

Bryostatin 1 is a cancer drug that has been shown to boost an enzyme, PKC episilon. This enzyme both helps form synapses and protects them against plaque. A trial that will test this drug in people with Alzheimer’s is about to begin.

Patricia Salinas and her colleagues at University College in London have shown that soluble beta-amyloid raises concentration of a synapse destroying enzyme called Dkk1. When the enzyme was blocked in cultures of brain cells, synapses remained intact. Potentially this could provide a way to protect the aging brain.

Gary Landreth and his team at Case Western University have found that another cancer drug, bexarotene, got rid of half the plaques within three days in an experiment using mice. The drug also reduced levels of beta-amyloid and the animals rapidly recovered their cognitive abilities.

The Healthymemory blog always takes pains to note that although these amyloid plaques appear to be a necessary condition, they do not appear to be a sufficient condition for Alzheimer’s. There have been autopsies of individuals whose brains all show conspicuous signs of Alzheimer’s, yet these individuals never evidenced any of its symptoms when they were alive. The explanation offered for this finding is that these people had built up a cognitive reserve during their lifetimes. The healthymemory blog is a strong advocate of building this cognitive reserve through cognitive exercise (e.g.,mnemonic techniques), and by remaining cognitively active and engaging in cognitive growth throughout one’s entire life.

1Hamzelou, J., (2012). A New Direction. New Scientist, 29 September, p. 7.

© Douglas Griffith and, 2012. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Douglas Griffith and with appropriate and specific direction to the original content.

Astrocytes and Alzheimer’s

October 14, 2012

Astrocytes are star shaped glial cells found in the brain and the spinal cord. An interesting article1 explains how these astrocytes could possibly prevent or provide a cure for Alzheimer’s. It is thought that these astrocytes make up a large percentage of the brain and have an important role supporting neurons to include clearing the beta-amyloid plaques associated with Alzheimer’s. It was recently shown that cells in the brains of people with Alzheimer’s “senesce.” This mechanism stops them from dividing and starts them on a path of destruction.

It is generally believed that cell senescence evolved to protect us from cancer. Cells can accumulate DNA damage as they age and they senesce to avoid incorrect division that can lead to cancer. The benefit of senescence over self-destruction is that it sends out a call to the immune system to destroy nearby cells that might also be affected. If the damaged cell is not killed, it goes on pumping out inflammatory proteins, which can cause damage thought to underlie age related ailments such as Alzheimer’s.

To provide some empirical data, brain slices were taken from cadavers. Slices were taken from fetuses, from people aged 35 to 50, and from people aged between 78 and 90.  The healthy brains from adults over 35 had six to eight times more senescent cells than those taken from fetuses. Cells from corpses who had had Alzheimer’s had more of these cells than their Alzheimer-free pairs of similar age. About 30 percent of the of the astrocytes seem to have senesced, a figure that was 10 percent higher in those with Alzheimer’s.

The theory is that the plaques and aging astrocytes get caught in a vicious cycle.  As the astrocytes senesce, they are less able to perform their plaque cleaning duties, and the accumulation of plaques drives more cells to senesce.2 If the astrocytes could be kept young, they could clear the plaque. The problem with preventing senescence is that it could increase the risk of cancer. Another approach is to get rid of the senescent cells. Research using mice has found that a technique for removing all of the senescent cells in a mouse prevented the onset of a range of age-related disorders. If this technique can be adapted for humans and the senescent cells can be cleared, then Alzheimer;s could probably be cleared.

Another approach might be to stop senescing brain cells from secreting their inflammatory brew. They have been found a compound that suppresses the secretions of senescent cells in the laboratory. That needs to be transitioned and tested with humans.

This work is quite promising. However, it should be remembered that beta-amyloid plaque might be a necessary condition, but it is not a sufficient condition for the onset of Alzheimer’s. There have been autopsies done of individuals whose brains were plagued by beta-amyloid plaque who had never shown any of the symptoms of Alzheimer’s when they were alive.

It is thought that keeping cognitively and physically active, and continuing to grow cognitively as we age builds up a cognitive reserve that resists or offsets these physical symptoms.

1Hamzelou, J. (2012). Why Alzheimer’s Hits Older Brains. New Scientist, 29 September, 6-7.

2Bhat, R., Crowe, E.P., Bitto, A. , Moh, M., Katsetos, C.D., Garcia, F.U., Johnson, F.B., Trojanski, J.Q., Sell, C., Torres, C. (2012). Astrocyte Senescence as a Component of Alzheimer;s Disease. PloS,

© Douglas Griffith and, 2012. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Douglas Griffith and with appropriate and specific direction to the original content.

The Exploitation of Patients with Alzheimer’s Disease

June 17, 2012

The Outrage of the Month published in the Public Citizen Health Letter1 begins “For the second time in less than two years, the Food and Drug Administration (FDA) at the behest of companies seeking to exploit the large market for Alzheimer’s Disease has approved a product with little proven benefit and documented risks.” According to the article, the earlier of these unwarranted FDA approvals occurred in July 2010 when the FDA approved a new high-dose version of the top selling Alzheimer’s drug Aricept 23. The article states that the agency approved the drug over the objections of most of its own scientists who argued that the drug did not improve overall functioning, but caused considerably more side effects than the older, lower does version of the drug.

According to the article, the most current example is the dye Amyvid that is injected into patients with possible Alzheimer’s disease and on the basis of a brain scan is used to detect amyloid plaque in the brains of such patients. Although amyloid plaque is found in the autopsies of those who have died from Alzheimer’s disease, it can also be found in individuals who never evidenced any symptoms of the disease. This test is inaccurate. It has been found to detect plaque in some patients who do not have Alzheimer’s disease and failed to detect the plaque in some patients who have the disease. Nevertheless, the dye is a financial boon for the drug manufacturer as was Aricept 23.

It is important to realize that there is no drug that cures Alzheimer’s disease. Some drugs have been shown to slow the progression of the disease. A friend of mine has a father-in-law who is suffering from Alzheimer’s and is undergoing expensive drug treatments. His father-in-law has no idea who is son-in-law is or even who himself is. This raises an interesting question. Are these drug treatments enhancing life or delaying the release from suffering that death provides? I stress that this is a question for each individual to decide.

See the Healthymemory Blog post “The Myth of Alzheimer’s” that reviews the book written by Peter J. Whitehous, M.D. Ph.D. Whitehouse is a renowned researcher into drugs for the treatment of Alzheimer’s. He has given up on there being a drug to cure the disease and is researching other methods for coping with dementia. He does not believe that Alzheimer’s is a distinct disease, but is rather a manifestation of dementia. It is interesting to note that the founder of Alzheimer’s disease, Alois Alzheimer, never was convinced that it was a distinct disease.

It should be realized that this is just another instance of the problem with medical care in the United States. Hardly anyone in the United States receives the best medical treatment. The plight of the uninsured is well known, but few realize that those at the other end of the treatment spectrum, those who receive treatment in the most expensive health care system in the world, are also ill-served. People at this end are grossly overmedicated and undergo unneccesary costly operations. See the book, Worried Sick: A Prescription for Health in an Overtreated America,” by Nortin M. Hadler, M.D.

1May 2012, 28, 5. Sidney M. Wolfe, M.D. (ed).

© Douglas Griffith and, 2012. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Douglas Griffith and with appropriate and specific direction to the original content.

Alzheimer’s and Amyloid Plaques

July 6, 2011

Much research is being done to develop tests for the early diagnosis of Alzheimer’s Disease. But conclusive diagnosis must await death and an autopsy. Amyloid plaques are the defining characteristic of Alzheimer’s Disease.1 But these require an autopsy to observe. Virtually everyone with the ailment has these plaques present in their brain. Thus, the presence of amyloid plaques appears to be a necessary condition for the disease. However, their presence is not a sufficient condition. There are people whose autopsies find that their brains are ravaged by amyloid plaques, yet they never exhibited any signs of cognitive impairment.

So the question is are the amyloid plaques the cause of Alzheimer’s or are they a symptom? An earlier Healthymemory Blog Post, “Glial Cells and Alzheimer’s Disease”, discussed the possible role that glial cells play. In spite of a large amount of research, we still don’t know what causes Alzheimer’s. Nevertheless, drugs have been developed. To this point, no drug has been found to cure or stop the progression of Alzheimer’s, but there are drugs that slow the progression of Alzheimer’s. A friend of mine told me about his father-in-law who suffers from Alzheimer’s. The father-in-law’s disease has progressed to the point where he does not remember who his son-in-law is. He no longer remembers who he himself is. Still he receives expensive drugs that will slow his death as well as slow his release from his miserable state.

Much work is also being done to develop tests that can diagnose Alzheimer’s early. The hope is that early diagnosis will enable early treatment which will either cure Alzheimer’s or reduce the progression of the disease to a crawl. But, there are no treatments yet. Personally, I have no interest in taking a test that will inform me I have an incurable condition. I do, however, applaud those who take tests and participate in experimental trials of drugs with the hope that they will lead to a successful treatment.

It should be remembered that all tests are flawed and produce false alarms. That is they can inform you that you have the condition, when in fact you do not. Also remember the cases discussed above in which brains that are ravaged with amyloid plaques belonged to people who exhibited no evidence of cognitive decline. How can this be? The most prominent theory is that these people had a cognitive reserve that either prevented the occurrence of the disease or slowed its progression to the point where it was not noticeable. These cognitive reserves are thought to be the result of people who stayed mentally active. Leading a healthy lifestyle is also important. So the path I am following is to build up this cognitive reserve. The Healthymemory Blog is devoted to activities and information that should be helpful in building this cognitive reserve.

1Weir, K. (2011). Memory keepers. Monitor on Psychology, June, 32-35.

© Douglas Griffith and, 2011. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Douglas Griffith and with appropriate and specific direction to the original content.

Glial Cells and Alzheimer’s Disease

May 8, 2011

A preceding post (“Our Neurons Make Up Only 15 Percent of Out Brain Cells”) highlighted the importance of glial cells to brain function. It was based on an article1 in Scientific American Mind, on which this current blog post is also based. The discoverer of Alzheimer’s Disease, Alos Alzheimer noted that microglia surround the amyloid plaques that are the hallmark of the disease. Recent research suggests that microglia become weaker with age and begin to degenerate. This atrophy can be seen under a microscope. In aged brain tissue, senescent microglia become fragmented and lose many of their cellular branches.

One more sign of microglial involvement can be found in the way Alzheimer’s courses through the brain. Damage spreads in a predetermined manner. It begins near the hippocampus and eventually reaches the frontal context. Microglial deneneration follows the same pattern but precedes the advance of neuronal degeneration, Alzheimer and most experts had presumed that microglial degeneration was a response to neuron degeneration. This new research suggests that the senescence is a cause of Alzheimer’s dementia. The hope is that once researchers learn why microglia become senescent with in some people but not in others, new treatments for Alzheimer’s could be developed.

It is also interesting to note the path of progression of the disease. It begins near the hippocampus, a cortical structure critical to memory. Memory loss can be an early indicator of Alzheimer’s. The disease then progresses through the cortex to the frontal cortex. So more memory loss occurs as more cortex is destroyed. The frontal cortex is where most planning occurs. It plays an important role in focal attention. The executive functions of the frontal lobes include the ability to recognize future consequences from current actions, to choose between good and bad actions, to override and suppress unacceptable social actions, and determine similarities and differences between things and events. In short, it is key to higher mental functions.

1Fields, D.R. (2011). The Hidden Brain. Scientific American Mind. May/June, 53-59.