Tuberculosis Has Been Shown to Cause Dementia

Tuberculosis has a long history with dementia and specifically Alzheimer’s disease, one type of dementia.

Tuberculosis (TB) is caused by a slow growing bacterium with the name of Mycobacterium tuberculosis. The “myco” in mycobacterium refers to a thicker than normal cell wall. Because it grows slowly, TB spreads from person to person only through frequent and close contact. By breathing the bacterium, TB usually starts by attacking the lungs first and then spreads (seeding) to other parts of the body, including your kidneys, brain and spine. Wherever it seeds it damages the organ. In the kidneys it causes urine and blood in the urine (sterile pyuria), Pott disease (spondylitis) in the spine, hepatitis in the liver, lack of steroid hormones (Addison’s disease) in the adrenal gland, swelling in the neck (scrofula) in the cervical lymph nodes, and inflammation (meningitis) in the brain. Meningitis is the inflammation of the three membranes (meninges) protecting your brain and spinal cord. The tough outer membrane is called the dura mater, then the arachnoid and finally the delicate pia mater, the inner most layer that touches the brain. TB meningitis affects one in fifty cases of TB (much higher among children and those with HIV.) When these protective layers are attacked there are serious consequences to the brain.

The average survival with such TB–ridden brain was seven years, similar to the mortality span of Alzheimer’s disease. Most patients with Alzheimer’s disease typically die from infection or pneumonia and not cognitive decline—we will revisit this again later.

In 2010 Neil Anderson with Auckland City Hospital, New Zealand and his colleagues reported that people with TB meningitis had serious complications. Around a third suffered from a stroke, problems with eye/eyelid, pupil and lens, and epileptic seizures.  Around one in twenty suffered from the treatment itself (iatrogenic) through drug-induced hepatitis, while a fifth of the patients died early from the disease. For those that survive, one in ten had long-term cognitive impairment and/or epilepsy. With such dramatic complications it is surprising to realize how common TB remains to this day.

After HIV, TB is the major cause of death from a single infectious agent and is one of the top 10 causes of death worldwide with 1.8 million people dying from the disease in 2016. Drug-resistant strains of TB have already been identified in 105 countries including the U.S., and once infected, we cannot do anything but watch helplessly as the person dies.

But there is another twist to the story of this bacterium.

In 2017 Lawrence Broxmeyer with the New York Institute of Medical Research, undertook a historical review of how TB might have been the cause of Alzheimer’s disease even during Alois Alzheimer’s time. Broxmeyer argues that Alzheimer must have known this but elected to ignore it. By 2013 Francis Mawanda and Robert Wallace with the University of Iowa, reported that one of the prime suspects for Alzheimer’s disease was chronic bacterial infections like tuberculosis. The brilliant Oskar Fischer of the Prague clinic, a contemporary of Alois Alzheimer, noted this as well. The competition between Alzheimer’s Munich clinic (headed by Emil Kraepelin) and Fischer’s Prague clinic (headed by Arnold Pick) predestined animosity. And there was no collaborative effort to reconcile these observations about TB and Alzheimer’s disease. Instead the Munich clinic was out for glory and the creation of a “new” disease to enhance their legacy.

We continue discovering that there are many causes of Alzheimer’s disease. The disease is a reaction to these many traumas. In response to this trauma, studies are now strongly pointing to inflammation—a reaction to these traumas—that causes the damage to brain cells. Inflammation, seen as a penumbra on imaging techniques, is a shadow of dying cells in the brain. The question still remains how the inflammation—the penumbra—can be reduced and eliminated while for others the inflammation continues to grow nonstop. Each cause of dementia—for example, physical trauma from playing football or TB—will have its own pattern of progression. And this is the rub.

While federal funds are squandered on looking at the progression of the disease, the causes of dementia remain in the shadow of the research spotlight. The outcome of this ignorance is the utter lack of progress made in the last 100 years and the zero clinical outcomes from forty years of U.S. National Institute on Aging funding. Zero.

An alternate approach would be to focus on preventive measures. Not as sexy as “finding the cure” but we can guarantee success on day one. Diet and exercise, always a good strategy for a fulfilling life, is not enough. The low hanging fruit would involve protecting the head during contact sports and other activities where physical trauma eventually leads to dementia. Better vascular management, treatment and control are a second line of attack that will significantly reduce dementia rates. The third line of attack is to understand and control inflammation. It seems contradictory, but overall, in order to prevent dementia, research needs to move away from dementia and move again to basic science. Dementia is broader than what our focus has been so far. Historically politics dictated this narrow approach, but science is pointing in a different direction, but we seem to remain shackled to the past.

Emerging research shows that one type of trauma that causes dementia are bacteria, with TB being a very common bacteria agent among humans. But this is not just about “killing the bacteria.” Bacteria, and especially TB that we see today are not the same bacteria we saw a hundred or a thousand years ago. They have evolved with us. And they are still evolving and matching our development. We are evolving with them both as a species, as a community (different TBs across the globe) and as we age. This could (partially) explain why some people can control the spread of the penumbra, the inflammation, while others relent to its power.

Laura Pérez-Lago, from Madrid General Hospital and her colleagues found that there are many different types of tuberculosis bacterium within the same patient. They also found that individuals infected with TB might have genetics that promote TB to mutate. It seems that we continue co-evolving with the TB bacterium and some people allow for the bacterium to change within us while others restrict it from changing. Peng Yi-Hao, along with the China Medical University Hospital in Taiwan, looked at more than six thousand patients newly diagnosed with TB patients. Although patients that had TB were more likely to have other existing health problems—including; irregular heartbeat (atrial fibrillation), hypertension, diabetes, heart failure, stroke, depression, and head injury, all of which are correlated with increased risk for dementia—after controlling for these factors the overall risk of developing dementia in six years was higher, by an additional one person for every five in the non-TB patients. Among the patients with TB, men and people between 50 and 64 years were more likely to develop dementia compared to the TB-free group. Except for the patients with TB, those with a head injury exhibited the highest risk of developing dementia.

What seems to be emerging is that there is likely a genetic predisposition to allow TB to mutate and cause damage to many organs in the body, including the brain. Also with age we become more susceptible to TB and our inflammation response becomes a greater problem for the brain to cope with.

Nicholas Dunn with the University of Southampton, UK and his colleagues confirmed this point when they showed that elderly patients with dementia have a higher ratio of infection episodes in the four years preceding the diagnosis of dementia.  We become more prone to infections, which causes inflammation which harms us as we age.

The lesson that TB is teaching us is that we need to look at the many possible ways that the brain can be hurt. Focusing on the trauma that starts the cascade of inflammation is a sure bet to eventually be able to first understand the dementia and then perhaps cure it. Like cancer, dementia is neither simple nor static. The role of TB in causing dementia has waited too long to be given the importance it deserves.

© USA Copyrighted 2017 Mario D. Garrett  

References

Alvarez, P (1919). Relation between tuberculosis and dementia praecox. Dement. Praecox. Stud, 2, 1-2.

Amor, S., Puentes, F., Baker, D., & Van Der Valk, P. (2010). Inflammation in neurodegenerative diseases. Immunology, 129(2), 154-169.

Anderson, N. E., Somaratne, J., Mason, D. F., Holland, D., & Thomas, M. G. (2010). Neurological and systemic complications of tuberculous meningitis and its treatment at Auckland City Hospital, New Zealand. Journal of Clinical Neuroscience, 17(9), 1114-1118.

Broxmeyer, L. (2017). Are the Infectious Roots of Alzheimers Buried Deep in the Past?. Journal of MPE Molecular Pathological Epidemiology.

Castañeda-García, A., Prieto, A. I., Rodríguez-Beltrán, J., Alonso, N., Cantillon, D., Costas, C., ... & Tonjum, T. (2017). A non-canonical mismatch repair pathway in prokaryotes. Nature Communications, 8, 14246.

Dunn N, Mullee M, Perry VH, Holmes C. Association between dementia and infectious disease: evidence from a case-control study. Alzheimer Dis Assoc Disord. 2005;19(2):91-94.

Eikelenboom, P., Hoozemans, J. J., Veerhuis, R., van Exel, E., Rozemuller, A. J., & van Gool, W. A. (2012). Whether, when and how chronic inflammation increases the risk of developing late-onset Alzheimer's disease. Alzheimer's research & therapy, 4(3), 15.

Garrett, M (2015) Politics of Anguish: How Alzheimer’s disease became the malady of the 21^st century. Createspace.

Glass, C. K., Saijo, K., Winner, B., Marchetto, M. C., & Gage, F. H. (2010). Mechanisms underlying inflammation in neurodegeneration. Cell, 140(6), 918-934.

Mawanda F, Wallace R (2013) Can infections cause Alzheimer's disease? Epidemiol Rev 35: 161-180.

Peng, Y. H., Chen, C. Y., Su, C. H., Muo, C. H., Chen, K. F., Liao, W. C., & Kao, C. H. (2015). Increased Risk of Dementia Among Patients With Pulmonary Tuberculosis: A Retrospective Population-Based Cohort Study. American Journal of Alzheimer's Disease & Other Dementias®, 30(6), 629-634.

Pérez-Lago, L., Palacios, J. J., Herranz, M., Serrano, M. R., Bouza, E., & García-de-Viedma, Dario. (2015). Revealing hidden clonal complexity in Mycobacterium tuberculosis infection by qualitative and quantitative improvement of sampling. Clinical Microbiology and Infection, 21(2), 147-e1. 

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Is Mouth Bacteria Causing Dementia?

In the 1897 fictional book War of the Worlds, H.G. Wells kills off the invading Martians and their gigantic robotic machines, by microbial infection. Two hundred years later we are just now appreciating the power of this microbial world.  We have been resisting studying how bacteria influence our behavior, including our mental health, in favor of the obvious low hanging fruit: a malfunction. Areas of study include the gut, but the best way to study bacteria is to look at it as it gets into our system through our mouth. [1]

In 2017 Kenji Takeuchi, with Kyushu University, Fukuoka, Japan and his colleagues reported that people in their 60s, who lost their teeth were more likely to get dementia five years later. And there was a dose effect, with fewer teeth the higher the rate of dementia, peaking at nearly twice as high. Only when older people completely had no teeth did this rate of dementia drop slightly.

What was interesting was that the same result was not found for vascular dementia—when dementia is caused by lack of blood supply to the brain. Having fewer teeth promoted dementia through something other than a problem with blood supply to the brain—the main cause of dementia.  Could this be the elusive cause of Alzheimer’s disease?

In a comprehensive review of periodontal disease and its relation to aging, the Brazilian Eder Abreu Huttner and Eduardo Hebling and their colleagues reported that although aging alone does not cause periodontal disease, aging does increase the risk by having less resilience, fostering conditions promoting the disease, and having a biological reaction that is more damaging than for younger people.

Controlling for other effects is difficult. For example Kenji Takeuchi also reported that teeth loss was related to having less than 10 years formal education.. After age, lack of formal education by itself remains the best predictor of dementia. Education has a protective function, perhaps delaying rather than eliminating dementia. Related to education is also income.  

In 2008 Nora Donaldson with King’s College London, and her colleagues reported data on 3,817 participants in the UK and found that social economic status had direct influence on the number of good teeth participants had. Richer people made better use of preventive care and also independently had better teeth. There is also a genetic component to teeth loss. With the main contender for dementia being the apolipoprotein E epsilon 4 gene we also find that this gene is also related to teeth loss. All of these factors can moderate and mediate the susceptibility to teeth loss.

Then in 2006 Margaret Gatz with the University of Southern California and her colleagues addressed these factors by using a Swedish study of identical twins. By controlling for most of these social and genetic factors, the authors report that the twin who had tooth loss before age 35 was 5.5 times more likely to develop Alzheimer’s disease. Tooth loss is directly involved in Alzheimer’s disease. We also observe that  centenarians—those that have lived to a 100 years and older—and their offspring have slight but significantly better oral health than their respective peers when they were in their early 60s.

Tooth loss can be caused by many factors, but the main contender seems to be periodontal disease. Periodontal disease is caused by bacteria that initially forms a sticky “plaque” which if not removed by brushing can harden and form “tartar” that attacks the gum causing “gingivitis” and eventually infects the tooth and bone as ”periodontitis.” The association of periodontal disease with dementia has been reported in many studies. In one recent 2017 review Yago Leira Feijóo and his colleagues with the University of Santiago de Compostela, Spain concluded that those with severe forms of periodontal disease are nearly three times more likely of getting dementia.

The cause of periodontal disease is primarily bacteria. But the story is more nuanced.  There are some 400 bacterial species populating the mouth in symbiosis with some viruses and maybe even fungi. A concoction that is also capable of invading the brain.  Although we still do not know how they get there. [2] It could be that the effect on the brain is indirect. Angela Kamer with the NYU College of Dentistry, and her colleagues proposes that it is likely that this mouth cocktail causes an inflammatory reaction throughout the body that also affects the brain.[3] But the brain also has traces of these microbes.

It is surprising to learn that the brain can be infected with the same microbial world that H.G. Wells wrote about 200 years ago. But unlike the story, in reality these microbes are killing humans instead of Martians. Autopsy studies find bacteria, fungi, viruses and a host of other microbial infections in our brain, especially among people that die with dementia. In 2011 Judith Miklossy confirmed these associations when she found that in four out of five autopsied brains of Alzheimer's patient there were spirochetal bacteria that originate in the mouth. [4]

In some cases these infections can be activated—both the rate of infection and the response—when the immune system is compromised through stress or other unknown mechanisms. This initial infection can cause inflammation in the brain and it is this inflammation that attacks the brain from inside. Ruth Utzhaki and her colleagues, in a 2016 review, came up with incontrovertible evidence that Alzheimer’s disease has a microbial component. Although always present, the authors report that this microbial world is woken up by an iron imbalance in the brain. An iron rich brain causes microbes to flourish, causing a reaction. There might be many such tipping points—that awaken this sleeping and toxic world—among older adults.

In fact the hallmarks of Alzheimer’s disease—plaques and tangles—are observed in mice and in cell culture after an infection with herpes simplex virus or bacteria. These plaques and tangles have been found to have anti-microbial function against multiple bacteria, yeast and viruses. In response to a microbial world that exists around and within us. The World Health Organization estimates that 3.7 billion people under age 50 have the non-sexually transmitted herpes simplex virus infection globally. Around a third to half of all adults in developed countries have periodontal disease. So bacteria and viruses are already present, the issue is how does bacteria, in particular, invade and damage our brain.

Bacterial infection is not simple. With periodontal disease, bacterial infection is dependent on the presence of the infection together with the susceptibility of the individual, including a direct genetic susceptibility. However age seems to be the main reason why we become more susceptible to these infections. With greater susceptibility and immune deficiency, older adults are more likely to suffer bacterial infection that results in periodontal disease that promoted dementia. And this is bi-directional, as memory lapses, dental care is further ignored, increasing the continual onslaught of infection in the brain.  A central aspect of this theory is that there is a multiplying effect with the infection causing an initial inflammatory reaction in the brain, making it susceptible to more infection. [5]

Since the plaques and tangles are in fact not dead cells as presumed, but very much alive, the idea that the plaques and tangles—characteristic features of Alzheimer’s disease—are protecting the brain seems plausible. Despite the success of drugs eliminating these plaques and tangles there has been no improvement in cognition. As a result there is now enough evidence to accept that the plaques and tangles are a reaction to lesions in the brain rather than what Alois Alzheimer initially proposed as the disease itself. They are brain scabs caused by a brain lesion. Bacterial infection is such one of many such lesions that the brain has to contend with on a daily basis. Bacteria that enters the mouth and is cultivated through periodontal disease is an important sources of infection.

Overall these studies indicate that it is biologically feasible for oral bacteria to go through the bloodstream, reach the brain and either initiate or promote existing lesions and cause an inflammatory response. The brain reacts by protecting itself through inflammation and surrounding the toxic substance with plaques and tangles. If this inflammation mechanism is the cause of dementia then perhaps simple medication can lower the inflammation in the brain.

Jeffrey Rich with the Sentara Cardiovascular Research Institute, Norfolk, Virginia; USA and his colleagues conducted a follow-up study looking at the use of non-steroidal anti-inflammatory drugs (NSAIDs)—include aspirin, ibuprofen, naproxen, COX-2 inhibitors, and other medications They found that the group using the NSAIDs had slower progression of the disease a year after initiating treatment. Although in a much later study, when they performed autopsies on these same patients, the authors reported that some had vascular dementia as well as Alzheimer’s disease (which diffuses the effect of inflammation on Alzheimer’s disease). However the results are still positive. In a review of the literature, the Dutch William van Gool and his colleagues make the argument that the body is maintaining a balance, that not all inflammation is bad, that some of the benefits of these medication might have nothing to do with inflammation and that the timing is important and they might only work at the early stages of the disease.

It seems that we are still on the periphery, searching for answers to a complex disease, in a piecemeal fashion, without coordination. Perhaps we are reaching our own tipping point in science and will have to admit that the body is a supraorganism. [6] The appreciation that other organisms live in harmony with and within us is a finely tuned symphony that aging has a way of disrupting.

© USA Copyrighted 2017 Mario D. Garrett  

This blog was initiated by a discussion with Peter Kraus.

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[1]

It has long been known that there is a direct effect of oral bacteria such as Porphyromonas gingivalis and Streptococcus sanguis on induction of platelet activation and aggregation, which in turn contributes to heart disease such as atheroma formation and thrombosis. See earlier blog

https://www.psychologytoday.com/blog/iage/201305/aging-teeth

Also studies have consistently shown that mothers with significant periodontal disease had a 7.5 fold increase in the risk of having a preterm, low birth weight baby.
There is also a relationship between periodontal disease and diabetes, with improved metabolic control seen in poorly controlled diabetics following periodontal therapy.
The periodontal bacterium P. gingivalis has also been linked to rheumatoid arthritis through the enzyme peptidylarginine deiminase.

[2]

Among periodontal bacteria, species such as A. actinomycetemcomitans, P. gingivalis, T. denticola and F. nucleatum are capable of invading the brain. 

[3]

This reaction involves; cytokines—substances, such as interferon, interleukin, and growth factors, that are secreted by certain cells of the immune system and have an effect on other cells; and C-reactive protein (CRP)—substance produced by the liver that increases in the presence of inflammation in the body. CRP increases up to 1000 folds in acute inflammatory diseases. These cytokines and CRP stimulate glial cells to produce amyloid-β 1-42 peptide (Aβ42) and hyperphosphorylated tau protein (P-Tau).

[4]

But there is also an indication that the infection can also come from outside infection such as Lyme bacteria.

https://www.psychologytoday.com/blog/iage/201705/the-coming-pandemic-lyme-dementia

[5]

Characterized by the production of high levels of inflammatory mediators such as IL-1, IL-6, IL-17 and TNF-α, and low levels of anti-inflammatory molecules such as IL-10

[6]

We are becoming Gods

https://www.psychologytoday.com/blog/iage/201511/we-are-becoming-gods

Geography of Aging and the Illusion of Self

https://www.psychologytoday.com/blog/iage/201505/geography-aging-and-the-illusion-self

References
Donaldson, A. N., Everitt, B., Newton, T., Steele, J., Sherriff, M., & Bower, E. (2008). The effects of social class and dental attendance on oral health. Journal of Dental Research, 87(1), 60-64.

Gatz, M., Mortimer, J. A., Fratiglioni, L., Johansson, B., Berg, S., Reynolds, C. A., & Pedersen, N. L. (2006). Potentially modifiable risk factors for dementia in identical twins. Alzheimer's & Dementia, 2(2), 110-117.

Itzhaki, R. F., Lathe, R., Balin, B. J., Ball, M. J., Bearer, E. L., Braak, H., ... & Del Tredici, K. (2016). Microbes and Alzheimer's disease. Journal of Alzheimer's disease: JAD, 51(4), 979.

Kamer, A. R., Dasanayake, A. P., Craig, R. G., Glodzik-Sobanska, L., Bry, M., & De Leon, M. J. (2008). Alzheimer's disease and peripheral infections: the possible contribution from periodontal infections, model and hypothesis. Journal of Alzheimer's Disease, 13(4), 437-449.

Leira, Y., Dom’nguez, C., Seoane, J., Seoane-Romero, J., P’as-Peleteiro, J. M., Takkouche, B., ... & Aldrey, J. M. (2017). Is Periodontal Disease Associated with Alzheimer's Disease A Systematic Review with Meta-Analysis. Neuroepidemiology, 48(1-2), 21-31.

Miklossy, J. (2011). Alzheimer's disease-a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria. Journal of neuroinflammation, 8(1), 90.

Rich, J. B., Rasmusson, D. X., Folstein, M. F., Carson, K. A., Kawas, C., & Brandt, J. (1995). Nonsteroidal anti-inflammatory drugs in Alzheimer's disease. Neurology, 45(1), 51-55.

Ridley RM, Baker HF, Windle CP, Cummings RM. Very long term studies of the seeding of beta-amyloidosis in primates. J Neural Transm. 2006;113:1243-1251
Sochocka, M., Sobczy_ski, M., Sender-Janeczek, A., Zwoli_ska, K., Bachowicz, O., Tomczyk, T., ... & Leszek, J. (2017). Association between periodontal health status and cognitive abilities. The role of cytokine profile and systemic inflammation. Current Alzheimer research.

Stein, P. S., Scheff, S., & Dawson, D. R. (2006). Alzheimer’s disease and periodontal disease: mechanisms underlying a potential bidirectional relationship. Grand Rounds Oral-Sys Med, 1(3), 14-24.

Takeuchi, K., Ohara, T., Furuta, M., Takeshita, T., Shibata, Y., Hata, J., ... & Ninomiya, T. (2017). Tooth Loss and Risk of Dementia in the Community: the Hisayama Study. Journal of the American Geriatrics

Immortality: With a Lifetime Guarantee

Immortality:
With a Lifetime Guarantee

Survival is our final ambition as a species and the only way to survive is to ensure that we are a good fit in our environment. There are two ways to survive as a species. One is to produce an enormous number of offspring and hope that a few survive long enough to pass on their genes. Another approach—one that humans are following—involves having a few children whom we nurture for more than 18 years. Nurturing is an important—and integral—component of our survival strategy. Nurturing involves having things to teach and living long enough to be able to teach them. This involves having a larger brain and longer life—and the two go together. Aging is not a dustbin of genetics, but an integral part of our strategy for survival as a species. With aging also comes the opportunity to learn about the environment. We learn in terms of our skills and also through our biology. As we age we pick-up new genetic material, modify existing genes, and fine-tune them before we pass our genes on to our children. Our lives are devoted to just this aim, except we remain ignorant of this fact for good reason. We create a model of reality in our brain. For us to engage in the world we have to be at the center and we have to believe that we are unique and have a free will. Our impression of reality, dictated by having a world that is just, fair and constant, also requires that we do not think about our own death or our model of the world becomes untenable. This is where our belief in immortality comes in. We want things to stay constant so that we can retain some level of control. Anticipating our death destroys this impression that the world is orderly and just. But there is one problem with this made-up reality, we do eventually get old, frail and die. We point at aging as the culprit. Aging is the problem that we need to solve rather than a survival strategy.  But if we understand aging we will understand the tricks of our psychology. By looking across ecological biology, genetics, biology and anthropology we can form an understanding of how aging came about as a positive attribute. With aging came a whole new dimension of human development. A life-long symphony is playing, that has a beginning, a middle and an end.  It is not just about tweaking genetics, or taking supplements, or curing aging. Our aging is an integral part of our environment and our history. We are meant to die, as much as it is detrimental to the individual, aging and death form our strategy as a species. Our personal salvation is that we delude ourselves this reality.

https://www.createspace.com/7082507

The Coming Pandemic of Lyme Dementia

There are many known causes of dementia. One of these causes are bacteria. Bacteria are usually ignored despite its historical and current significance in dementia research.  A hundred years ago it was well known that syphilis—a bacterium—was the only known cause of dementia. The bacteria interferes with the nerves until it reaches the brain where it destroys the brain from the inside. In the end, the expression of long-term syphilis is dementia—Neurosyphilis. Alois Alzheimer wrote his post-doctoral thesis (Habilitationsschrift) entitled “Histological studies on the differential diagnosis of progressive paralysis.” on neurosyphilis before his supervisor Emil Kraepelin propelled him into the history books by defining Alzheimer’s disease as a new disease in 1911. [1]

Neurosyphilis was very common in the 1900s. Between one in four to one in ten people in mental institutions were there because of neurosyphilis. Eventually syphilis kills its victims. Before the introduction of penicillin in 1943, syphilis was a common killer. In 1929, among men, the death rate from syphilis was 28.3 per 100,000 for Whites and 97.9 per 100,000 for Blacks [2]. The similarities between syphilis and dementia were addressed repeatedly in the early literature in Alzheimer’s disease [1]. Because syphilis can now be treated easily and cheaply, it has nearly been eradicated. But there is a new bacterium threat emerging—one that can also cause dementia.

Today, the main bacterial threat to acquiring dementia comes from Lyme disease—a bacterium borrelia burgdorferi. Lyme disease is transmitted to humans through the bite of infected blacklegged tick. These ticks are themselves infected by feeding off diseased insects and birds, which bring the infection from across the globe. Worldwide there are 23 different species of these Lyme disease-carrying ticks.

Lyme disease is the most common disease transmitted by animals in the northern hemisphere and it is becoming an increasingly public health concern [3]. Not only because Lyme disease is a debilitating disease, but because eventually Lyme disease has been shown to cause dementia—Lyme dementia [4]. Science has not identified the mechanism for the development of Lyme dementia. The American psychiatrist  Robert Bransfield has been documenting some of its neurological expressions, but so far there is a lack of emphasis in the research community on exploring these clinical features. There is great resistance by the U.S. Center for Disease Control and Prevention (CDC) to acknowledge the importance of this infection.

Ernie Murakami, a retired physician, has been monitoring the spread of Lyme disease across the world. With more than 65 countries that have the blacklegged ticks which transmit Lyme disease. This is a worldwide pandemic.The prevalence of Lyme disease reporting varies dramatically, primarily we are not looking for it.  Canada reporting the lowest cases in the world, with 1 case per million, while Slovenia reports 13 cases per 10,000. In the United Sates the CDC reports that more than 329,000 people are likely to be infected every year in the U.S. alone. Only one in ten cases are reported since clinicians are not looking for Lyme disease. This estimated number of annual infections is higher than hepatitis C, HIV, colon cancer, and breast cancer. Lyme disease accounts for more than 90% of all reported cases of diseases transmitted by animals (vector-borne illness).

With any good public health strategy there needs to be a two pronged response--prevention and control: addressing the clinical effects of the disease and the underlying cause. In the United States, although there are minimal research funds to examine and explore cures for Lyme disease, this avenue is likely to see the most significant increase in funding. But this would be folly without addressing the underlying cause of the disease. Addressing these underlying causes will however be challenging.

Harvard Medical School Center reports that areas suitable for tick habitation will quadruple by the 2080s. But there are more pressing changes that will happen in our lifetime. Deforestation and climate-induced habitat change are affecting insect which carry diseases like malaria and Lyme disease. Slow climate change, urban growth in areas next to forests, reforestation following the abandonment of agriculture, and increases in the deer, mice and squirrel populations (among many others) which harbor these ticks.

Malaria and Lyme disease are both projected to increase. Even taking a more conservative estimate (all of the USA, most of Canada, all of Europe, Middle East and China), more than half the world’s populations are exposed to Lyme disease. A proportion of these populations will become infected with Lyme disease and eventually some will develop dementia. Pure Lyme dementia exists and reacts well to antibiotics [4].  Is public health ready to address this?

© USA Copyrighted 2017 Mario D. Garrett 

References:

[1] Garrett MD (2015) Politics of Anguish: How Alzheimer's disease became the malady of the 21st century. Createspace. USA.

[2] Hazen H.H. (1937). A leading cause of death among Negroes: Syphilis. Journal of Negro Education, 310-321.

[3] Pearson S. (2014). Recognising and understanding Lyme disease. Nursing Standard, 29(1): 37-43.

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[4] Blanc F., Philippi N., Cretin B., Kleitz C., Berly L., Jung B., ... & de Seze J. (2014). Lyme Neuroborreliosis and Dementia. Journal of Alzheimer's Disease, 41(4): 1087-93.

Learning about Aging through Film: The Narrative Arc

The use of film to explore concepts in gerontology. This is one of a series of five lectures on the role of film in gerontology. Spoiler alerts, if you have not seen these films, this analysis necessitates exposing the plot. These notes are intended for you to click on the movie trailer sequentially with the analyses.

The narrative arc in film is a static story board of how a story evolves and develops, both evident as well as imagined. How older people are portrayed in film is best described through the interpretation of this narrative arc. An arc is the linear development of a story—a beginning, a middle and an end.  An alternate method of analyses would be through the more limited interpretation of context, character, symbolism, and other constructs.

One of the first films describing a simple story about older people is the 1952 Japanese film Ikiru by the acclaimed director Akira Kurosawa—acclaimed for the Seven Samurai, Rashomon, and Ran. Ikiru has a fairly simple narrative arc. A bureaucrat, on the cusp of retirement, is informed that he has terminal cancer. The narrative arc focusses on the main character in the film attempting to find meaning and leaving behind a legacy in his life before he dies.

https://www.youtube.com/watch?v=yCSiL2wmxuE

This simple story highlights that after one’s entire life spent doing what you are supposed to do—work, maybe family—that at the end what is important is relationships. At the end, he finds some solace among his younger mates, where he finds friendship.

This narrative arc, an old man at the end of life, was further developed by another seminal director, Ingmar Bergman who in 1957 wrote and directed Wild Strawberries.

https://www.youtube.com/watch?v=0RzOCwer-gc

Filmed in black and white, perhaps in homage to Ikiru, the film goes further in search of the meaning of one’s life and leaving a legacy. Following a fairly similar story of an accomplished bureaucrat—this time a professor—Wild Strawberries explores the question of what was it all about? The lost meaning is a reflection that the character’s internal story did not go far enough to include getting old. We do not have ambitions for getting old, and once we get there, we remain without a plan. Wild Strawberries has been described as Bergman’s attempt to justify himself to his own parents. The narrative arc told through actual and dream experiences, mixes ghosts, fantasies and reality. Admired but not loved, the protagonist starts to explore what the continuation of his story in older age should be. Like Ikiru, relationships seem to be the answer.

Such a conclusion is not far-fetched from what we observe at the end of life.

In 2012 Bronnie Ware, an Australian palliative care nurse, wrote The Top Five Regrets of the Dying: A Life Transformed by the Dearly Departing. Our two male protagonists in Ikiru and Wild Strawberries follow these regrets. These misgivings focused on having unfulfilled dreams and unrequited loves. Not having the courage to follow their dreams, where (mostly) men tended to regret working so hard. Stifling feelings in order to settle for a mediocre existence. And not staying in touch with their friends, and loved ones. And the final regret is not allowing oneself to be happy. They got stuck in a rut. The agreement between the narrative of these two films and the five regrets of dying people is stunning.

The films’ narrative arc, from a negative view of aging, exposing a slow hemorrhaging of life force, the story transforms to positive highlights of friendship and family. That it is not too late to address these regrets.  But what if this transformation did not take place? If the dystopian view of aging remains without the salvation of a new-found narrative what would be the result? This is the story of the two protagonists in the 2015 Italian film Youth.

https://www.youtube.com/watch?v=-T7CM4di_0c

Paolo Sorrentino’s film centers on two close friends sharing a vacation at an exclusive Swiss spa. The two protagonists are, a director who continues producing the same kind of films, surrounded by increasingly younger writers. While the other protagonist is a music composer who has decided to retire. What we have to work out is that the composer stopped composing—to the chagrin of many—because of his wife’s dementia which he hid from everyone including his daughter. He has made changes to address this trauma and his aging. Negative events in life change our narrative arc. In contrast, the other character, the director, only had one story—to remain doing what he did in the past. He did not have a different story for when he got old, and the quality of his work diminished. At the end, his suicide was the only answer to his failing career since he did not have a plan B, an evolving narrative arc. We have a starkly different outcome for what is portrayed as equally successful early careers.

This theme of different projections of the story line is best seen in the whimsical 2013 documentary, directed by Zachary Heinzerling, on Cutie and Boxer. Two married aging Japanese visual artists, living in New York city, where one reached their azimuth of success a few decades ago, while the unknown and subservient wife is launching her trajectory of ascendence in her narrative arc.

https://www.youtube.com/watch?v=YXS6Aby5AUg

Cinematographically, a narrative arc can also be reversed. This is the beauty of film, we can explore the importance of a narrative arc by manipulating the sequence. This is a popular method in film, to imaging that a life’s story can go backwards or stay static, anchored to a particular age where you do not have to have a narration for an older age.

The digital masterpiece of the 2008 The Curious Case of Benjamin Button directed by David Fincher—of the fame, Fight Club, Se7ev, and Gone Girl—is based on the premise that while the main character is born old and starts becoming younger, everyone else gets older and dies. The only connection the main character develops in the film, is when his (descending) timeline converges with another character’s (ascending) timeline. This is the meaning of the story, that a meaningful relationship is shared with people in similar (time) context.

https://www.youtube.com/watch?v=VqeqaweXBV0

This theme is again is explored in the later 2015 film the Age of Adaline by Lee Toland Krieger where the main character is involved in a car accident resulting in a traumatic physical shock that enigmatically stops her aging.

https://www.youtube.com/watch?v=7UzSekc0LoQ

The story focusses on two aspects of how meaningful relationship is shared with people in similar (time) context, when she experiences the aging and ultimate death of her daughter and the aging of her lovers.

What if you can go back and change your narrative arc. What would you choose? In Francis Ford Coppola’s 2007 Youth without Youth an older man is struck by lightning and starts to regress into his past. Not only was he getting younger, as the cases with The Curious Case of Benjamin Button, in his mind time was flowing back as well. This is the proverbial what would you do if you had to do it all over again.

https://www.youtube.com/watch?v=l8VfptBUCg0

Another technique used in film is to explore the “What If?” question. Made in 2009 Mr. Nobody was written and directed by Jaco Van Dormael. In this science fiction world where the last mortal is about to die at age 118, the protagonist explores three options that he could have made differently. Would the narrative arc result in a better outcome at the end of life?

https://www.youtube.com/watch?v=mpi0qsp3v_w

In the end, the protagonist acknowledges that although every choice he has made had far reaching results in the future, ultimately none of the choices are good or bad. The interpretation is that as long as we make allowance for getting old everything will turn out well. Each will option will result in slightly different outcomes but all will have a coherent story. The narrative arc is written as we live life, and sometimes we are just too “busy” to envisage that anything will change. Despite us knowing, intellectually at least, that everything changes all the time.

A limited narrative arc, one that is missing a component for later life, relegates older age to a dystopian existence. Only by having an internal narrative that includes future dreams can there truly be a fully lived life. What better than a story of Burt Munro, a New Zealand amateur motorcyclist who wanted to break the world speed record and in so doing ignored age completely. This is the adaption of his story: The World’s Fastest Indian.

https://www.youtube.com/watch?v=3bu9dGRQvJY

It took 20 years for the New Zealand director Roger Donaldson to make this film. In it, the protagonist narrative arc is changed when he tells of the death of his brother Ernie by a fallen tree—and, in Burt Munro’s real life, his stillborn twin sister—which changes the real life Burt Munro’s story and view of life. Negative events in life change our narrative arc. The beauty about this film is that the narrative arc ignored age completely. Suffering from angina and later a stroke in 1977, the real Munro at the age of 68 while riding a 47-year-old machine continued to set world speed records for 1,000 cc bikes. He did not use his experiences to dictate his age and his narrative arc did not stop at older age. He had his own ongoing story. In the film although there are characters that try and stop him from pursuing his narrative, the protagonist simply ignored them. Some of us are not so lucky.

Where we collude in this restriction is that we promote a restricted narrative arc for older people. Do a little exercise for me.

Let’s imagine that you have a 100-year-old woman that you are going to interview. What is the single question that you will ask her.

Write it down.

Then assume that you have a 16year-young girl coming to be interviewed. What single question would you ask?

Write that down.

The prediction is that you probably ask the older woman about her past and the younger woman about her future. You have already hemmed them into you view of what their narrative arc should be. With this knowledge in hand, let’s review a recent interview with Jerry Lewis.

http://www.hollywoodreporter.com/video/watch-7-painfully-awkward-minutes-jerry-lewis-957299

An awkward exchange where Jerry Lewis’s narrative arc focusses on the future while the reporter is trying to force him—unsuccessfully, to the great strength of Jerry Lewis—to focus on his past.

To age successfully we must not only have a story that goes beyond adulthood—to extend into older adulthood—but we must also be vigilant against those who unintentionally try and demolish our narrative for living in older age, by translating it to “old” age. Our narrative arc is important because it is how we conduct our life, including into older age.

© USA Copyrighted 2017 Mario D. Garrett 

Big Pharma Against Dementia

The World Alzheimer Report of 2011 reported that we do not know the benefits of screening and early diagnosis of dementia. We all assume that people should be checked early for dementia, but we do not know whether there is an advantage to be diagnosed with the disease. There are definitely negative repercussions—losing your driving license, right to conduct professional duties, enter into financial agreements, and sometimes even the right to conduct your own affairs. It seems that once you get diagnosed with dementia then you are left to fend on your own with your loved ones if you have any.

There is a disconnect between diagnoses—the identification of the disease—and prognosis—forecasting the progression of the disease and suggested treatment, therapy or support services. In the field of dementia, as with other diseases especially cancer, there lies an expectation that an early detection brings better outcomes: You live longer with less pain. But the reality is very different. New emerging research shows that our ambition to help dementia patients because of an early diagnosis is failing miserably.

In a French study in 2015, Clément Pimouguet and his colleagues reported that people with dementia who had consulted a specialist at the start of their disease, died earlier than those who only saw their general practitioner (GP) or did nothing. Sadly they found that there was no difference between participants who visited their GP and those who went without any clinical care.  Although those that went to see a specialist had much faster functional decline, their thinking ability was not much different from the other group. Why would seeing a specialist increase your likelihood of dying?

The lack of follow-up by the specialist was one of the reasons given for the higher rate of death. In 2017 Paula Rochon  and Jeremy Matlow and colleagues in Toronto, Ontario, reported that half of 2,998 nursing home residents with dementia were still getting questionable medication in their last year of life.  These medications might have had some benefit at the early stages of the disease but definitely have negative affect on the wellbeing of these confused patients. That a third of the residents did not see a specialist in the last year of life suggests that the medication was prescribed earlier on in the diagnosis and had not been reviewed since. Regular medication reviews will help to curtail unnecessary prescriptions.

It is likely therefore that too much and inappropriate medication is a culprit. In France only the specialist can prescribe drugs and this study found that half were prescribed antidementia drugs (46.2%); while the rest 12% prescribed antipsychotic drugs, 28% anxiolytic drugs, and 9% took psychostimulant. It is only when the diagnosis of dementia was vascular dementia and where some fo these drugs are not to be prescribed that seeing a specialist was found to be beneficial. Amelie Bruandet with the university of Lille, France and her colleagues found that with vascular dementia the shorter the delay between first symptoms and first visit, the longer patients survived. It could be due to medication, specialist do not prescribe medications that are killing dementia patients earlier.

It seems that we do not have any medication for dementia that is both effective and safe. In fact, all evidence points to dementia medication as being ineffective and in most cases dangerous. A conclusion that was arrived at by a 2014 study by two Dartmouth professors Steven Woloshin and Lisa Schwartz reporting for Consumer Reports. In addition to their costs—ranging on average $177-$400 a month—there was not one drug that they could recommend. Not one drug.

The logical assessment would be that since physicians have no medication to provide patients with dementia then following the Hippocratic Oath and “first, do no harm,” no medication should be prescribed.  But a 2015 study of elderly patients showed that anticholinergic medications given to patients with dementia—including antimuscarinics, tricyclic antidepressants, and first-generation antihistamines—are associated with an increased risk for dementia. Drugs being prescribed have an established evidence to increase dementia. Sometimes this dangerous medication is given for non-life-threatening disease such as overactive bladder. Christian Meyer from the University Medical Center Hamburg–Eppendorf in Germany, and his colleagues reported that more than one-quarter of older Americans with overactive bladder are given a prescription for oxybutynin, and one-third are given a refill, despite the established link between this drug and cognitive dysfunction in the elderly. In a 2015 survey of Medicare patients with dementia more than one in four were being prescribed "potentially inappropriate" anticholinergics.

The overuse of prescription of medication among older patients is ageist. We need to address this final bastion of stereotyping. We know that younger people with a similar disease are more likely to get therapy. But there is another negative consequence of this lack of knowledge. Physicians become shy at making prognoses. Although diagnosis is relatively easily, they can easily say it is Alzheimer’s disease or Vascular dementia without any liability issue, and most do despite evidence that they are likely to be wrong.  The patient is seriously sick, we can all see that. But once physicians start to define a timeline or sequence of how the disease will enfold, then they become exposed not only to the patient, but more importantly to the patient’s family, their medical institutional and legal liability.

In a short paper, Sonali Wilborn, and Navdeep Grewal, with Seasons Hospice and Palliative Care, Madison Heights, Michigan USA found that predicting mortality using current prognostic guidelines, fails in approximately a third of Alzheimer’s patients. Nicholas Christakis, a hospice physician takes it much further. He rightly laments the neglect of prognosis in medicine. Making a prognosis is messy and inaccurate. In 2000, he reports a study where only one in five timelines were accurate in forecasting death, more than half were over-optimistic while one in six were over-pessimistic. Being over-optimistic ensures that patients delay too long in sorting out their affairs.

The symbol of medicine is the rod of Asclepius—which has a snake coiled around a cane. It is carried by the Greek god Asclepius, a deity associated with healing and medicine. It is often confused with the caduceus which has a very different meaning.

The caduceus—depicting two snakes wrapped around a winged rod—is carried by Mercury the mythical messenger of the gods. Mercury is the guide of the dead and protector of merchants, shepherds, gamblers, liars, and thieves. In dementia care we might be confusing both the symbol and the objectives becoming the protectors of big pharma: merchants, gamblers, liars, and thieves. The abuse of older patients with dementia remains an unwritten chapter in the low point of medicine.

© USA Copyrighted 2017 Mario D. Garrett 

References

Bruandet, A., Richard, F., Bombois, S., Maurage, C. A., Deramecourt, V., Lebert, F., ... & Pasquier, F. (2009). Alzheimer disease with cerebrovascular disease and vascular dementia: clinical features and course compared with Alzheimer disease. Journal of Neurology, Neurosurgery & Psychiatry, 80(2), 133-139.

Pimouguet, C., Delva, F., Le Goff, M., Stern, Y., Pasquier, F., Berr, C., ... & Helmer, C. (2015). Survival and early recourse to care for dementia: A population based study. Alzheimer's & Dementia, 11(4), 385-393.

Rait, G., Walters, K., Bottomley, C., Petersen, I., Iliffe, S., & Nazareth, I. (2010). Survival of people with clinical diagnosis of dementia in primary care: cohort study. Bmj, 341, c3584.

© USA Copyrighted 2017 Mario D. Garrett  

Reminiscing Therapy and Dementia

In 1959, Erik Erikson published the first theory of personality that included older people. Before this, theories stopped at adulthood. His mentor, and father of psychodynamic therapy, Sigmund Freud, discounted older people since he believed they are not able to learn after the age of 50. Older age was defined as simply a decline from the apex of adulthood. This changed with Erikson’s final stage of personality development: Wisdom, Ego integrity vs. Despair. This stage related to those over the age of 65. The theory proposed that this is a time of acceptance of past life. By looking back and reconciling one’s accomplishments and losses, wisdom can be attained. If this process remains unfinished however then despair will ensue. Within this first theory of aging, “looking back” is integral to attaining wisdom and deflecting despair in older age.

At the same time, a new theory of older age emerged and can be traced to an earlier article published by Elaine Cumming, Lois Dean, David Newell, and Isabel McCaffrey in 1960. A year later Elaine Cumming and William Henry consolidated their thinking in a book, Growing Old: The Process of Disengagement which created such a backlash within the gerontology community. The idea behind this theory was to validate why older adults disengage from society. Criticisms of this theory were quick and harsh. But disengagement argument is much more subtle, and includes a discussion how society disengages older adults as worthless.

When older people face discrimination that insults their self-esteem, this creates conflict between one's past and the present self-concept.  One way to deal with this conflict—like any reaction to a trauma—is to move away. Older people move away from society in order not to get hurt. Around this time in 1964, in a book chapter, Robert (Bob) Butler argued that the vividness of the past is motivated by emotional needs in old age. These emotional needs he later labeled “ageism.”   Continuing with the Cumming and Henry argument that society mistreats older adults and that reminiscing allows older adults to maintain their sense of self.

Then in 1971 Charles Lewis in Reminiscing and Self-Concept in Old Age reported an experiment to test whether remembering the past allows older people to re-affirm their importance in the world. There were already studies showing that older men who reminisce tended to be less depressed and tended to have better survival (short-term studies.) But Lewis wanted to find out if reminiscing improved older men’s self-esteem especially after experiencing a threat. Lewis’s study showed that those that reminisce deflect some of today’s stressors by inflating one’s sense of self on the basis of past accomplishments or states. All of these set the stage for the pivotal experiment that was done in 1979.

Just under 40 years ago, a classic experiment became known as the counterclockwise study.  Then Harvard University social psychologist Ellen Langer and her colleagues conducted a strange experiment with a group of men between the ages of 75 and 80. For five days, the men were randomly assigned to one of two groups. Both groups were asked to imagine themselves at 55 years of age. One group was placed in an environment which mirrored the 1950s, with a redifusion (hard-wired radio), black and white tv with 1950s old radio and tv programs to match. Newspapers, magazine, decorations, furniture, food all matched the time period. While the second group was instructed to behave like they were 55 years old, but without the added environmental changes.
After only five days, the results were unexpected and dramatic. Men in both groups objectively looked younger by about three years, had improved hearing and memory, gained weight, increased muscle mass and had improved hand strength. These surprisingly quick results were more distinct for the group that lived “in time of their 50s” rather than the group that just reflected as their life was 20 years ago, although both groups improved.

Counterclockwise study catapulted the popularity of Reminiscing Therapy (RT). RT involves many variations. Traditionally—because it was the least expensive—RT involved the older adult discussing past activities, events and experiences. This was helped by the use of photographs, household and other familiar items from the past, music and archive sound and video recordings. Over the last decade, RT has become one of the most popular psychosocial interventions in dementia care. A quick review comes-up with more than 1,000 research papers published in 2016 on this topic. With a century of failures in finding any medication to help people with dementia, at least there was some hope that some therapy exists.

In 2005 Welsh scientist Bob Woods and his colleagues performed a review of four clinical trials—with controlled groups—and RT was found to improve thinking (cognition), mood and general behavior.  In addition, and as an added bonus, those caring for the patient also showed reduced level of stress and strain. Best of all, there were no known harmful effects. Outcomes that were again supported by more recent review in 2012 by Maria Cotelli and her colleagues. Although there are some reviews that show weak outcomes, the mounting evidence suggest that RT is—to varying degrees—effective in improving mood, thinking and well-being in patients with dementia. In a clinical area littered with failures, RT looked like a prime candidate for a miracle intervention. But how does it work?

Living with Alzheimer’s disease means to live in the moment, because the anchoring to the present and being able to predict a future has been disrupted.  Which explains why the placebo effect doesn’t appear to work with Alzheimer’s patients since they are unable to anticipate the future.  But could they relate to the past better, especially a time in the past when they were at their peak?  Anecdotally we know this to be the case.

Time constitutes an important factor in how we think of ourselves. The mind contains specialized areas for storing and retrieving knowledge about our personality traits across time. For example how we behaved as children.   People with dementia may be operating from knowledge of a former self, which may not match their current status. Neurological studies show how damage to certain brain structures result in very specific problems with time. So we know that time is an important function for the brain to process. Stanley Klein with the University of California Santa Barbara has studied this effect, summarizing these studies by identifying at least five functionally—and they argue—neurologically distinct components of how the brain stores time.

The brain is “concerned” with time. There is agreement among philosophers and neurologist that perception of time is an important human component. By thinking ourselves younger we allow our body and mind to behave as though we are younger and therefore we exercise these capacities more. Eventually such exercise improves our capacity. Becca Levy with Yale University and her colleagues has shown that positive age stereotypes, presented subliminally across multiple sessions in the community, lead to improved physical function that lasted for 3 weeks.  The same is true when competitive sportspersons are told that they are testing a new drug (placebo.) Not only do they perform better but their biomarkers all improve as well. This is not just a delusion, but an improvement. It seems that we have some control, or plasticity over our physical and mental functioning. And by pushing this plasticity—either up or down—we can modify our trajectory. This works with healthy sportspeople, people with dementia (because they can relate to the past) and also influence people’s longevity.

The idea that how we think of ourselves, regardless of our actual health, determines longevity seems outlandish. But numerous studies show just that. In a 23-year longitudinal study, Becca Levy reported that those individuals who had a more positive self-perception of aging lived an average of 7.5 years longer than did individuals with less positive self-perception of aging, even after adjusting for gender, socioeconomic status, loneliness, and functional health. In fact, perceived health was a better predictor of mortality than objective measured health (i.e., smoking and being overweight). Older adults who reported their health as poor, regardless of their actual health status, were six times more likely to die earlier than those who reported their health as excellent. We have some plasticity, some control over our physical health as well as mental health. We can “will” this plasticity.

The surprising outcome therefore, is that through Reminiscing Therapy, older adults with dementia are given a way to aspire to a time when they were better and this pushes them to try harder and as a result improve. Such plasticity is a degree change in a trajectory, not a cure.  Right now, there are some interesting developments in Reminiscing Therapy with dementia patients. The surprising take-home lesson for us is that it might also work for people without the disease, to push that plasticity as far as it will go to slow down that trajectory of aging.


References
Butler, R. (1964). The life review: An interpretation of reminiscence in the aged. In R. Kastenbaum (Ed.), New thoughts on old age. New York: Springer Co.

Erikson, E. H., Paul, I. H., Heider, F., & Gardner, R. W. (1959). Psychological issues (Vol. 1). International Universities Press.

Cumming, E., & Henry, W. (1961). Growing old. New York: Basic Books.

Langer, E. J. (2009). Counterclockwise. Random House Digital, Inc..

Some examples of Reminiscing Villages

Cedar Lake Village retirement community Olathe, Kansashttp://www.cbsnews.com/news/reminiscence-therapy-to-trigger-dementia-patients-memories/

The Meadows, assisted living facility in Elk Grove, CAhttp://www.providermagazine.com/archives/archives-2011/Pages/0611/Reminiscence%20Therapy%20Benefits%20LTC%20Residents.aspx

Town Square of George G. Glenner Alzheimer’s Family Centers, San Diego, CAhttp://www.sandiegouniontribune.com/news/health/sdut-glenner-center-town-square-san-diego-opera-2016sep08-story.html

Alexa Seniors’ Residence, Dresden, Germany
http://www.telegraph.co.uk/news/2017/03/02/dresden-retirement-home-recreates-communist-east-germany-helpresidents/

The Easton Home, an elder-care facility in Easton, Penn.http://abc7.com/health/reminiscence-therapy-helping-those-with-alzheimers-and-dementia/1125661/Complete dementia village, Hogewey, Weesp, Netherlands
http://www.alzheimers.net/2013-08-07/dementia-village/

© USA Copyrighted 2017 Mario D. Garrett