Why Does God Want to Kill Me?

We know that we will die.

Yet four out of every five younger adults aged between 18 and 29 believe in the afterlife. At the same time fewer of them say they believe in a god. These Millennials born around 1980-1994—despite doubting the existence of God, believing the Bible is a book of fables, not attending religious services, never praying, and  reporting “being not religious at all”—still believe that they have aspects of immortality. They feel entitled enough to be saved after they die without the necessity of a god to save them. The more entitled they feel—white and middle class—the more likely that they do not believe in god but that there is an afterlife waiting for them. Minorities do not feel this entitlement to the same degree.
This resurgence in the belief of immortality without the shackles of believing in god is new. But they have to ask themselves why does god want to kill them in the first place. Such an entitled group needs to face this question head on. For the answer might hold a greater insight then religion, and to address this question we have to look at physical (biological) anthropology.
As a specie, survival is our only ambition.  The only way the successive generations prosper is if they are a good fit in their environment and survive long enough to create a new generation. Nature has two extreme methods to achieve this single aim. 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 followed by humans—involves having few children whom we nurture until adulthood. This is our survival strategy as a species. These strategies have mythological names: Semelparity refers to “r” strategists (large number of offspring and then die), and Iteroparity for “K” strategists (a few offspring whom we nurture).
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. Which is why we live so long and have such a big brain, the two go together. Aging is not a dustbin of genetics, but an integral part of our strategy for endurance as a species. Aging and having a big brain go hand-in-hand as nature’s plan for our survival.
With aging also comes the opportunity to learn about the environment. We learn in terms of our skills and also through our biology. We develop immunity from the day we are born and some of these biological adaptations end up in our genes through the transfer of genetic material. Our genes are more permeable then we once thought. We get genes not just from our parents but also from the environment. We get gene transfer from bacteria (plasmids), fungi, viruses, sometimes siblings, mothers from their children. We are a magnet for adaptive genetic material from our environment. As we age we pick-up new genetic material and modify existing genes (epigenetics) before we pass these genes on to our children. Our lives are devoted to just this aim.
Because of our big brain we need more than that…we need a more substantial meaning in life because out brain has made us solipsists—at the center of the universe.
Our brains create virtual realities. We create a model of how the world works. For this world to have meaning to us—other than a simple mental toy that helps us predict our environment—we have to be at the center and “own” this world. We therefore believe that we are unique and have free will. Our impression of reality, dictated by having an image of the 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. But god wants to kill us, because that is how our species improves. The faster the turnover, with new generations coming through, the better our species can adapt to the environment.  But this clashes with our model of the world.
We want our world to stay constant so that we can retain some level of control over this finely tuned balancing trick. Anticipating our death destroys this impression that the world is orderly and just. But there is one problem with this made-up reality, we see others eventually get old, frail and die. We point at aging as the culprit. That is when we see aging as 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. Our strategy for survival—Iteroparity “K” strategy—means that we nurture younger generation. With our increasing lifespan we have been extending this nurturing longer. Could it be that we have been nurturing them too long? That this younger generation have forgotten how to be adults themselves.  The younger generation increasing sense of entitlement is but a reaction to the knowledge that they are truly one mortal link in the immortal chain of life. The shackle of religion that buffers us from this realization is no longer strong enough.
For this new generation, we have nurtured them to the extent that they feel important enough that they do not have to consider death. The model created by their brain includes an afterlife to alleviate the possibility that they are not at the center of the universe. Emerging generations are rejecting death and they are also not having children. By liberating themselves from religion, norms and expectations they are rejecting the need to have children. Children will necessitate them to move away from being at the center of the universe.
 Our aging is an integral part of survival up to a point. Because we have extended our longevity we are nurturing our children too long. Our human psychology that relies on us being at the center of the universe feeds off this nurturing and becomes a prominent feature of our existence. Throughout all this nature wants too maintain a turnover. 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 and for emerging generations they are doing this by avoiding god and believing in an afterlife.

  © USA Copyrighted 2017 Mario D. Garrett 

References

Garrett, M (2017). Immortality With a Lifetime Guarantee. Createspace. USA.

Harley, B., & Firebaugh, G. (1993). Americans' belief in an afterlife: Trends over the past two decades. Journal for the Scientific Study of Religion, 269-278. 

Twenge, J. M., Sherman, R. A., Exline, J. J., & Grubbs, J. B. (2016). Declines in American adults’ religious participation and beliefs, 1972-2014. Sage Open, 6(1), 2158244016638133.   

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Age Apartheid

I sometimes stray off in class. Like some students, the classroom becomes my own little world of fantasy. Except, unlike my students, I am teaching the class.

Last week I was discussing how peer-ist our society is. We tend to only mix with people our own age. As I was lecturing I tried to recall the last time I held a baby in my arms, and in front of 110 students I realized that it must have been more than two years ago. I joked that I see a lot more older people because that is my job. But unless you live in an extended family, and most students in the United States do not, then it is unlikely for them to interact with children or older adults on a consistent basis. By not engaging with older adults my students are likely to develop negative ageist stereotypes

In 1992 Joann Montepare and her colleagues looked at how college students’ spoke with their grandparents and parents on the phone. They found that with their grandparents, college students had a higher pitch used more babyish, feminine voice, while at the same time being more deferential and congenial. Different from the type of speech exchanged with their parents. And this differential treatment starts much earlier than college.

Children tend to evolve a negative view of older adults early on. Negative views of older adults seem to come naturally to young minds. For example in 1990 Charles Perdue and Michael Gurtman asked children to recall traits after they were introduced to the person they are recalling the traits for. They could recall more negative traits when their reference was an “old” person and more positive traits about a “young” person. Children already have preferential memories. They remember AND recall negative traits because they are already associated with older adults. The author argue that these age biases are automatic, unintentional and unconscious. It seems that such discrimination is pervasive and results in negative behavior towards older adults.

In 1986 while observing behavior of children as they interacted with elderly people Leora Isaacs and David Bearison found that children were quite discriminating.  When faced with either of two study helpers—one was much older, but both dressed similar and professionally—when with the older helper, children sat farther away, made less eye contact, spoke less and initiated less conversation and asked for less help. Children have already learned to keep older adults at a distance.

Could closer interaction remove these stereotypes?

One way to deal with these negative stereotypes is to develop a closer association with older adults. But the results were initially surprising. The University of Maryland professor, Carol Seefldt in 1987 found that 4 and 5-year-old children who had visited infirm elders in a nursing home once a week for a full year held more negative attitudes towards older adults compared to a similar group without this contact. However, the day care and nursing home staff, reported positive and long-lasting benefits to both the children and elders.

I remember my children coming home from Montessori School proud to tell me that they visited a nursing home with “old people.” Knowing that this was my interest they knew I was interested in what they learned and I was anticipating a positive response. Smelly and horrible was their response. But then in hindsight it should not have surprised me. If my experience of older adults is exclusively based on a nursing home, I similarly would have a very negative view of aging.

Which explains why the evidence that intergenerational contact influences children's attitudes is mixed. In 2002 Molly Middlecamp and Dana Gross enrolled 3-to-5 year old children in either an intergenerational daycare program or regular daycare program. They found that the two groups were very similar in their attitudes to older adults. In general, children rated older adults less positively than they did younger adults, and these children believed that older adults could participate in fewer activities than children could. The take home lesson is that not all prejudices can be overwhelmed by knowledge, only through appropriate knowledge.  

Without appropriate engagement, we get a voluminous amount of information about older adults exclusively from the media, especially as reflected in adolescent literature. David Peterson and Elizabeth Karnes reported that in fiction literature older persons were underdeveloped and peripheral to the major action in the books reviewed. And there are nuances in perception that are determined by the socio-economic context. Tom Hickey and his colleagues as early as 1968 found that among the third grade, students from higher socioeconomic groups looked more favorably on older persons (although perceiving loneliness problems), and children from poorer homes did not anticipate loneliness but expected senility and eccentric behavior. A social component of the type of stereotypes is evident.

If my information is coming from a negative source, then my negative views are unlikely to be assuaged. My social class or culture might modify these stereotypes. By designing an appropriate intervention, where young people interact in a meaningful way with older people, only then can negative views of aging be replaced with more realistic perceptions. This was the intention and success of a 2002 program initiated by Eileen Schwalbach and Sharon Kiernan. The program was designed for fourth grader to visit an elder "special friend" at a nursing home every week for five months. They were primed before their visit by describing some of the issues that might come up during their visit. During the course of the study, the 4th graders’ attitudes toward their "special friends" were consistently positive and their empathy increased.

Milledge Murphey, Jane Myers, and Phyllis Drennan wrote a review of such effective programs. They especially focus on the seminal program begun in 1968 by Esstoya Whitley.  As part of their school curriculum, 6-8 years old students "adopted" a grandparent from among residents of a nearby nursing home.  As anticipated the children’s attitudes became more positive towards their adoptee. But what was unexpected was that the children continued visiting their adopted grandparents for a few years at least three times per week. The children gained a positive attitude toward the elderly and a more realistic view of aging and developed a true relationship with their adoptees.

But perhaps the most memorable study of interaction was a recent 2017 British factual entertainment program—euphemism for reality TV in the United States—by Channel 4. Although such intergenerational programs have been conducted in the United States for more than half a century, this was the first time it was televised from the start. The nursing group participants came from St Monica Trust retirement community in Bristol where once a week for six weeks a group of 4-yer old kindergartners descended upon the sedentary tranquility of the nursing home and infused it with ambulant energy. The weekly television series updates the viewers with funny and eccentric interactions. But at the end what the show clearly shows is how the older residents improve their cognition, physical ability and mental health across the six week of interaction with the children. In turn the children develop greater empathy for their older playmates.

And the question is why were we separated in the first place? How and why society become so age-segregated?

Looking across a sea of young faces in class I realize that we start at school and the best place to disaggregate is schools. Ivan Illich, the infamous activist from the 1960s already covered this topic. In the 1971 book on Deschooling Society Illich discusses ways of removing the barriers to education and to incorporate education into the general social network through social hubs like libraries. With the incredible amount of money that educational institutions make—especially publicly funded ones—there is no incentive to change the status quo. Until then, we have to suffer the consequences of age apartheid that we continue promoting, while feeling enriched and uplifted when we see those barriers removed, even if for our brief viewing pleasure, albeit on television for now. In the meantime I need to get back to my age-disaggregated class.

 © USA Copyrighted 2017 Mario D. Garrett 

References

Atchley, R. C. (1980). Social forces in later life. Belmont, Calif.: Wadsworth.

Brubaker, T., & Powers, E. (1976).The stereotype of 'old': A review and alternative approaches. Journal of Gerontology, 31, 441-447.

Channel 4 (2017). Old Peoples Home for Four Year Olds. Accessed online 12/9/2017: https://www.youtube.com/watch?v=Xm2z5468htA

Duncan, R. Preface. In E. Whitley (Ed.), From time to time: A record of young children's relationships with the aged. Florida: College of Education Research Monograph No. 17, University of Florida, 1976.

Gruman, G. J. (1978). Cultural origins of present-day ageism: The modernization of the life cycle. In S. F. Spicker (Ed.), Aging and the elderly: Human perspectives in gerontology. New Jersey: Humanities Press.

Henderson, M. E.; Morris, L. L.; 8c Fitz-Gibbon, C. T. (1978). How to measure attitudes. Beverly Hills, Calif.: Sage,

Hickey, T., Hickey, L. A., & Kalish, R. A. (1968). Children's perceptions of the elderly. The Journal of genetic psychology, 112(2), 227-235.

Holmes, C. L. (2009). An intergenerational program with benefits. Early Childhood Education Journal, 37(2), 113-119.

Illich, I. (1973). Deschooling society (p. 46). Harmondsworth, Middlesex.

Isaacs, L. W., & Bearison, D. J. (1986). The development of children's prejudice against the aged. The International Journal of Aging and Human Development, 23(3), 175-194.

Middlecamp, M., & Gross, D. (2002). Intergenerational daycare and preschoolers' attitudes about aging. Educational Gerontology.

Montepare, J. M., Steinberg, J., & Rosenberg, B. (1992). Characteristics of vocal communication between young adults and their parents and grandparents. Communication Research, 19(4), 479-492.

Murphey, M. & Myers, J. E. (1982). Attitudes of children toward older persons: What they are, what they can be. The School Counselor, 29 (4), 281-289.

Perdue, C. W., & Gurtman, M. B. (1990). Evidence for the automaticity of ageism. Journal of Experimental Social Psychology, 26(3), 199-216.

Peterson, D. A., & Karnes, E. L. (1976). Older people in adolescent literature. The Gerontologist, 16(3), 225-231.

Robertson, J. (1976). Significance of grandparents. Gerontologist, 16, 137-140.

Schwalbach, E., & Kiernan, S. (2002). Effects of an intergenerational friendly visit program on the attitudes of fourth graders toward elders. Educational Gerontology, 28(3), 175-187.

Seefeldt, C. (1987). The effects of preschoolers' visits to a nursing home. The gerontologist, 27(2), 228-232.

Whitley, E. (1976) From time to time: A record of young children's relationships with the aged, Florida: College of Education Research Monograph No. 17, University of Florida.

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Dawn of the Age of Parrhesia

"Parrhesia" comes from the Greek playwright (tragedian) Euripides meaning literally "to speak everything" and by extension "to speak boldly", or "boldness". It is a form of extreme candor. It implies more than just freedom of speech, but the obligation to speak the truth for the common good, even at personal risk. 

Parrhesia was a central concept for the Cynic philosophers, and then later on applied by the Epicureans in a manner of frank criticism. This was a common method of discourse in philosophy at the time, which was later championed by the post modernist Michel Foucault. This was in contrast to rhetoric, which was a method to help persuade the audience. Rhetoric, the art of effective or persuasive speaking or writing, designed persuade and impress its audience. Often regarded as lacking in sincerity. In todays context some would (incorrectly) refer to it as fake news.

For the parrhesiastes--the one who uses parrhesia--they say everything that is on their mind, hiding nothing. By opening one's heart and mind completely to other people through their discussion, the speaker gives a complete and exact account of what they feel and think, unfettered by niceties or eloquence,  so that the audience is able to comprehend exactly what the speaker thinks. One who uses parrhesia must be critical of everything including themselves. They must also not bend to popular opinion or cultural norms, even if this endanger their life. Publicly the user of parrhesia must be in a subordinate to those being criticized. 

In todays world we are lost between the rhetoric and the false parrhesiastes. 

Those that tell the truth--parrhesiastes--are many, but they are necessarily individual. In a complex society, to be able to be fully knowledgeable and honest you have to be a specialist, an expert. Non experts are the rhetoricians. They persuade others that they are telling the truth but they truly do not understand the truth. And those are the rhetoricians. Unfortunately it is very difficult to tell them apart. So the knee jerk reaction is to disqualify all experts, Like a serpent that swallows its tail we have dismissed those individuals that can help us understand the truth.

The serpent that swallows its tail is the symbolism for alchemists. History can teach us the fate parrhesiastes. Alchemists were another set of individual experts that have been vilified throughout history.  While the symbol of Ouroboros--the snake eating its own tail--represent infinity and wholeness, it does have some strange bedfellows.

Reference

Foucault, Michel (Oct–Nov 1983), Discourse and Truth: the Problematization of Parrhesia (six lectures), The University of California at Berkeley.he parrhesiastes uses the most direct words and forms of expression he can find. 

Aging In Montclair and bevival

Aging In Montclair and bevival present Oct 20-22nd Aging in Montclair and bevival.com are proud to present the east coast debut of San Diego’s popular film event, Celebrating Aging In Film. Curated and moderated by series founder, aging expert and author, Professor Mario Garrett Ph.D., this three-day weekend event is designed to shed light on how the aging narrative is transforming our culture. For film enthusiasts, this weekend educational series is an exciting opportunity to watch four iconic films and participate in illuminating, post-screening discussions with two fascinating educators. Themes include multi-generational relationships, humor, culture, romance, and the enduring creative spirit.   Screening venues were made possible through the generosity of Montclair State University, School of Communication and Media, and the Montclair Art Museum. order your tickets now Celebrating Aging In Film Series and VIP Reception TICKETS + INFO aginginmontclair.org/film-series AIM Book Group bevival Instagram Copyright © 2017 Aging in Montclair, All rights reserved. You are receiving this email because you are a member of AIM. Thank you for your support! Our mailing address is: Aging in Montclair 13 Trinity Place The Salvation Army Building Montclair, NJ 07042 Add us to your address book Want to change how you receive these emails? You can update your preferences or unsubscribe from this list.

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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