Introduction & What Me, Worry?
The reader should understand that this book represents the informed opinion of the author, and is not intended to provide a complete scientific treatment of any of the subjects considered herein. There are hundreds of thousands of scientific studies that have generated data relevant to the topics at hand. No scientist in the world has a full grasp of this subject. It necessarily receives short shrift here. And while the author is an acknowledged authority on this subject, it is simply not possible to give credit for all of those other scientists in the world who could—and should—be cited, for the annotation in this treatment to be complete, or completely fair. I ask the reader to accept these limitations, and to view this book as a starting point for their education about this incredibly deep and rich body of scientific work. I ask my fellow scientists to forgive my limitations in annotation if I have not given you—or others you are aware of—appropriate primary credit for the conclusions drawn in this treatment. I invite all of you to add to this annotation and to enrich the conversation begun with these book chapters by adding “your two cents worth” to this dialog via the “comments” box following these notes related to the issues discussed in each book chapter.
At the same time, this is, for me, a serious treatment. I can support, in my own mind, through hundreds of laboratory studies and through a broad understanding of the scientific literature, every statement made herein. That is NOT to say, of course, that this broad perspective is not open to correction or improvement. Again, please avail yourself of the “comments” platform, if you would like to rise to further support, extend, or disagree with the subjects considered on these pages.
SPECIFIC COMMENTS ON CHAPTERS 1 & 2:
- Population estimates for Alzheimer’s Disease and other causes of dementia—and for all other neurological and psychiatric disorders in these introductory (and in the following) chapters come from:
- Center for Disease Control (U.S.) statistics: www.cdc.gov/datastatistics/
- World Health Organization (United Nations) www.who.int/gho/publications/world_health_statistics/2012/en; and www.who.int/entity/healthinfo/EN_WHS2012_Full.pdf
- Or from a Lancet issue (Volume 380, number 9859, pp. 2053-2260, 2012-13) summarizing world disease burden issues: www.thelancet.com/themed/global-burden-of-disease Also see Brookmeyer R. et alia, Projections of Alzheimer’s Disease in the United States and the public health impact of delaying disease onset. www.ncbi.nim.nih.gov/pmc/articles/pMC1509089/pdf/amjph00021-0049.pdf Brookmeyer and colleagues point out that a delay in the onset of AD by an average of 1 year would decrease the number of AD patients in the US by 1 million. According to the American Association of Retired Persons (AARP), the average care costs for an AD patient in the US is $56k/annum. Thus, our math problem is a simple one. A 1-year delay in AD onset would save $56 billion in the US alone. One of the goals of this book is to contribute to moving AD risk in an onset-delaying direction, not primarily to save money—although those savings could be enormous, and great good could come from them—but to reduce the numbers of individuals who have to endure dementia, and to weaken and shorten its grip on the innocents amongst us to a substantial extent—hopefully, by multiple years—in the US, and in the world.
- I have included all the other dementias under the “Alzheimer’s Disease” label when describing the neuropathologically “diseased” aging brain. See the Alzheimer’s Association’s 2012 Alzheimer’s Disease Facts and Figures www.alz.org/downloads/facts_figures_2012.pdf for descriptions of the other common non-Alzheimer’s dementias. There are (of course) diagnosis-specific features of the neuropathology recorded in each of these maladies, and their pathological origins scenarios significantly differ from Alzheimer’s itself. Still, most of my narrative about origins and strategies that relate to increasing resilience against AD onset also apply for these variants (Lewy Body Disease; frontotemporal dementia; dementia accompanying Parkinsons; et alia), just as they apply for AD itself. I’ll discuss those relationships and arguments about growing resilience for other dementia subtypes a little more, in my notes following a later chapter (26) on AD itself (see http://www.soft-wired.com/ref/ch26)
- The German neurologist/pathologist Alois (Aloysius) Alzheimer first described the AD pathology in 1906, with an initial focus on early-onset cases. Alzheimer was initially motivated to understand the neuropathology of a 51-year-old dementia patient. It took him 6 or 7 years to locate a handful of patients whose brains, at autopsy, exhibited the signature amyloid plaques and microtubule tangles that we now identify as the primary neuropathological markers of AD. In parallel, other neurologists/anatomists (including Sigmund Freud) began to record the same physically-expressed pathology in elder demented patients, using a relatively new (late-19th Century-developed) brain cell staining method developed by a colleague and friend of Alzheimer, Franz Nissl.It should not have been for lack of patients that these AD brains were initially so hard for Alzheimer to find. Alzheimer was a professor at the Städtische Anstalt für Irre und Epileptische (Asylum for Lunatics and Epileptics) in Frankfurt in the densely populated German Rhineland, and had extensive working connections with scientists in another German population center, Munich. The relatively late recognition of Alzheimer’s Disease as a distinct medical condition, evidence for variations in prevalence in different world demographics, and growing evidence that there are dozens of life-passage risk factors that can significantly increase the risks of disease onset raise questions about environmental or social factors that may contribute to differences in the numbers of affected individuals and to a probable rise in incidence of AD in human populations over the past several centuries. To cite one of many examples, the incidence of AD in modern-day India, for age- (and in other ways-) matched populations, is estimated to be about ½ that in the US or Korea or Germany.
When my mother initially realized that she was failing, she told me that in her childhood and young life in her farming community she did not know anyone who was demented in their old age. “There were lots of old people.” She declared. “We didn’t know anyone (her emphasis) who was struggling like so many struggle nowadays.”
Of course the biggest factor contributing to increasing AD prevalence in the U.S. and in the world is the continuing increase in human longevity itself (see, e.g., Kalaria R N, et al., Alzheimer’s disease and vascular dementia in developing countries; disease management, and risk factors. Lancet Neurol 7:812-26, 2008. See www.ncbi.nim.nih.gov/pmc/articles/PMC2860610/
- For a further description of the diagnosis of “mild cognitive impairment” (MCI), see a Mayo Clinic report on this subject. www.mayoclinic.com/health/mild-cognitive-impairment/DS00553 Mayo Clinic and Washington University at St. Louis scientists made seminal contributions to the recognition and formal definition of this pre-Alzheimer’s condition.
- When scientists (initially at Carnegie-Mellon University in Pittsburgh) developed the ability to label amyloid so that AD pathology was visible in Positron Emission Tomography images in the living brain, it was quickly realized that the majority of “normal” citizens past their 70th birthday are growing the AD pathology. See, e.g., Jagust W (2009) Imaging the Aging Brain, Oxford U Press, Oxford; or see PET And The Evaluation Of Alzheimer’s Disease And Related Disorders (2010). As we’ll discuss later (www.soft-wired.com/ref/ch26) the emergent AD pathology is paralleled by the differential physical shrinkage of—and the “functional disconnection” of—“highest” cortical system levels. For an illustration of the extents of shrinkage of the cortex in advanced AD, see http://www.alz.org/braintour/alzheimers_changes.asp … or to witness 2 years of change in the thickness of the cerebral cortex as AD advances, see sequenced brain shrinkage reconstructions (“movies”) created by neurologists at UCLA http://www.loni.ucla.edu/~thompson/AD_4D/dynamic.html Note, there, how the shrinkage is initially most prominent in cingulate and other medial cortical zones, and in the inferior temporal, frontal and posterior parietal cortex. These “highest” cortical areas are the first to undergo loss and disconnection in older age; their physical reduction parallels cognitive loss and senility onset.
- For a little more about Avram, the 93-year-old paragon in Chapter 2, and his cellulose-to-sugar project, see http://www.rexresearch.com/hclcleantech/baniel.htm
- For general references on “brain plasticity” written for the informed layperson, see: The Brain That Changes Itself, by Dr. Norman Doidge Train Your Mind, Change Your Brain; How A New Science Reveals Our Extraordinary Potential to Transform Ourselves, by Sharon Begley
- For a general references to plasticity-compatible training principles as they relate to issues of rehabilitation, see: Move Into Life: The Nine Essentials of Lifelong Vitality, by Anat Baniel.