You CAN Prevent Alzheimer’s!
A Neuropsychologist’s Secrets to Better Brain Health
By Thomas Harding, Psy.D., M.A.
Published
by Beach Hill Publishing at Smashwords
Copyright 2010 Beach Hill
Publishing
First Edition, 2010
This ebook is licensed for your personal enjoyment only. This ebook may not be re-sold or given away to other people. If you would like to share this book with another person, please purchase an additional copy for each recipient. If you’re reading this book and did not purchase it, or it was not purchased for your use only, then please return to Smashwords.com and purchase your own copy. Thank you for respecting the hard work of this author.
All rights reserved. No part of this book may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording or by any information storage and retrieval system, without written permission from the author, except for the inclusion of brief quotations in a review.
Beach Hill Publishing books are available at special quantity discounts to use as premiums and sales promotions, or for use in corporate training programs. For more information, please write to:
Beach
Hill Publishing
P.O. Box 276
Aiea, HI 96701
www.Be-Dementia-Free.com
This book is available in print at most online retailers.
Dedication
In memory of James Forrester Craine, Ph.D.
“The
Mentor cannot stay forever—otherwise, how would we know that their
knowledge was passed on?”
— Yoda, from the movie Star Wars
Acknowledgments
Writing this book fulfills a promise that I made to Dr. Craine in sharing his wisdom. Along this journey, I have been especially blessed to have the help, encouragement, and support of many.
Some very good friends and colleagues took these many pages of manuscript, trekked their way through, and provided suggestions and insights. Thank you, Drs. David Demarest, Ph.D.; Frederick Manke, Ph.D.; Audrey Hoo, Psy.D.; and Keith Pedro, Psy.D.
I am indebted to a talented writer, Mike Park, for helping me find my “voice” and offering his critique. For endless constructive criticism and patience with my propensity for sentence run-ons, I am grateful beyond words to Maile Tsutsumi.
The knowledge base contained herein exists due to the devotion and pursuit of knowledge from thousands of neuroscientists and graduate students worldwide. The human race thanks you.
I have been able to sketch for you only a fraction of the evidence supporting our conclusions. But I am not a lone voice, simply a herald of the coming revolution in the fight against dementia.
Table of Contents
PART I: How Senior Moments Found Us
PART II: Meet Your Brain
4. The Forming and Fading of Memories
PART III: KEY FACTOR #1:
Proper Brain Stimulation
5. The Nuts and Bolts of Neurotraining
PART IV: KEY FACTOR #2:
Avoid Known Risk Factors
PART V: KEY FACTOR # 3:
Proper Brain Nutrition
11. The Skinny on Fat and Cholesterol
12. Nutrition for Brain Plasticity
PART VI: KEY FACTOR #4
Physical Exercise and Rest
13. To Sharpen the Brain: Hone the Body
14. Sleep Your Way to a Better Memory
PART VI: Slowing the March of Time
16. Inflammation and “Inflammaging”
17. Neurohormones and Brain Aging
About the Author
Dr. Thomas Harding learned from his mentor, Dr. James Craine, the nuances of developing specific neurotraining plans for brain-injured patients.
So moved by witnessing firsthand the progress made by his patients, he analyzed over 20 years of data collected by his mentor in Hawaii and reported his positive findings in 2005.
A skilled neuropsychologist in both the geriatric and brain-injured populations, Dr. Harding has often provided court testimony for patients whose mental capacity for legal matters was brought into question.
Dr. Harding has made guest appearances on radio talk shows discussing dementia-related topics. He is also a frequent speaker at conferences on topics including proper brain stimulation and other dementia prevention strategies, as well as educating attendees on various mental health issues pertaining to the geriatric population.
Being community minded, Dr. Harding has served as Vice Chair of the Hawaii State Traumatic Brain Injury Advisory Board, Department of Health. While working in Maui, he was a member of the Maui Geriatric Board (Hui), helping his community identify service gaps in treatment provision for the elderly.
Disclaimer
Every effort has been made to make this book as complete and as accurate as possible. However, there may be mistakes, both typographical and in content. Therefore, this text should be used only as a general guide and not as the ultimate source of information. Furthermore, this book contains information that is current only up to the printing date.
The purpose of this book is to educate and entertain. The author and publisher shall have neither liability nor responsibility to any person or entity with respect to any loss or damage caused, or alleged to have been caused, directly or indirectly, by the information contained in this book.
If you do not wish to be bound by the above, you may return this book to the publisher for a full refund.
About the Book
America is at a point in history where Baby Boomers are turning 60-plus years of age, and half are predicted to succumb to some form of dementia by the time they reach their 80s. Every 70 seconds, someone in America develops Alzheimer’s Disease (AD). With AD and other dementias rapidly on the rise, threatening to bankrupt an already failing federal healthcare system, researchers have put much effort into searching for answers, with no cure in sight.
If the odds of acquiring a disease for which there is no cure is as risky as the flip of a coin, how do you feel today about making that call? Wouldn’t it be better to confidently predict and know that you will be on the right side of the coin when the call is made?
This book gives you the predictive powers to confidently make that call.
Fortunately, when it comes to winning the dementia coin toss, science has given us predictive powers in the form of risk factors. Knowledge of all risk factors allows one to live as I call, “Out with the bad, in with the good.”
By taking the multitude of known risk factors and categorizing them into four main elements or keys, it becomes easier to remember them and apply them to your life. Mastery of the four keys will keep the 800-pound gorilla called Dementia away from your doorstep.
The following chapters are organized into seven parts:
Part I explains how a typical person may develop Alzheimer’s (AD) and gives a brief overview of the dementia process and various forms such as AD and vascular dementia, the two most common types. Also included in this section is an introduction to Dr. Craine and how our paths crossed, along with an explanation of a wonderful thing called “neuroplasticity.”
Part II shares with the reader brain basics and how the brain functions and forms memories. Also discussed is why memories fade when the 800-pound gorilla named Dementia comes a-knocking.
Parts III–VI cover the four key factors for optimal brain health:
The 1st Key: Specific brain stimulation. Researchers now acknowledge that specific brain stimulation can slow and even reverse the decline of cognitive function (e.g. memory).
The neurotraining program shared within this book is the 1st key, which provides that much-needed specific stimulation. It consists of the principles and games of Dr. Craine’s neurotraining program. It shares with the reader a time-tested neurotraining program designed to create and strengthen new and existing synaptic connections between brain cells and promotes neurogenesis (formation of new brain cells). There is no need to buy expensive computer software or pay online subscriptions to stimulate your brain.
The 2nd key: Avoidance of known dementia risk factors. Included is a risk profile. Fill it out to familiarize yourself and discover which risk factors are present in your life today. Following the risk profile is the chapter where you will learn prevention strategies (out with the bad, in with the good) to eliminate or reduce risk factors, such as stress, from your life. Stress is such a crucial risk factor that we all deal with, and I consider it “Public Enemy #1.” It gets its own chapter.
The 3rd key: Proper brain nutrition. Here is discussed how the modern-day food supply resembles nothing of what our DNA evolved on. Also discussed is how the food we eat contributes to brain degeneration and the importance of changing our eating habits. After learning to take the bad out, next is discussed what to put into our diet, with a focus on the nutrients that science has discovered to improve brain plasticity and function.
The 4th key: Physical exercise and rest. Yes, physical exercise helps keep the brain healthy. Several studies now indicate this fact. Also in this section, recent research shows how a good night’s sleep is vital for memory formation. The consequence of not getting enough sleep and the effects on memory and increased risk for dementia are discussed.
Part VII, “Slowing the March of Time” is an updated view on what constitutes successful brain aging. Our behaviors have a major influence on the speed by which our brains age. Much has been learned through research, and there is much that we can do to slow down this process.
Remember, mastery of the four keys revolves around the mantra, “Out with the bad, in with the good.”
It Could Happen to You
Margaret looked nervously at me from across my desk. Her daughter, sitting anxiously next to her, fidgeted with a tissue in her hands. They both expected the bad news although neither was really sure they wanted to hear it. “Well, what do you think, Doctor? Is it Alzheimer’s?”
In my experience, there’s never a good way to deliver bad news. Just some methods that seem more tactful than others. As a neuropsychologist, however, whose job it is to assess individuals’ brain functions in a fast-growing geriatric population, it comes with the territory.
Margaret, or Margie as she prefers to be called, is typical among them. She’s in her 70s and living in a body weathered by time and neglect. And yet, in her mind, she identifies with a woman half her age. She’ll be the first to tell you she’s lived a healthier lifestyle than many of her peers. She was never a heavy drinker or smoker, though she occasionally imbibed, and she felt she maintained a fairly active and normal existence, never going so far as to do anything that might destroy her golden years. But it is that very definition of what we deem “normal” that perhaps is at issue. We’ll discuss more on that later.
The Typical Patient
Margie’s journey to my office reads like a blueprint for many previous patients. It began innocuously enough when her daughter, April, noticed a certain cognitive decline in her mother’s mental acuity. Things that used to come easily, like remembering recent events, or why she had walked into a room, or where she had placed common items like her car keys, were now suspiciously beyond her ability to recall. Up until now these suspicions were shrugged off and were commonly referred to as “senior moments.” As these so-called senior moments increased in their frequency, April shared her concern with a friend, who recommended her to me.
After an initial interview, I administered a series of tests that form the foundation of what is referred to as a “dementia battery.” A few days later, Margie and April returned for the news: Margie did not have dementia—not yet, anyway.
Here the term “dementia’” does not refer to being psychotic or “crazy.”
The relief in Margie’s face was palpable. Already she envisioned herself on a cruise with friends sipping wine and enjoying dinner shows well into her 80s and 90s. But April wasn’t ready to share in her jubilation.
“What do you mean ‘not yet’?”
A person’s brain function, I explained, is like a continuum spread out between two outstretched hands. The hand on the left represents dementia, a general term used to describe the symptoms that occur (memory loss being the most common) when the brain is damaged by one of several diseases, such as Alzheimer’s Disease, or cerebral vascular disease.
The hand to the right, meanwhile, represents normal brain function.
Margie’s results put her squarely in the middle of the continuum, in an area that for her age is described as Mild Cognitive Impairment, or MCI for short. In other words, her current mental abilities were not at the level they should be for someone her age, though they were not so bad as to label her demented.
A little concerned, April asked, “Are you saying that my mother will eventually reach the dementia hand, or will she stay where she is—in the middle?”
It’s a good question, and a common one. In Margie’s case it was simply too early to tell. “The good news,” I told them, “is that not everyone who develops MCI moves down the continuum to reach the dementia hand. There are many variables at play that can affect a person’s progression up or down the continuum and not all of them necessarily move you all the way into dementia. On the other hand, there are those, like Alzheimer’s Disease, that most certainly will.”
Disease, Dysfunction, and the Brain
Let’s look closer at the word dis-ease. It means to be not at ease, or, on a cellular level, out of balance, unhealthy cell function, or dysfunction. Poor cell health and dysfunction open the door for an increased potential for decreased cell maintenance activities and other things to go wrong, such as the formation of neuritic plaques, neurofibrillary tangles, and inflammation in the brain that are associated with Alzheimer’s Disease.
The 800-Pound Gorilla
As we age, it is commonplace in our society to experience “senior moments” just as Margie did. Of course, it is only natural that as these instances become more frequent we begin to assume the worst: Am I losing my mind? Am I getting Alzheimer’s? Will I be that parent who becomes a burden on my children because I can no longer remember how to do even the simplest of tasks?
And it’s no wonder. Alzheimer’s Disease (AD) is the most notorious attributable factor to dementia in the world—and for good reason. AD is a type of neurodegeneration caused by an accumulation of amyloid plaques and neurofibrillary tangles within the brain that decrease brain plasticity and interconnectivity, and which eventually leads to cellular death. Put simply, AD kills brain cells—and lost brain cells equal lost brain function.
AD is a progressively degenerative brain disease that accounts for approximately 62 percent of dementia cases worldwide and will eventually rob you of your friends, family and loved ones. They will ultimately become nothing but strangers to you, shadows moving through an unfamiliar world. What is possibly worse for those you leave behind, however, is that you will also no longer resemble the person they knew and loved either. In time, AD will eventually even rob you of your life. For most people worried about a decrease in their mental acuities, AD is the ultimate 800-pound gorilla looming over them.
Is Memory Decline Inevitable?
But let’s take a step back for a moment and look at the facts. There are many reasons as to why we have these so-called senior moments as we age. Not all of them lead to AD. In fact, there are various forms of dementia. Some of them are reversible, while others are entirely preventable if we have the tools and understanding of how to prevent them. A little early tip: How we treat our brain today will have a significant effect on our brain function tomorrow.
Take a look at the chart that follows. The “Z-scores” are nothing more than statistical data points, so don’t be intimidated. All you need to know is that 0.0 represents average memory function; just as a 100 IQ score would represent average intelligence.
Average Lifespan Memory Function
Verbal Memory is the ability to remember that phone number you just heard, or a list of words read aloud to you. Visuospatial Memory is the ability to remember things like where you parked your car or how well you do on a memory card game. Notice how on average both types of memory function reliably decline as we age down to –1.0, or what is considered a very low average range of function. “Is this an inevitability?” you may wonder. Is it the future that is in store for all of us?
The answer is a resounding NO! This chart is based on data collected from a population unaware of how to maintain their brain function over time. It is based on a public enamored with junk food, fad diets, lazy lifestyles and unstimulating mental pursuits. It is our goal here to change all that you think you know and show you how to prevent that decline so that your golden years are everything you want them to be!
Before we can do this, however, we must first provide you with a foundation for understanding how the brain works and ages in relation to the rest of your body. Following is a table that shows healthy brain aging compared to AD and mild cognitive impairment (MCI):
Age-Related Brain Atrophy
Just like the rest of your body, your brain goes through changes as you age. Because you can’t see it, though, you aren’t typically aware that these changes are occurring. So let’s talk about an organ you can see—your skin.
Close your eyes for a moment and think back to when you were ten years old. You are looking at yourself in the mirror, perhaps brushing your teeth or combing your hair. Puberty hasn’t set in yet, so there isn’t a blemish on your face. The word “wrinkle” has no meaning to you. Now, through your mind’s eye, you look at the back of your ten-year-old hands, fresh and spotless. Remember how if you suffered a minor scrape or cut you could almost watch your skin knitting itself back together? A wound like that would heal in something like a day. It was absolutely amazing!
Now open your eyes and look at the back of your hands. Wrinkles. Scars. Age spots. Sure, you call them freckles, but we all know what they really are! And the wrinkles—they just gradually get deeper over time, and more pronounced. But some of you, maybe, see skin that is remarkably smooth and supple for your age. Why do you think that is?
There’s no trick to it, really. Aside from some genetic factors, the quality of your skin today comes down to how well you have taken care of it throughout your life. Too much sun, cigarette smoking or alcohol, all have an impact on the health and vitality of your skin. Take notice, though, that these are environmental factors we can control, and how well we take care not to expose ourselves too much to these factors today will determine what our skin will look like tomorrow.
Like our skin, our brains have similar reactions to negative environmental factors. And as in our care for our skin, those environmental factors that adversely affect the brain’s development and sustainability are entirely under our control. How well we take care not to expose our brain too much to these risk factors is a major player in determining our brain function for tomorrow.
Risk Factors, Briefly
You’ll hear me use the term “risk factor” a lot. A risk factor is something that increases a person’s chances of developing a disease. I will cover many of these at length in subsequent chapters, but I at least want to give you a working knowledge of what they are before we go on. A health risk factor can be your age, your sex, lifestyle, personal health history or family health history. Environmental risk factors are things such as smoking, air pollution, stress, or toxins in your food or water supply.
If you are exposed to certain risk factors, you may be considered at “high risk.” For example, if you have a family history of heart disease, you are considered at high risk for heart disease. However, being at high risk does not mean you will definitely develop that disease, just as being “not at high risk” does not necessarily mean you will escape getting that disease. The number and severity of risk factors your brain has been or will be exposed to plays a large role in how far down the brain aging graph your brain function has declined or will decline.
Dispelling Common Misconceptions about Dementia
Many people associate dementia solely with Alzheimer’s Disease and are thus surprised to find themselves in the preliminary stages of the disorder with no sign of AD in sight. They fail to realize that there is a plethora of diseases and/or disorders that can lead to some form of demented state. Perhaps the most common misconception with regard specifically to patients who are diagnosed with AD, however, is that they did not think they could get it with no previous family history of the disease.
Take a look at the pie chart shown here. It describes the percentages by population of the numerous degenerative brain diseases that could cause a loss of mental function:
While it is true that AD accounts for a whopping 62 percent of dementia cases, there are a slew of others to consider as well. And that patient who was diagnosed with AD but had no family history of the disease? What he doesn’t realize is that AD comes in two forms—Familial AD, or FAD, and Sporadic AD. Only a small percentage of total AD cases are diagnosed as FAD, the genetic variant that runs in families. The overwhelming majority of AD cases are Sporadic, and they are caused by certain lifestyle choices, or other risk factors (hypertension, diabetes, etc.) that lead to poor brain cell maintenance and function. We are all at risk of developing Sporadic AD if we do not adhere to the prevention strategies we will be discussing later in this book.
Neurodegeneration
Many of the risk factors that cause the onset of Sporadic AD are, in fact, preventable. Inadequate nutrition (due to the typical American diet), decreased oxygen levels (due to constricted capillaries—again, poor diet and other lifestyle factors), coupled with little to no stimulation of memory systems (due to inactivity), and an environment filled with toxins set the stage for the beginnings of a complex neurodegenerative cascade. This downward spiral involves multiple changes in decreased levels of neurohormones, neurotransmitters, lipids, enzymatic activity, increased cytokines (involved in the inflammation response), changes in the cellular structure itself, and even changes in the genetic material of the DNA. All of these changes contribute to cellular dysfunction, loss of synaptic connectivity between neurons (30 percent or more in the case of AD), and even neuronal death.
What you may be surprised to hear, however, is that this imbalance begins quite early in life. Some researchers have uncovered evidence suggesting that the process starts extremely early. Atherosclerosis, or vascular disease, has been seen even in babies. Research has also shown significant inflammation and plaque buildup in arteries of 20-year-olds! One study of young soldiers with an average age of about 20 who died in the Korean War found that over half had significant atherosclerosis in their coronary arteries and aortas.
As this neurodegenerative downward spiral continues into our later years, the brain will continue to lose neurons and the synaptic connections between them. In place of these healthy neurons and connections are occlusions such as amyloid plaques and neurofibrillary tangles that are the hallmark of AD, and which accumulate over time. Research presented at the 2010 International Conference of Alzheimer’s Disease indicated that biomarkers such as amyloid beta levels rise significantly long before (15-plus years) any behavioral changes such as measurable memory changes occur. While some neuronal loss is normal, how much is presently unclear. What is clear is that unhealthy neuronal cells cannot produce the chemical messengers, known as neurotransmitters, in enough quantity to keep up with the demand we place on them to maintain the flow of information among the neuronal population, and this becomes especially so as they decrease in number. It isn’t until we are older that the damage we have perpetrated over a lifetime shows up in the form of cognitive dysfunction (e.g. poor memory) in our aged, slower, shrunken brains.
The Odds of Becoming Demented
So, what are the odds of becoming demented? I do a lot of seminars in the course of my work and I am often asked something to this effect. Would you believe 50/50? That is not to say that half of the people reading this book will develop Alzheimer’s. Rather, there is a 50 percent chance that whoever is reading this now, given what the typical person’s lifestyle is, will develop some form of dementia as he or she advances in age—whether it be vascular dementia, frontotemporal, Parkinson’s, or even the dreaded AD, among many others.
The ugly truth is that statistics show you will either become demented yourself, take care of someone who has become demented, or know of a demented person in your immediate family—unless we decide to do something about it now!
Even if you are already into your later years, there is hope. In a 2006 article in the journal, Neurobiology of Aging, researchers at the University of Illinois showed that with a little task-specific training (such as proper memory exercises), the brains of older individuals can blunt cognitive functional decline and even start to look and act younger. Using fMRI brain imaging, researchers discovered that training for specific tasks not only improved performance in older people, but also caused increased activity in the brain regions that were being targeted (in this case the ventral prefrontal cortex, a common site of age-related atrophy). The results suggest that age-related functional decline is not an inevitable process of aging, but can be reliably reduced, and possibly reversed, via brain stimulation, or neurotraining. Other studies across the country are showing similar results, and it is now generally accepted that stimulation of the mind is good medicine for the brain and can even help maintain brain health.
Sharp vs. Dull
Have you ever known of an elderly person who possessed the mental acuity or sharpness of a person half their age? They do exist—Dr. James Craine, my mentor and the principal researcher whose material this book is based on, was one of them. He worked on neuropsychological evaluations with me right up until the day he passed away. He loved the field of neuropsychology, and had the mental acuity to carry out such complex work up to the very end of his life.
So why then is it that some individuals stay mentally sharp while others, although they may not become demented, clearly have dulled mental function? Dr. Craine attributed his superior brain function to neurotraining exercises (he was also a track-and-field athlete, holding several titles in his age group). He claimed that you didn’t have to be the recipient of a traumatic head injury to benefit from neurotraining. “There’s always room for improvement,” he would often say, and he was living proof.
The Goal
Dr. Craine was the embodiment of what I call “Mature Body—Youthful Mind,” a concept I encourage you to take on as a goal while you progress through this book, learning the techniques put forth in it. After all, you’ve most likely worked long and hard to obtain your life’s achievements and get to where you are today. But what good is it to accomplish so much and not be able to remember any of it in the end? You should want to retain your memories and sustain or improve you brain health so that you can enjoy yourself well into your golden years. This is certainly better than being strapped to a wheelchair drooling into your lap and not knowing anybody or anything around you, right? If you’ve never been to a care facility with an Alzheimer’s Unit, go take a look for yourself and see what you think then. I’m sure, after working hard all your life (or perhaps you’re still working and want some reassurance against a future living with dementia), your goal is to retire and enjoy life. Not to let that 800-pound gorilla rob you of what you’ve worked so hard for!
The Solution
Let me make this clear right now: There isn’t a magic pill we can swallow or a surgery we can undergo that can fix what we have done to our brains throughout years of abuse and neglect. Not long ago, when poor cardiovascular health began resulting in a significant increase in number of heart attacks, the medical community got busy figuring out how to perform heart repair and replacement surgeries. The result is that today our health care system is more prepared than ever to handle serious heart problems. However, brain dysfunction due to similarly poor cardiovascular health usually does not show up until later in life, and even if it did make itself apparent earlier in the game, there are no methods at a surgeon’s disposal to repair the damage that has been done. Likewise, there are no “new pills” as purported in magazine and late night television advertisements to restore memory loss. Bottom line—there is no magic bullet or miracle cure.
But the damage that has been done is reversible, if it isn’t too severe or too late in the game. Back in the mid-1970s when science thought the brain was static, my mentor, Dr. Craine, postulated that the brain was plastic and had the ability to modify itself—to grow new connections that may have been lost from an injury. Today science has confirmed that the brain can indeed grow new connections and even produce new neurons (brain cells) through a process known as neurogenesis (more on this later). Based on his plasticity premise, he developed a cognitive rehabilitation or “neurotraining program,” as he liked to call it. Over a 25-year period, he refined this program and applied it to the head-injured populations in Hawaii, where his institute was located.
As a neuropsychology doctoral student, my dissertation investigated the efficacy of his program. It turned out those individuals with mild to moderate head injuries were able to regain much of the brain function they had lost, although patients with extremely severe head injures did not respond to the rehabilitation. (It appears that there is a “point of no return” for the brain). Now, if mild and moderate brain-injured patients benefited from Dr. Craine’s neurotraining program, imagine what it could do for you! Making his life’s work available to everyone was one of the last wishes he asked of me before he passed away. It was his hope that no one would have to live with dementia if it were at all preventable.
If you follow what’s written in this book, and apply what you have read to your life, I promise you can actually change the course of your future. It’s simple: The solution is all about choice, choosing to eliminate some bad habits and replacing them with good habits. With this book, you now possess the necessary tools to ensure that you will be the proud owner of a healthy, happy brain for many years to come. But you must apply what you will learn in these pages.
For those of you who have yet to develop any signs of dementia, if you apply what you learn in this book, your mind will be as sharp as it is now 20, 30, or even 40 years down the road. For those who have mild or even moderate brain injuries, this book is a ray of hope into your future. With the proper type of brain stimulation, you can regain some of the function that you have lost. Teaching you the specific and precise programmed stimulation or exercises for your brain is a key focus of this book.
I am speaking from firsthand experience, as I suffered a mild head injury during my teenage years and have regained my base level of function, and have subsequently gone far beyond what was thought possible by the “experts” (already a glimpse as to why I entered this field).
Working side by side with Dr. Craine, I have also helped many brain-injured individuals recover much of their cognitive function. If you want to learn how to do a new task, it makes sense to learn it from someone who has already done it and is willing to show you how. So, with that said, let’s go kick some gorilla butt!
Pioneers Before Their Time
Today it is widely known that brain plasticity and neurogenesis occur in the adult human brain. The acceptance of these concepts, however, and the subsequent press they have garnered are a relatively new occurrence. The pioneering researcher, Dr. Joseph Altman (1965 and 1969), was the first to report about the ongoing cell division that occurs in the adult brain. Dr. Altman discovered in rodent studies that an enriched learning environment resulted in improved brain function. Rodents living in an enriched environment ended up with slightly heavier brains, greater thickness in certain brain structures such as the hippocampus, increased levels of some neurotransmitters, and more connections between the neurons in their brains. These rodents went on to perform better in learning tests, such as in navigating mazes, than their control group peers. Dr. Altman postulated that perhaps some of the improvement in performance could be attributed to brain plasticity and neurogenesis—radically new ideas that flew in the face of conventional theory.
The Static Brain Paradigm
Dr. Altman’s lone experimental findings met with extreme prejudice when he first made them known. The prevailing theory at the time of his experiment held that the adult human brain was static rather than plastic. This so-called “static brain paradigm” did not allow for the idea that an adult brain could generate any new cells or synaptic connections during adulthood.
Dr. Altman’s findings thus stood in direct contradiction to the prevailing notions of the day and resulted in a widespread lack of acceptance. It was akin to Aristotle, in 330 B.C., telling stubborn believers of a flat world that it was in fact round!
It took over 30 years before the scientific community’s conceptual understanding of the brain expanded to gradually embrace the idea of plasticity and neurogenesis, thus vindicating Dr. Altman’s findings. Only after the introduction of empirical data provided by better neuroimaging technology did the credibility of the long-held theories become seriously challenged. Indisputable pictures and video footage of living brains remodeling themselves after an injury and creating new synaptic connections provided undeniable evidence and support for new theories of neural plasticity, thereby giving the field new direction, while laying to rest the old static brain paradigm.
Another Pioneer
Not everyone thought Dr. Altman was off his rocker, though. A handful of neuropsychologists chose to further investigate the new findings despite contemporary sentiments. Inspired by the legendary neuropsychologist Alexander Luria of Russia, and fueled by Altman’s findings, Dr. James Craine, the director of the neuropsychology department at a hospital during the 1970s, created and developed the neurotraining principles and stimulation games included in this book.
By 1981 he had perfected his program and written the book, The Rehabilitation of Brain Function: Principles, Procedures, and Techniques of Neurotraining. Using the principles and techniques he perfected over several years, Dr. Craine was helping brain-injured survivors in Hawaii recover from brain damage even while the scientific community stubbornly maintained their static brain theory, just as Aristotle’s flat-earth nemeses did 2,300 years before.
Meeting the Mentor
As a neuroscience graduate student in Hawaii, I was involved in stress experiments that highlighted the extensive damage inflicted upon brain regions from stress—not from brain trauma or some other form of physical injury, mind you, but from stress alone. I was witnessing actual empirical observations that told me the brain was changing according to the outside stimuli it was exposed to, and yet my professors persisted in maintaining that “the brain is static.” It just didn’t add up.
Around that time, Dr. Craine came into my life and told me not to believe everything I read in my textbooks; that the brain was plastic. He was my new supervisor on a project examining the effects of insect neurotoxins upon the brain function of children exposed to the toxin via their mother’s milk.
We had many discussions after work, and, to make a long story short, I switched academic programs and joined ranks with him. Later, as I got to know Dr. Craine better, I asked him, “How did you do it? How did you avoid all of the criticism and indifference toward plasticity for so many years?”
He smiled and replied, “I just went quietly about my work developing the neurotraining program and providing services to people in the local community who needed and could benefit from it.”
“But, people—the world—could benefit so much from your work,” I said.
He said, “The time isn’t right—when it is, you will tell them.”
A Life-Altering Event
Dr. Craine’s perspective on brain function was a better fit at explaining the experimental findings of my stress studies compared to what my professors were teaching me in the lab and in class. If stress is so damaging, and destroys connections between neurons and even the neuron itself, how was the average American, with their busy, stressful lifestyle, still able to function? With as much stress as I had endured in my lifetime, how was it that I could still remember anything?
As if stress weren’t enough of a factor, I was also a survivor of a major motor vehicle accident (see picture below) that changed my life forever.
I was a teenager in a time before airbags, and unfortunate enough to be the one sitting in the crumpled passenger’s seat of my friend’s pickup truck. To say that I am very lucky to be alive would be an understatement. I did not walk away from this vehicle. Instead, I spent the greater part of a year in casts and on crutches.
Unbelievable as it seems, I was knocked unconscious only momentarily. I say “momentarily” as I remember the events of that evening quite well. Had the concussion been severe, I would have amnesia of the events immediately before and after the crash.
That is not to say I did not suffer any brain damage; however. I survived what is known as an acceleration-deceleration brain injury, which results in something called a “diffuse axonal injury” where microscopic lesions, or nerve fibers, shear or stretch with consequent axonal (nerve cell) damage. Between the car crash and the stress levels I have endured in life, it suffices to say that if the static brain paradigm were true, I would not have been able to write this book today.
Brain Regeneration and Plasticity
Generally speaking, brain regeneration and plasticity is a product of two main components: stem cells and various neurotrophic growth factors, such as brain-derived neurotrophic factor (BDNF). BDNF is produced as a result of brain activity in neuronal circuits (e.g. memory).
Newly born stem cells in specific brain regions (e.g. hippocampus) can become a newborn workhorse brain cell called the neuron (covered in the Brain Basics chapter).
Neurogenesis
In this image, a stem cell is shown capable of generating different kinds of brain cells, depending upon need. The process by which these cells interact with existing brain cells to recreate the function of damaged brain tissue makes up part of the brain’s neuroplasticity.
These new neurons grow much faster and healthier when BDNF is present. BDNF acts like a fertilizer—similar to when you fertilize your lawn to grow greener grass faster. A healthy young neuron will branch out and connect to neighboring neurons, thereby becoming part of a neural network system, such as your memory system. It is important to note, however, that the process of a neuron surviving to integrate itself into a memory system is dependent on proper stimulation. Without stimulation, the newborn cell doesn’t integrate, and dies.
True neuronal integration depends on many complex variables and progressive events, and subsequently not all newborn cells make it through the integration process. Most newly generated hippocampal cells die, presumably by apoptosis (programmed cell death). It does appear, however, that essentially all newly born neurons that survive their initial two weeks will mature and persist. Their survival depends on genetic factors, as well as an appropriate microenvironment (BDNF) and various external stimuli.
Microenvironment and Plasticity
The second and more common way the brain rewires a memory neural network is by increasing the connectivity of existing neurons. Once again, by providing the proper microenvironment such as the fertilizer BDNF, existing neurons will add more connections and strengthen existing ones. This process, as with the previous one, is also dependent on proper stimulation.
Brain regeneration can be witnessed when stroke victims placed into medical boot camps begin regaining better brain function. Their medical boot camp regimens basically amount to rigorous stimulation programs. Animal studies show us that the hippocampus regenerates itself twice as fast when given learning tasks.
Take away the stimulation, however, and the brain does not regenerate. This is why animals grown in the dark lose vision, because the neurotrophins that sustain optic nerves aren’t produced without stimulation. Similarly, this is why people with less mental stimulation are more prone to develop Alzheimer’s. Less learning-stimulated nerve activity in the frontal cortex and hippocampus means less neurotrophic activity in the hippocampus. As activity decreases, researchers see shrinkage of the cortex and hippocampus. Hippocampus shrinkage is especially exacerbated in the brains of people with Alzheimer’s. To no surprise, levels of neurotrophins such as BDNF are low in people with Alzheimer’s.
Plasticity in Older Brains
The brain operates on a “use it or lose it” basis, much like the rest of our body. A good example is our skeletal muscles, which tend to atrophy if they are not properly stimulated (exercised). The brain is similar. If we don’t stimulate our memories as we age, the connections between our memory neurons, and even the neurons themselves, fade away over time until our first ”senior moments” occur.
If you are beginning to experience senior moments, it is a sign your memory systems are not being stimulated well enough to keep their connections healthy and intact. Don’t despair, though, as all is not lost. Older brains do in fact retain some of the plasticity found in newborns, and, with proper stimulation, they will also respond and grow new neural connections. In studies designed to test plasticity, such as those conducted by Dr. Huxhold (2008) that sought to compare a young group’s (20–30 years) to an older group’s (70–80) response to stimuli, both experienced substantial gains in practiced memory tasks.
Good news! Epidemiological data suggest that humans with active minds have a reduced risk for developing dementia as they age.
For a moment, though, let’s assume that for whatever reason you have chosen not to stimulate your brain. In that case, some researchers believe that how soon you start to show signs of senior moments depends on the size of your cognitive reserve.
Cognitive Reserve
Dr. Satz (1993) proposed a “threshold theory,” which postulates that the amount of brain reserve capacity (BRC) represents structural or physiological brain advantages (such as size and redundancy of interconnections). The idea here is the larger, denser brain regions will have a better chance at recovering from head injuries, or providing buffers between normal aging and AD. Researchers investigating AD determined that low educational and occupational levels were associated with an increased risk for developing AD (Bondi, et al., 1996; Schmand, et al., 1997). A common explanation of this finding is that people with higher levels of education have more “cognitive reserve” to compensate for the neuropathological changes resulting from the disease and to delay the onset of its clinical presentation.
Once the idea of neuroplasticity was firmly established in the scientific community’s paradigm, the cognitive reserve theory was expanded (Stern, 2002) to distinguish two classes of reserve models. First, the original passive model that focuses on brain reserve in terms of physical reserve capacity. This could be represented by neural network density. Second, an active model was described that focused on the ability of a person to recruit alternative cognitive capacity, or the plasticity, of the brain to reorganize cognitive networks when the brain has been compromised. Both active and passive components most likely play a role when the brain is affected by aging. Thus, an individual’s amount of cognitive reserve likely depends on factors ranging from genetics to how stimulating an environment a person exposes himself or herself to, and to active usage of his or her brain.
Brain Basics 101
Inside your head is a brain that consists of the same gray matter that figured out how to put a man on the moon. The gray matter that makes up your brain is shared by all humans. No matter what your skin color, religious beliefs, or political perspective, on the inside, we are all gray.
You will find it helpful to know some brain basics in order to keep up with later discussions regarding brain health, so here is what I consider the basics. I have filled this chapter with pictures for ease of explanation and to help those individuals who learn best with visual aids.
Quick Facts
The human brain typically weighs about 3 pounds (or 1–3 percent of total body weight). Although no one has actually counted the number of brain cells we have, the brain is generally estimated to contain approximately 100 billion neurons (electrically active nerve cells), with approximately 10,000 synaptic interconnections per healthy neuron. This means there are 100 trillion interconnections in the brain. Counting them at the rate of one a second would take 30 million years.
There are approximately 10 times as many support cells (glial cells) for neurons. This 10:1 ratio may be where the old myth that we only use 10 percent of our brain originated. However, nothing could be farther from the truth. Let me assure you that every neuron in your head is active—if it is inactive, it is either dead or close to it.
The Neuron
Your brain is made of various types of cells. The real workhorse in the brain is known as the neuron, and it will take center stage in our discussion. Following is a picture of a typical neuron. Neurons come in various shapes and sizes and perform different jobs.
Neurons are made up of three major parts: a cell body, an axon, and a dendrite.
Generally speaking, a neuron is a cell like any other cell: the cell body, or soma, has an enclosed membrane with its genetic material (DNA) in a nucleus embedded in its cytoplasm. Inside the soma are other organelles typical for any cell, such as the mitochondria, which are the engines or energy producers of the cell. Neurons are very metabolically active and the mitochondria require large quantities of glucose and oxygen to maintain appropriate energy levels for the neuron.
What makes neurons unique, however, is that the neuron sends out two kinds of threads. One of these threads, known as the dendrite, looks similar to a bush or tree. Each neuron has several main dendritic branches such as in the foregoing picture. The dendrites carry information from other neurons toward the cell body.
The other thread that a neuron extends out is called the axon. The axon carries an electrical impulse away from the cell body toward the other end of the axon where the terminal buttons are located.
Axons are covered by myelin, a type of support cell to the neuron. Myelin increases the speed of transmission of information, or electrical impulse, down the axon, much like gold plating or coating on an electrical wire or contact. It is often referred to as “white matter” as it appears white in color due to its fatty composition (see cross section photo below).
How Neurons Communicate
Neurons communicate with both electrical impulses and with chemicals known as neurotransmitters. The soma acts as the processing center of all the chemical information received from the other neurons via the dendrites. The soma will send an electrical impulse down the axon toward the axon terminal buttons located at the end of the axon (see following pictures). When the electrical impulse reaches the terminal buttons, a chemical cascade begins and the electrical impulse ends. Here at the axon terminal button is where a chemical message is transmitted to the dendrite of another neuron.
The synapse is the area where the axon terminal meets up with the dendrite of another neuron. The synaptic cleft is the tiny space between the axon terminal and the synapse.
Located inside the terminal buttons are synaptic vesicles containing a chemical neurotransmitter substance (e.g. serotonin, dopamine, etc.). When the electrical impulse reaches the terminal button, the synaptic vesicles release their contents into the gap of the synaptic cleft. The neurotransmitters are then taken up by receptors of the dendrite that makes up the other side of the synaptic cleft, where the dendrite is waiting to receive the chemical message.
This is the basis of neuronal communication. The electrical/chemical cascade between neurons happens in milliseconds. Think of a neuron as akin to a flickering light bulb—firing an electrical impulse along its axon several times a second.
Plastic Dendrites
Owing to their treelike structure, dendrites take up space, and the tree provides the surface area for as many contacts as possible (even from the other side of the brain), thereby giving every synapse message a direct path to the soma that it intends to communicate with. The growth of dendritic trees continuously adds new surface area for more contacts, not only in childhood, but also into adult life, and even into healthy old age. Axons and their lateral branches also grow and divide, allowing them to connect with other neurons.
Following is the main reason I elaborated on basic neuronal communication for you, and I believe that Dr. Walter Freeman, professor at UC Berkeley, said it best in his book, How Brains Make Up Their Minds:
“The competition for synaptic space is intense, and success in finding and maintaining a connection depends on the synapses being active. If they are inactive, owing to damage or disuse, the connections decay and the synapses disappear. Even the neurons themselves may vanish. The health of neuronal connections in old age, like muscles, requires stimulation. The lifelong growth and the maintenance of active connections provide the basis for learning, remembering, and adapting through modifications of the numbers and strengths of synapses, and they require daily exercise….” (boldface added).
Remember the old saying, “If you don’t use it, you’ll lose it?” We now know that this old adage applies to neurons and their synaptic connectivity. If you want to keep your memory system healthy and functional, stimulate it!
Basic Brain Anatomy
Throughout this book there are certain terms used to identify brain regions. The following picture shows the basics:
The foregoing image shows, on the left, the outside of the cerebral hemisphere, viewed from the left side, showing the major lobes (frontal, parietal, temporal and occipital) along with brain stem structures. The image on the right is the same side view showing the location of the limbic system inside the brain. The limbic system consists of a number of structures, including the hippocampus along with other regions. The hippocampus is still part of the surface of each cerebral hemisphere, but the folding and twisting of the hemisphere during its embryologic growth buries it like fingertips in a fist, placing it deep inside the medial temporal lobe in the base of the brain. The hippocampus is a key structure in the formation of new learning and memory. The hippocampus has been named the “gateway to memory” owing to its important and indispensable role in new learning and memory.
The main source of input into and output from the hippocampus is the adjacent entorhinal cortex, so the two parts constantly interact. The entorhinal cortex collects all bits of information from other brain regions, such as visual stimuli of a face and verbal stimuli of a name, and packages them together before sending it along to the hippocampus for encoding. After encoding, the hippocampus sends the data back out through the entorhinal cortex where it is sent to various brain regions for recall later.
Unfortunately the hippocampus and entorhinal cortex are the first areas affected by the ravages of neuritic plaques and neurofibrillary tangles of Alzheimer’s, making it difficult in the early stages for new memories to be formed, and impossible in the later stages of AD.
Two Hemispheres
The brain consists of a left and right hemisphere, with the two halves connected by the corpus callosum (picture below). Looking at the brain from the front and cut from ear to ear, you can see the outer cortex, or gray matter, and the white matter of the brain. It is the gray outer cortex where the neuronal bodies are located, and the axons of the neurons that are covered in a fatty myelin sheath make up the white matter (which gives it a white appearance). The corpus callosum consists of tightly bundled axons from both hemispheres that cross over to the other side to allow communication with the neurons from each side.
Brain Cross Section
Let’s say you are meeting someone for the first time at a social event, and you are trying to remember his or her name. The neurons involved for facial recognition reside in the cortex of the right hemisphere, and the neurons involved with language (name) reside in the left hemisphere. In order for you to put a name with a face, both sides of the brain must communicate with each other along the corpus callosum.
Blood Supply to the Brain
Turtles can walk around for hours with no oxygen supply to their brains. Your brain, however, is absolutely dependent on a continuous supply of well-oxygenated blood. An adult brain requires approximately a quart (750 milliliters) of oxygenated blood every minute to maintain normal activity. A stable and continuous blood supply is required, and the brain, which represents only 2 percent of your total body weight, uses about 15 percent of the normal cardiac output and accounts for nearly 25 percent of the body’s oxygen consumption!
Unlike most other cells in your body, which can burn either fat or sugar (glucose) for their energy production needs, neurons can only burn glucose under normal, non-starvation conditions, and they typically consume 50 percent of the total blood sugar. Unlike liver and muscle cells, which can store large amounts of sugar as glycogen, neurons can only store at most a minute or two’s worth of glucose, and so they are dependent upon a continuous and uninterrupted blood supply to maintain normal energy metabolism and avoid injury or death.
Without oxygen, the brain is like a fish out of water.
Brain Blood Supply
This picture is a simplified representation of the major arteries supplying blood to the brain, both deep inside the brain as well as on its outer surface.
The Blood Brain Barrier (BBB)
Every cell in your brain needs blood, and in place of an effective way to store oxygen and glucose there exists an extensive circulatory system that supplies that continuous quart of blood to your brain every minute. Getting blood to every brain cell is the job of the amazing capillary system of the brain, which also forms the blood brain barrier (BBB). Not only does this amazing capillary system keep your brain bathed in blood, it also protects the brain from foreign molecules. The BBB is formed by very tight junctions between cells that make up the inner walls of capillaries (endothelial cells). This results in a mechanism that controls the passage of substances from the blood into the brain (see figures that follow). The BBB lets essential metabolites, such as oxygen and glucose, pass from the blood to the brain but blocks most of the larger molecules.
This means that everything from hormones and neurotransmitters to viruses and bacteria are refused access to the brain by the BBB. It also means that many drugs, which would otherwise be capable of treating brain disorders, are denied access to the very regions where they would be effective. Here are some facts about your BBB:
• There are 100 billion capillaries in the human brain, and the endothelial walls inside these capillaries form the BBB.
• The surface area of the human BBB is about 20 square meters!
• There are about 400 miles of capillaries in the human brain!
• Every neuron is virtually perfused by its own blood vessel; therefore, the delivery places oxygen (and drugs) at the “doorstep” of every neuron in the brain.
In order to traverse the walls of brain capillaries, substances must move through the endothelial cell membranes and requires a transport system and specific transporters for glucose and other critical molecules. The following figures will show you the compactness of the extensive network of the capillary system in your brain. The next figure shows the arrangement of blood vessels in the cerebral cortex of a 66-year-old man. The blood vessels were injected with plastic, and the surrounding tissues were dissolved away, and an image of the resulting cast was made with a scanning electron microscope:
The scale mark corresponds to 55nm.
Today’s powerful electron microscopes allow us to see “up close” to view brain tissue. This next picture is close enough that you can actually see single red blood cells inside the capillary!
The BBB capillary system is so small that single blood cells flow through in single-file fashion. There is little room left. When the blood supply becomes constricted (e.g. inflammation, cholesterol or plaque buildup, etc.), and blood supply to the constricted area decreases, this is when neuronal health decreases and cellular dysfunction and even death may begin. Below are figures of various ways blood flow is decreased or lost to an area:
A ruptured aneurysm and hemorrhagic strokes are frequently due to hypertension (high blood pressure). Too much pressure on a weakened wall of a blood vessel area can lead to a rupture or “blowout.”
A thrombus is a buildup of inflammation, plaques and fatty acids that constricts the passageway for blood flow. The end result is decreased blood flow to the area on the other side of the buildup.
Spontaneous cerebral blood clots or embolisms can block the blood flow to a region and is a common pathology of Alzheimer's Disease and cerebral vascular dementia. Embolisms are frequently the culprit that causes silent cerebral infarctions or "mini-strokes" as well as transient ischemic attacks (TIAs).
Bottom Line: Less Oxygen = Decreased Metabolism & Increased Dysfunction
Vascular Dementia