Do I Have Alzheimer’s Disease?

I am a psychiatrist who specializes in the treatment of mental health disorders and brain illnesses in patients over the age of sixty. I practiced general adult psychiatry for seven years before I shifted the focus of my practice toward working with older adults. This new professional direction followed the loss of my father to Alzheimer’s dementia. Alzheimer’s disease is the most common form of dementia and the illness took approximately ten years to take away his autonomy, independence, and future. Since 2001, I have been the medical director of an inpatient psychiatric treatment unit for older adults. Approximately 75% of the patients admitted to our unit suffer from Alzheimer’s disease or another form of dementia. I wrote this article in response to the concerns of many of the sons, daughters and spouses of my patients, their concerns over the mental health, well-being, and outlook for their affected family members and for themselves. I hope this book is useful in answering some of your questions with regard to Alzheimer’s disease and, more specifically, how to differentiate Alzheimer’s disease from a benign condition that we call “normal aging” and another condition that may progress to dementia called “minimal cognitive impairment.” This e-book is a reference to help direct you to resources that may be able to answer questions that I can’t answer in this context. While the information may be helpful in determining whether you are at risk or need to be evaluated or screened for Alzheimer’s disease, this book cannot take the place of an actual face-to-face evaluation by a physician or other mental health care provider that specializes in the evaluation and treatment of Alzheimer’s disease.

Chapter 1: What is Alzheimer’s Disease?

Alzheimer’s disease is a brain illness that causes the cells of the brain (neurons) to function improperly and leads to cell death. It is one of many neurodegenerative disorders that affect humans. It is the diagnosis in approximately two thirds of all patients with dementia and is thus the most common type of dementia. Patients and families frequently ask me, “What is the difference between Alzheimer’s disease and dementia?” Dementia is a broad term that indicates that the patient has a brain illness impairing several areas of brain function causing a significant change in their social or work capabilities. Most patients with dementia have difficulty with short-term and/or long-term memory, and may have difficulties in understanding, planning, problem solving, judgment, using language correctly, insight, or their ability to manage complex medical, legal, or financial affairs.

Alzheimer’s disease is thought to be partially caused by accumulation of a protein called beta amyloid and damage to the brain from the subsequent response to this accumulation of beta amyloid. In some cases, the accumulation of this protein is related to a specific genetic mutation and, in these cases, the amount of beta amyloid accumulation and brain damage occur at a relatively young age, such as in the early to mid 50s. Most patients with this “early onset” or “presenile onset” have more trouble with the illness quickly and tend to decline more rapidly than patients with the onset of illness after the age of 65. Another microscopic finding in the brain cells of patients with Alzheimer’s disease are neurofibrillary tangles. There is a protein in the cells called tau that can be affected by the illness such that it essentially becomes tangled and can no longer transport nutrients and other products in the brain cell that are required for optimal health and function. This combination of beta amyloid plaques and neurofibrillary tangles are the classic microscopic findings in the brain of a patient with Alzheimer’s disease, however, it is possible to have some plaques and tangles and not have Alzheimer’s disease.

The number of patients with Alzheimer’s disease increases markedly with the patients’ age. For example, at age 65, approximately 5% of people have Alzheimer’s disease. Approximately 15% of people at the age of 75 are affected, and 35 to 40% of the people age 80 to 85 are affected, and more than 50% of people over age 85 show signs of the illness. Since the percentage by age range doesn’t seem to plateau as you look at older and older patients, it almost seems as though all of us would be affected if we were to live beyond the age of 100. The view that late onset Alzheimer’s disease is an almost unavoidable consequence of aging is not widely held. As more and more people live beyond the age of 100, a plateau may be seen in the percentage allowing some of us to escape Alzheimer’s regardless of age. It would then be possible that research efforts directed at finding out what was different about those people might lead to further treatment advances and eventually a cure for Alzheimer’s disease. Unfortunately, modern medicine has yet to “cure” any neurodegenerative disorder that is not infectious or nutritional.

Chapter 2: How Does Alzheimer’s Disease Differ from Normal Aging?

This question comes up frequently when working with patients and families of patients with Alzheimer’s disease. Having worked at a geriatric psychiatry unit for several years and having seen hundreds of mild, moderate, and severe cases of Alzheimer’s disease, it has become clear to me that, in the early part of the illness, many people mistake the illness for normal aging. As the illness progresses, it’s much more difficult to misidentify what’s going on as being similar to what happens to all older adults as they age. For example, in the very first stage of Alzheimer’s, patients begin to have difficulty with complex concentration and short-term memory problems. The portion of the brain that is affected early in Alzheimer’s disease, called the hippocampus, affects a person’s ability to keep day-to-day items, tasks, conversations, etc., in working memory and retrieve them minutes or hours or days later. We take our hippocampus and its functioning for granted, but without it functioning well, a person essentially becomes disabled.

They are unable to keep track of appointments, they can’t remember conversations with others, they are unable to remember directions that they are told, and they are unable to manage their own medications and checkbook. In normal aging, there is a decrease in processing speed and complex concentration that is likely unavoidable and will affect most of us over time. This is similar to the change that many people get, related to aging, in their eyesight or hearing. That is, most of us will require reading glasses at some point in time, and many of us will require the assistance of a hearing aid in our later years. The body and brain simply don’t work at the same level of efficiency across the entire life span, as anyone over the age of forty knows. However, with Alzheimer’s disease, this relatively benign change gradually but inexorably becomes something different. A patient with moderate Alzheimer’s disease can’t manage their own checkbook whereas someone who is experiencing normal aging generally can if they had done it across their lifetime.

A person who had always been able to manage their own medications without difficulty and later develops difficulty managing their medications, may not be suffering from the effects of normal aging but may need screening for dementia or Alzheimer’s disease. Many times family members can identify the earliest thinking and memory slippage and it predates the person seeking treatment by one to five years. Obviously, people are mistaking changes in their spouse or parent or other loved one as normal aging when there was another process occurring. Any previously complex function that is given up by a person over the age of sixty-five should make one wonder about the possibility of Alzheimer’s disease. When I say a complex activity, I mean things like doing your own taxes, managing a checkbook, managing a complex medication regimen, driving without difficulty, and making complex medical, legal, or financial decisions. A request by a spouse or elderly loved one to take over their checkbook may indicate an underlying problem with their ability to focus, attend, calculate, plan, and execute what had previously been a relatively easy task for them. I have heard people at lectures I give say things like, “I was told that if you’re worried about memory that you probably don’t have Alzheimer’s because Alzheimer’s patients don’t know there’s anything wrong with them.”

This turns out to be false information, as many patients are able to identify that there is something wrong with their attention, concentration, and memory early in the illness and they complain about these changes to family members, but these changes are attributed to normal aging. It doesn’t help to sort this out that approximately two thirds to three quarters of people over age sixty-five complain of memory or concentration problems. The dividing line between “I think I might have a little trouble with my memory” and “I think I might have Alzheimer’s,” has to do with the nature and severity of the concentration or memory problem. If the concentration or memory problem is enough to make the person alter their habits, hobbies, or clearly affects their ability to function in their work or social life, then an evaluation is warranted. With regard to my father’s difficulty with Alzheimer’s disease, his first symptom at the age of around age sixty-seven was slightly increased irritability and an increase in levels of frustration when presented with what had previously been easy or simple tasks.

A couple of years later, he asked me to put my name on his checking account and I thought nothing of it, assuming that as he was aging he wanted to have someone else on his account, for the most part in case he passed away. I learned within two years of this request that he was making errors in his checkbook and needed someone else on the account because he could not keep up with his checkbook and finances. His next complaint had to do with the idea that maybe he shouldn’t drive anymore because there were too many people driving too fast on the roads and he didn’t think he could keep up. It seemed to me that there was no major change in his hand-eye coordination or his general ability to walk and get around or drive safely; it was the complex nature of driving as a behavior. We take this behavior for granted and most of us can do it almost automatically since we have been doing it from our teenage years on. However, when I hear that an older person has decided to give up driving, if there is no clear physical reason such as poor vision, poor hearing, arthritic changes, or some other medical reason why the person can’t drive, it makes me think the person needs a dementia evaluation. Any clear change in functioning that requires help from outside where none was needed before should make one think about the possibility of a dementia evaluation for that patient or family member.

Chapter 3: MCI versus Alzheimer’s Disease.

There is a condition in the psychiatric and neurological literature called minimal cognitive impairment, or MCI. In recent years, the term minimal cognitive impairment (MCI) is commonly used to refer to a stage of cognitive impairment (and specifically a subtype with memory loss [i.e., amnestic MCI]) prior to attaining clinical criteria for dementia in Alzheimer disease and related disorders. However, no completely reliable means, other than long-term follow-up and eventual autopsy, exist to distinguish between patients experiencing MCI due to pre-clinical AD and patients experiencing MCI due to less frequently occurring conditions. In this context, MCI is regarded as a high-risk condition that precedes AD in a proportion of cases. It should be emphasized, however, that considerable controversy still exists considering the formulation of the concept of MCI and the practical implementation of the diagnosis. Furthermore, there is no consensus whatsoever as to treatments for this controversial condition.

There are many studies available to look at what happens with patients who are diagnosed as having MCI and generally, it can be said that minimal cognitive impairment is likely a pre-dementia condition for many MCI patients. Amnestic MCI is said to progress to AD at a rate of 10-15% per year, as compared with healthy elderly individuals who develop AD at a rate of 1-2% per year. In addition, in a study from the Mayo Alzheimer’s Disease Center, which monitored patients for over 10 years, the rate of conversion into AD was as high as 80% after 6 years of follow-up. This is significant from the perspective that AD is often cast as a leading cause of death in the United States in older adults.

Mild degrees of cognitive impairment, particularly when self-reported by patients, pose a substantial challenge to the clinician. The physician may be dealing with a patient with a mild or transient condition, a drug-induced adverse effect, or a depressive disorder; the patient may be in the early stages of a condition that will eventually lead to a dementia; or the complaint may be due to a psychological condition rather than an organic brain disorder. Because a variety of conditions may result in such a complaint, an individualized workup for such conditions and a consensus on a therapeutic approach should be sought.
In fact, the relatively recent formulation of MCI follows previous attempts to characterize cognitive decline associated with aging, including benign senescent forgetfulness, age-associated memory impairment, and age-associated cognitive decline. Therefore, this relatively new concept is perhaps best considered as a stage in the difficult process of understanding and characterizing mild defects in cognition that do not fit clearly within the scope of established neurological and psychiatric disorders.

It most often has to do with complex concentration and/or short-term memory difficulties, which can be the harbingers of the development of dementia. Over time, it will become more clear which patients with minimal cognitive impairment are likely to go on to develop dementia and which patients in that group that have minimal cognitive impairment would benefit from treatment of the MCI as a pre-dementia condition, that is, essentially treating it as though it is a mild dementia. No current proven treatments are available, but many compounds, vitamins, and herbal products have been tried.

Chapter 4: How Do I Get a Diagnosis?

If you have reason to believe that you need a dementia screening evaluation, you can get further testing and a diagnosis from a variety of healthcare providers. Many people initially discuss their concerns and complaints with their primary care physician or family practice doctor. This is a good strategy if the primary care physician or family practice doctor has an interest in the early diagnosis and treatment of dementia and pre-dementia conditions. If, however, the family doctor does not take the complaint seriously and automatically relegates them to “normal aging” without doing any sort of a thinking and memory screening test or checking into the complaints more completely, you are better of seeking a specialist that works in this area. Clinical neuropsychologists can do psychological testing focused on attention, concentration, memory sequencing, planning, problem solving, organizing, and collating different sorts of data. The testing with a neuropsychologist generally takes around two hours and a multi-page dictated report or written report is then available with the results from the testing. More commonly, a primary care physician or family practice doctor hears the complaints of difficulty with concentration and memory from a patient, and arranges for a specialist evaluation with a geriatric psychiatrist or general adult psychiatrist who treats a large number of patients with dementia.

Another health care provider that can provide a dementia screening evaluation would be a neurologist. Neurology is the medical specialty dealing with brain illnesses and illnesses of the peripheral nervous system, and many neurologists have an area of interest in the care of dementia, as many neurological illnesses produce dementia, including Parkinson’s disease, Huntington’s chorea, multiple sclerosis, etc. There are screening tools available on the Internet for self assessment that can help determine whether you need a dementia evaluation via one of these specialized health care providers. However, one should exercise caution with regard to using screening tools that may over- or underestimate the actual problem. In short, it is fair to say that if you believe you have a significant problem with attention, concentration, memory, or more specifically, short-term memory difficulties, you should seek an evaluation with a provider who has expertise in this area in order to allow yourself the best chance of getting an early diagnosis and starting treatment at the earliest possible phase of the illness.

The diagnosis of Alzheimer’s disease involves a history and physical exam and can include memory screening tests that can be done in the psychiatrist’s or neurologist’s office or, in special cases or cases that are unclear, via referral to a neuropsychologist for more extensive testing. In addition, a group of laboratory tests to exclude medical conditions that can mimic dementia is undertaken, as well as a brain scan to look for other causes of problems with concentration and memory. Most doctors that screen dementia patients either order a CAT scan or an MRI of the brain to help with their diagnostic workup. In some cases where the history, physical exam, neuropsychological testing, and laboratory results and brain scan are not definitive in terms of providing a diagnosis, a PET scan may be pursued and can push the diagnostic accuracy above 95%. A PET scan is different from an MRI or CAT scan in that it maps, in color picture, blood flow patterns and sugar utilization by the brain and thus gives a way to measure brain function, whereas CAT scans and MRIs show pictures of brain structures but don’t help in any way to determine anything about brain function.

In the hands of a competent specialist, the information gleaned from all of the sources above will lead to a diagnosis that is 90-95% accurate, and thus Alzheimer’s disease is no longer a disease that can only be “diagnosed at autopsy,” which is what I was taught when I was in medical school. It is true that in order to be 100% certain, an autopsy would be required, but most of the patients that I have seen are still using their brain at the time that I am doing their evaluation, and are not quite ready for an autopsy.

Chapter 5: What Treatments are Available for Alzheimer’s Disease?

The mainstay of treatment for Alzheimer’s disease is a group of medications called acetylcholinesterase inhibitors. This group of medications includes Aricept, Razadyne, and Exelon. These three medications are similar in their mechanism of action, although there are some subtle differences that can be considered in choosing a medication for a specific patient. This entire class of medications has, as its major side effect, upset stomach or possible nausea and vomiting. That is because the acetylcholine that increases in the brain and compensates for some of the damage related to Alzheimer’s disease also stimulates a receptor in the brain that causes nausea and/or vomiting. For most patients, starting at a low dose of these medications and slowly building up decreases the likelihood of this side effect becoming a problem. It should be noted that this group of medications does not cure Alzheimer’s disease and simply helps to prevent further decline and provide some improvement for many patients when the medication is started, especially those in the earliest stages of the illness. In the later stages of the illness, from Stage four of seven until the end of the illness, the majority of the effect of the medication can be summarized as “reducing behavioral symptoms and delaying nursing home placement.” In late 2003, another medication received FDA approval for the treatment of moderate and severe Alzheimer’s disease.

The name of this medication is Namenda and its chemical name is memantine. This medication has had a very good track record in Europe and became available in US pharmacies in January of 2004 and is now widely prescribed as an adjunct or add-on to the mainstay of treatment, the acetylcholinesterase inhibitors mentioned above. Namenda is a glutamic acid acceptor blocker, or an NMDA receptor blocker, which seems to delay the decline associated with the illness. It is believed that, through blocking this receptor, that some of the events that can lead to brain cell loss can be slowed down or stopped in some patients such that the illness progresses at a slower pace. Again, this medication, like the acetylcholinesterase inhibitors, is not a cure but can help delay the progression of the illness. No other medications are currently available for the treatment of Alzheimer’s disease, however, many patients develop behavioral or mood or psychotic complications of Alzheimer’s disease and require treatment with medications that target those symptoms. For example, mood stabilizers can be used for patients with excessive irritability or poor frustration tolerance or agitation. Antipsychotic medications can be used for agitation, disorientation, paranoia, delusion thinking and/or auditory and visual hallucinations. Antidepressants can be used for the roughly half of all Alzheimer’s patients who develop depression during the course of the illness. Antidepressants tend to help with depressed mood, irritability, poor sleep, poor appetite, decreased interest or decreased enjoyment of hobbies or activities, and suicidal thoughts. In addition, the antidepressants can sometimes help generally with impulse control problems and excessive irritability or anxiety.

It is very important to get a diagnosis early in the course of the illness because the medications that are primarily used to treat Alzheimer’s disease seem to work best early in the course of the illness and may delay the progression of the illness until other, more comprehensive, or better treatments are available. For example, let’s say that you were going to develop Alzheimer’s disease and you would show some mild symptoms at age seventy-five, and you were not aware that you had anything other than normal aging and did not seek treatment until age eighty when you were roughly halfway through the illness. At that point, you would have difficulty with daily functioning, medication management, management of your checkbook and finances, etc. If the medications are started at that point, it is similar to trying to treat diabetes when the person has already lost a limb or their vision or is on dialysis. The medications will help at that point, but may not have as robust an effect as they might have had the medication been started at age seventy. In addition, let’s just say for example, that you were going to die at age eighty-five. Had you sought treatment at age seventy-five and pushed noticeable symptoms farther into your future by as much as two to four years, then you would not have as significant and noticeable symptoms that affected your quality of life or ability to function until you were over age eighty, effectively reducing the amount of time spent dependent on others or in a nursing home setting. This strategy of preventing Alzheimer’s by, in essence, dying of something else first, may seem a marginally useful approach, but any functional time is better than nonfunctional time where one would be dependent on the care of others. Seeking treatment early and effectively pushing the time when one is dependent on others back several years can be very useful, not only for the strategy of, in essence, “trying to die of something else first,” but also to preserve a brain function for more effective treatments if they become available.

Chapter 6: Alzheimer’s Disease Prevention Strategies

I have treated hundreds of Alzheimer’s disease patients since I began to shift the focus of my psychiatric practice around 1995. One of the things I have noticed is that many of the spouses and siblings of the effected patient and the children of the effected patients have worries about their own brain function and are concerned about what they may be able to do to delay or prevent Alzheimer’s disease. It has become clear over the last decade or so that, for many patients, there are two processes going on in the brain that contribute to the degree of symptoms that one sees at a given age, and the rapidity of decline that one sees in a given patient after diagnosis of dementia is given. One process in the brain has already been described, and that is the accumulation of beta amyloid plaques and neurofibrillary tangles that are the microscopic findings in the brain of Alzheimer’s patients on autopsy. In addition, however, there are vascular changes in the brain that have to do with hardening of the arteries that we call “vascular changes.” When these vascular changes are severe, they can culminate in an actual stroke.

For many patients, though, the damage is microscopic and shows up on CAT scans and MRIs of the brain, and is described as “periventricular white matter hyperintensities that signal chronic ischemic change.” This is doctor speak for little tiny white dots that we wish were not there on our brain scans or the brain scans of our patient that represent brain damage from blocked microscopic blood vessels, resulting in poor oxygen and blood flow to affected areas. Most people who have a large amount of these “white dots” have what we call “vascular risk factors.” These risk factors include high blood pressure, diabetes, cigarette smoking, high cholesterol, and eating a diet high in saturated fat and being obese or having a sedentary lifestyle. Finally, there are some modifiable risk factors for Alzheimer’s disease. It turns out that many patients with Alzheimer’s disease have vascular damage in the brain in addition, and the patients who have the most vascular damage look the most ill with regard to their Alzheimer’s disease and have a more rapid functional decline. This was shown in a book entitled, “Aging with Grace: What the Nun Study Had to Tell Us about Alzheimer’s…” In this book, they monitored a group of patients who had similar lifestyles, diets, etc., (a group of nuns in a convent) and found that many of the nuns who looked quite demented when they were interviewed or tested had very little Alzheimer’s plaques and tangles in their brain, but had a lot of these vascular lesions that are referred to above as “white dots.” The number and severity of these white dots in their distribution tended to correlate with their degree of dementia and functional decline that was seen in these patients. It was interesting to note that some patients who had very few plaques and tangles, but had extensive vascular changes in the brain, were quite demented, and some patients who had a large amount of plaques and tangles, but very little vascular damage in the brain, seemed intact and did well in clinical testing and on neuropsychological testing measures.

From this information, it became clear to me that there was a group of modifiable risk factors for decline related to Alzheimer’s disease over which one could exert some control. You can’t choose your genetics, but you can choose to aggressively treat high blood pressure and diabetes if you have them, and you can also choose to aggressively treat problems with high cholesterol if you have that. In addition, one can stop smoking and eat a diet that is focused on eating a large amount of whole grains, fruits and vegetables, and very little red meat or foods high in saturated fat. By avoiding fried foods and foods high in saturated fat or foods that have large amounts of trans fats in them, it may be possible to reduce vascular damage in the brain. Thus, if one were to begin to have some accumulation of beta amyloid plaques and tangles, the effect might not be as marked if your brain was otherwise healthy. So, for those of us that would like to keep our brains in good shape (since they haven’t perfected brain transplant surgery yet) it would help to pursue a healthy, active, vigorous lifestyle with a healthy diet, and to aggressively treat high blood pressure, diabetes, high cholesterol, and quit smoking.

In addition to modifying these vascular risk factors, there is some evidence that some vitamins and nutraceuticals and antioxidants can help prevent or delay the onset or progression of Alzheimer’s disease. This is a controversial area despite the fact that there are some relatively good studies that show benefit for some of these agents. Suffice it to say that I personally do not take antioxidants such as vitamin E, or vitamin C, or alphalipoic acid, but some doctors recommend these. In addition, a B complex vitamin and a combination fish oil or flaxseed oil capsule that provides extra omega 3 fatty acids have been suggested by some. These essential fatty acids seem to help with brain cell membrane fluidity and function, and the antioxidants, vitamins, and alphalipoic acid seem to decrease age-related oxidative injury to brain cells. In essence, what this means is that these substances help scavenge free radicals or toxic food and diet breakdown products and products of routine metabolism, and may help reduce damage to brain cells over time. At the very least, these substances and vitamins that I have mentioned above have very few known side effects and are generally safe to take. I am not personally betting on their benefits in terms of longevity and a longer intact brain function and have chosen to get the same substances from actual food items that contain them instead of taking supplements.

Chapter 7: Summary or Take-Home Message

Alzheimer’s disease is a brain illness characterized by the abnormal accumulation of beta amyloid plaques and neurofibrillary tangles in the brain that cause premature dysfunction and cell and brain cell death. The cumulative effect of the inflammation and brain cell death related to these plaques and tangles over time cause difficulty with many areas of brain function. These areas include short-term memory, complex concentration, calculation, and later in the illness, the ability to think, plan, execute, problem solve, judge things, and also impair insight such that halfway through the illness, many patients are not aware that they are ill. Early diagnosis is helpful to start the available treatments as early possible in order to preserve brain function for more comprehensive or better treatments that may become available over time. In addition, the early diagnosis of Alzheimer’s disease allows the patient to plan for needed changes and modifications in lifestyle and long term plans and arrange for appropriate care in the later stages of the illness. It also allows time for one to get one’s affairs in order and provide a living will to make ones needs known in advance of a time when the patient will no longer to make complex medical, legal, and financial decisions. Unfortunately, most patients usually show up for treatment halfway through the illness and are already beginning to lose insight into the nature and severity of their problem and may already be too ill to assign a durable power of attorney or make their wishes known in a legal document.

Getting a diagnosis is important because there are treatments available that can delay functional decline and help preserve quality of life. Prevention strategies with regard to Alzheimer’s disease include aggressively treating high blood pressure, diabetes, high cholesterol, and quitting cigarette smoking. In addition, the adoption of a healthy, active lifestyle with adequate aerobic exercise and healthy diet focused on whole grains, fruits and vegetables, and a reduction in saturated fat and trans-fat intake, can reduce the likelihood of vascular damage, which accelerates the decline in Alzheimer’s disease and increases stroke risk. Some vitamins and nutraceuticals have been shown to help delay onset and/or progression of Alzheimer’s disease and are worth looking into. Taking moderate doses of vitamins E and C as well as a complex multi-vitamin, alphalipoic acid, and a flaxseed and/or fish oil supplement may also be helpful. I hope you have found the information in this e-book helpful to answer some of your questions with regard to Alzheimer’s disease. It is important to seek a competent evaluation by a health care provider experienced in the treatment of Alzheimer’s disease if you believe that you are at risk or having symptoms. Don’t wait to get an evaluation or seek treatment; the brain you save may be your own.