Media & Press
Mild Cognitive Impairment Article excerpted from The Johns Hopkins Memory Bulletin
by Dr. John C. Morris, Dr. Peter V. Rabins, originally published in The Johns Hopkins Memory Bulletin, January 2006
Forgetfulness. It's pretty much guaranteed to catch up with you at some point in time. You are in your 50s, 60s, 70s, or older when suddenly it seems that you're "losing it." The name of the movie you saw last week? Can't remember. You grope for the title of a book you just finished reading yesterday. You find yourself standing in front of the open refrigerator door, wondering what you were looking for. At a party, you've been speaking to a man for 15 minutes; when your wife comes over, you start to introduce her but can't remember the man's name.
Embarrassing, to be sure. "Another senior moment," you may mumble to yourself as you experience one of these minor mental setbacks. However, others have darker thoughts when their memory starts slipping: "I must be developing Alzheimer's disease." There's another possibility.
Such instances of forgetfulness may be neither "senior moments" nor Alzheimer's. Instead, these amnestic difficulties may signal mild cognitive impairment, or MCI, a subtle but usually measurable change in memory that many researchers see as a transitional state between the memory changes due to normal aging and the earliest indication of serious memory problems triggered by Alzheimer's. With MCI, memory loss is more severe than would be expected in a person of a particular age and education level.
The good news is that the forgetfulness typical of normal aging is relatively minor-more of a nuisance more than anything else, and nothing to be concerned about. Nearly all of us take more time to learn and recall information as we age. This occurs because the transmission of nerve impulses between cells and across cell membranes (synapses) in the brain inevitably slows as we get older. The decline usually progresses almost imperceptibly, over several decades.
By midlife, most of us occasionally find ourselves staring blankly into a kitchen cupboard or dresser drawer trying to remember what we were after. Although some people fear the worst, these memory changes are not dementia -a significant loss of intellectual abilities (such as memory capacity) severe enough to interfere with social or occupational functioning.
Normal age-related memory changes usually involve a slight delay in getting access to a memory that is in your brain. That's why you recall your acquaintance's name five minutes later, and why you eventually remember why you went to the refrigerator. In fact, although just about everyone experiences some degree of age-related memory loss, only 1 out of 100 people in their 60s have dementia.
Dementia, and Alzheimer's disease specifically, is a major concern for most people 60 and over. Granted, dementia is not a natural consequence of aging, but its incidence does, unfortunately, increase with age. People who reach age 85 have a 20 to 35 percent chance of developing some significant cognitive impairment.
We currently have several therapies for AD, and many more are in various stages of development. Neurological experts hope that the development of improved therapies will be paralleled by the development of diagnostic tests that can uncover cognitive impairment at its earliest stages, including MCI. We know that AD doesn't have a sudden onset; by the time symptoms appear, the disease has probably been developing in the brain for some time. Some researchers believe that MCI could be the earliest manifestation of AD.
When does normal forgetfulness end and MCI begin? Unfortunately, the question is difficult to answer. Because MCI is of intense interest and a topic of ongoing research, and because there still is a great difference of opinion and controversy as to what constitutes MCI, Dr. Rabins (PVR) and Dr. Morris (JCM), two experts on dementia and MCI, offer their counsel on a spectrum of frequently asked questions about MCI.
Q. What happens to a person's memory during the course of normal aging?
PVR: Memory is power. It allows us to navigate our way through the world, learning, storing, and retrieving bits of information that will allow us to safely differentiate friend from foe, tonic from poison. Memory helps us plot a safe course from point A to point B, and to and from all points in between, if we so desire.
Moreover, our memories define who we are. Philosophers and scientists alike have long recognized that our memories and our selves are interwoven; perhaps they are even one and the same. Memories link us with the things that make us happy and those that make us sad, the things we've accomplished and the things we hope to accomplish in the future.
Memory has been described as a warehouse of knowledge. Actually, however, there is no single location or central warehouse in your brain where all your memories are processed and then neatly stored. Thanks to the neuroscientists who have begun unlocking the many secrets of the brain over the past few decades, it is now recognized that all new ideas and past information are reviewed, analyzed, compared, and connected, allowing you to create integrated experiences. Representations of these episodes are then stored in the form of electrochemical changes and altered neural circuits in various parts of your brain.
It is not uncommon to think of memory as an abstraction-a compilation of sensations, feelings, thoughts, and images that are mysteriously called upon when needed. However, that abstraction has a clear, if not yet fully understood, physical basis. Our brains are composed of hundreds of billions of cells that encode our memories, making them available through communication fueled by chemical and electrical interactions.
What you learn and are able to remember depends on your ability to make associations, or mental linkages, among experiences, store them in an organized fashion, and then search for them efficiently when retrieval is needed. This involves the functioning of several brain regions, and the neurons (brain cells) within each one.
While memory loss is one of the earliest signs of AD and a host of other dementias, a major difference between "age-related memory loss" and dementia comes down to declarative memory, the aspect of memory that stores facts and events.
If you compared the memories of a group of normal 25-year-olds to a group of normal 75-year-olds, the memory changes in the older group would be quite modest. What is interesting is that declarative memory, or free recall, is what starts to wane, along with speed of retrieval.
For example, if I were to read aloud a list of ten words to the younger and older groups, wait three minutes, and then ask each person to repeat as many words as they could remember, the average 25-year-old would remember about 8.5 words, while the average 75-year-old would remember 7.5 words. Many researchers believe that this difference in declarative memory is due to the normal aging processes.
Here is what I find fascinating about memory: If, instead of asking the older people to spontaneously recall as many of the ten words they can, I gave them a piece of paper with the ten words written on it but mixed in with other words, and asked them to circle only the words I had read to them, they would get just as many words as their younger counterparts! Having a visual prompt seems to help overcome that change in free recall memory.
However, if the same word test were given to people suspected of having AD, the difference would be striking. After three minutes, some would recall two or three words. Others might ask what a list is. The difference in word recall between a normal aging person (7.5 words remembered) and someone with AD (0, 2, 3, or 4 words remembered) is huge, and it's evident that a serious cognitive gulf exists between the two.
But what does it mean when an older person remembers five or six words instead of the expected 7.5? Are they are simply at the furthest extreme of age-related memory problems? Or, on the other hand, do they have the earliest form of AD, a stage we now call mild cognitive impairment? At this point, unfortunately, no one can say for sure.
Q. What is mild cognitive impairment?
PVR: Mild cognitive impairment is a general term that researchers now use to describe a subtle but measurable memory disorder marked by lapses in shortterm memory. It probably includes two groups of individuals, one in the transitional stage between the cognition of normal aging and mild dementia, and another group who will not progress to dementia, at least within five years. This group has a little more decline in memory than is usually seen with normal aging.
A person with MCI is one who has memory complaints and performs worse- but not all that poorly-than expected when compared to others the same age and education level. However, they do not show other signs of dementia, such as impaired judgment or reasoning. Even so, there are researchers who believe that in some patients these mild memory lapses may actually represent the earliest stages of Alzheimer's disease.
In order to better understand MCI and its relationship to AD, in 1999 the American Academy of Neurology convened a group of specialists from around the world (I was an invited guest, as was Dr. Morris) and asked them to develop a set of criteria that researchers could use to study MCI. The group proposed the following criteria for making a positive MCI diagnosis:
- The report of an individual that he or she is having memory problems, a complaint preferably confirmed by a spouse or close friend
- Measurable, greater-than-normal memory impairment detected with standard assessment tests
- No decline in overall thinking or reasoning skills
- Ability to still perform usual daily activities
It's now agreed that these criteria did not settle the debate about what constitutes MCI, but as we work toward a deeper understanding of early dementia, this definition of MCI will continue to evolve. Eventually, it may be discarded altogether and another term used in its place. Then, too, it may be modified so that it more accurately predicts what will happen to a person's memory and other thinking functions in the future.
Q. Do patients diagnosed with MCI eventually develop Alzheimer's disease?
PVR: If you take a group of people who complain about their memory and give them standard memory tests, and they perform below 1.5 standard deviations (about 32 percent) what is considered normal for a person their age and education, they are neither in the AD category nor in the normal aging category. They have MCI. And when researchers follow this group of people over five years, 50 to 60 percent will go on to develop AD. Some researchers think the percentage may be even higher.
Therefore, the still unanswered question is, "Is this MCI group at higher risk of developing AD?" All we can say is, "Not necessarily." Even after five years, depending on the study, as many as 40 to 50 percent of people diagnosed with MCI haven't really changed at all. In fact, a few have even gotten better, perhaps because they weren't in top form the day they were originally tested-perhaps they had a cold, or were taking one or several of the medications that affects memory, or were mulling over an argument they'd had with their spouse the previous day.
Q. Why has MCI research accelerated recently?
JCM: Interest in MCI began with the appreciation that dementia reflects brain disease rather than the normal aging process. As recently as 20 years ago, people thought it was normal for the elderly to fail in their memory and other mental abilities-that it was just an inevitable aspect of aging. What we have learned in the past two decades is that almost everyone who has substantial memory changes as they age has an underlying illness that explains this condition. The most common-and the most feared-is AD. With the understanding that substantial memory change is not part of normal aging, and with the development of therapies in the past ten years to treat the symptoms of AD, researchers have begun to focus on recognizing the disorder as early as possible. That is why MCI has become such an intensely studied entity. The research is not easy. Unlike heart disease, which has a variety of blood and diagnostic tests for identifying disease processes, we don't yet have a blood test or MRI scan to let us know when an individual is developing the brain changes that are the beginning of dementia.
Q. How are people with the earliest forms of dementia identified?
JCM: To try to get a handle on this, a group of researchers led by Ronald Petersen, M.D., Ph.D., a neurologist and director of Alzheimer's Research Center at the Mayo Clinic in Rochester, Minnesota, proposed criteria for MCI so researchers could see who fits into the MCI category and what eventually becomes of them.
These criteria are arbitrary and the evaluation is made only after taking an extensive medical history that is verified by someone who knows the person well. Ultimately, the diagnosis of MCI is a judgment call made by the examining doctor.
Q. How many people have MCI?
PVR: It is now estimated that 4.5 million Americans have dementia and this number will double every 20 years this century unless a prevention or cure is discovered. The number of people with MCI has been harder to determine, but research to date suggests that at least twice that many individuals currently have MCI, most of which is undiagnosed.
Q. At what age do people develop MCI?
JCM: We are typically looking at people with MCI who are 75 and older, although, like AD, it can strike people in their 40s.
Q. What are the causes of MCI?
PVR: Because MCI is likely a category containing multiple problems, its causes are probably multiple. As I mentioned earlier, there are brain changes that occur over time with normal aging. The cause of this is not known, and some scientists have argued that even these "normal" changes are the result of disease that could someday be prevented. Others suggest that these changes are due to inevitable deterioration of nerve cells or some other process that occurs over many years.
In the popular amyloid plaque theory of AD, it's theorized that damage occurs to the brain when toxic pieces of the beta amyloid protein, either on their own or after coalescing into plaques and tangles, cause the degeneration and ultimate death of brain cells and their connections. Some evidence suggests that this may begin ten years or more before memory problems are first noticed. As more amyloid plaques form and brain cells die, memory loss begins, followed by more damage over time that eventually impairs and destroys all the thinking functions. Again, this is just a theory, but currently it has the most science behind it Nonetheless, it's one that could be replaced in the future as more research discoveries are made.
Q. How is MCI diagnosed?
PVR: Diagnosing MCI is tricky. Typically, a doctor will take a good history and perform a complete psychiatric, neurological, and medical exam of the patient. It's best to have a partner or good friend present during the exam because this person will report problems that the person with MCI is either unaware of or has not recognized. If the patient is an accountant, for example, and says his memory problems are slight, but his partner says he can't even do the math necessary to pay his bills, the doctor might then diagnose dementia.
A brain X-ray may be taken to rule out a stroke or other possible causes of MCI. In some cases, a CT scan or MRI can be used to determine hippocampal size (the hippocampus is a part of the brain heavily involved in memory) and identify brain abnormalities. Currently, this is only helpful in research studies of groups of people. Neuropsychological testing, a battery of assessments that examine many cognitive functions in a standardized manner-and is more extensive than a standard mental status or cognitive examination-is invaluable.
This testing can assess memory, attention, problem-solving abilities, judgment, and other thinking abilities and provide results that can be compared to others of similar age and education level. It is the availability of these "normative values" that allows for an assessment of the severity of the memory problems and a determination whether it is within the range of expected values or worse than this.
I sometimes find that some individuals who don't seem that impaired on my examination are found to test like people with true AD or some other dementia. Other times, though, tests show a little more decline than expected based on age and education, but it's not so severe that you are sure the patient has AD.
Testing is not always conclusive, and when it's all finished, I sometimes have to tell patients and their families that I'm not sure their current memory difficulties will worsen, placing the patient in a neurological "gray area." Upon hearing this, my optimistic patients will say, "So, there is a real chance that I won't get worse." And I will agree. However, the more pessimistic patients will say, "So, you think I have early Alzheimer's." To which I'll reply, "No. But you might develop it in the future."
In either case, I emphasize that they are still healthy and able, and urge them to forge ahead, live life to its fullest, and try not to worry about the memory problems because worry usually makes mild memory problems worse. I also tell them that there is a good chance the problem won't worsen, and that if it does, it will not happen for several (or many) years. Although that is bad news for some, it's not a death sentence. When I am not sure what a person's future holds, I will have them return in six to nine months for re-testing.
Q. Are medications prescribed for the treatment of MCI symptoms?
PVR: Many doctors will prescribe an AD drug, such as Aricept, for their patients with MCI. However, the only published study from a study directed by Dr. Ronald Petersen found that one drug, donepezil (Aricept), decreased the likelihood of developing dementia at 18 months, but not at three years. (See box below). I do not prescribe an AD drug for MCI unless I think it is likely that the person has the form of MCI that is a harbinger for AD, or unless the patient specifically asks for one. As I mentioned before, I reassess patients with MCI in six to nine months. If at that time their MCI has worsened, I then recommend an anti-AD drug.
Q. Based on your research, what is your thinking about MCI?
JCM: I have to preface my remarks by saying that my ideas about MCI are somewhat controversial and not everyone in the dementia field agrees with what I have to say. I believe that standard neuropsychological test scores alone are not enough to make a diagnosis of MCI, as I will explain. I also believe that some physicians who are labeling patients with MCI may be "underdiagnosing" and that many of the patients actually are demented.
Here are three key points I want to make about MCI to help put the disease in proper perspective.
Point One. We know that MCI can be a manifestation of many medical conditions. It could also be the furthest end of what we consider the normal spectrum of aging.
Then again, it could be caused by things that have nothing to do with the primary problems of the brain. For instance, it could be triggered by side effects of certain medications that dull the brain, causing a person to feel groggy and to become cognitively impaired. Medicines that act on the brain, such as anti-seizure medications, have cognitive side effects that cause people not to think as clearly or quickly as they used to.
We now know that drugs taken for overactive bladder (OAB) can cause memory problems for some people. In addition, medications for serious psychiatric problems, agitation, and psychosis are well known to cause a dulling of mental senses. Remember, too, that older people take a variety of medications that individually may not affect thinking or memory, but that when taken in combination with other drugs may have side effects that disrupt cognition.
Another factor that may cause MCI is depression. People who have lost their spouse or loved one are often physically and emotionally devastated, and this brings about changes in the neurochemical balance in the brain. I think the subsequent bereavement and withdrawal from normal activities is responsible for memory problems seen in many older people. When suffering from depression, people are not registering information in their brains as they once were. They are distracted and are going to be forgetful because they are simply not paying attention. However, as the bereavement clears, the cognitive impairment clears with it.
Some forms of MCI neither progress nor get better. A good example of this is in someone who has suffered a concussion and no longer remembers as well as they used to. These memory deficits don't worsen, but they cause a problem with short-term memory that may persist forever. We call this a static MCI.
My point here is that there are many potential causes of MCI and that not all MCI is going to progress to a dementia state.
Point Two. For the most common type of dementia, which is AD, and for other types of dementia, such as Lewy body dementia, the first change that occurs is mild cognitive impairment. To state it another way, almost everyone with AD begins with the mild cognitive impairment stage. All AD patients will go through it. Although not everyone with MCI is going to become demented, virtually everyone with dementia experiences MCI at some point as an early manifestation before it evolves into a more overt dementia, replete with language and judgment difficulties.
Point Three. Our job as clinicians is to try to identify that subset of MCI patients that is really on the way to dementia. We need to distinguish their problems from those with reversible causes (medicines, bereavement) and static causes (concussion) because the treatment of those who are very likely to have the beginnings of a dementing illness is quite different.
Unfortunately, we don't have a test for this. But what we have learned-and this is the controversial part-is that if you carefully interviewed someone who knows the patient well, and if they told you that the person has deteriorated in their mental abilities, that they have changed relative to their own past mental performance, and {{that these changes are characteristic of AD} (forgetful; can't carry out usual activities at quite the same level as they once did; tend to have difficulty with complex reasoning), then I would say that this person most likely has what I call "MCI of the Alzheimer's type."
While everyone else makes the diagnosis of MCI based on how someone performs on a battery of neuropsychological tests compared to someone of their own age and educational level, what we do here at Washington University is make the diagnosis of MCI of the Alzheimer's type based on distinct changes noted in an individual. It's done in one visit to our Center with the help of a collateral source-a loved one who knows the patient very well.
What we have found is that MCI of the Alzheimer's type has the same features as AD, but it's much milder. The memory loss is not remotely as severe as it will eventually become. The change of function is very minimal, and in many ways, the patient looks and acts normal. They are still participating in many everyday activities, including driving, but they are just not performing these activities as well as they once did.
Not everyone is comfortable with my definition of MCI of the Alzheimer's type. However, if you took this subset of people, you would find that they have all the same features as early AD patients. If you take an MRI scan, for example, the volume of their hippocampus will be smaller. If you test for the apolipoprotein E 4 (APOE-4) gene, the gene that is associated with late-onset Alzheimer's disease, it will be over-represented in these people. Most people with MCI of the Alzheimer's type are going to live for several years more, but some will die sooner. If you were to subsequently examine the brain pathology reports of the people who died, you would typically find definite evidence of early AD.
Q. If there is no effective therapy, why should patients be told they have MCI of the Alzheimer's type?
JCM: I will give you both sides of this controversial issue. Pro: You need to take MCI seriously. I think patients and their families want to know what they have rather than being told that it's some vague entity they can't fully understand. Our best chance of helping people is by intervening early in the disease process when drug therapy might have some positive effect on disease progression, memory, and behavior.
We should tell people if we think they have early AD so they can begin to deal with it. By and large, these people appear and act normal. They are only mildly impaired. This is exactly the stage where they should be involved in planning for their future and how they want it structured. They should get a durable power of attorney, make their will, and decide on a future living situation. They should be as involved as they can at this point instead of waiting until their cognitive powers deteriorate to the point where it's just too late to have any substantive involvement in decision making.
Since we think this disease is caused by underlying AD, patients with MCI of the Alzheimer's type are candidates for treatment with AD medication. The current drugs, which are moderately effective and approved by the FDA to treat mild to moderate AD, are not approved for treating people with an MCI diagnosis.
However, we satisfy this by telling patients that we suspect that they have early AD and what we are treating with the drugs is not MCI but AD. Our ultimate hope is that one day we will have drugs for MCI that can cure MCI, thereby intervening before more damage can be done. Con: Labeling someone with AD can have serious implications. For example, once a person is diagnosed with AD it is extremely difficult, if not impossible, to get long-term health insurance. In addition, in some states, the diagnosis of AD alone is sufficient cause for immediate revocation of all driving privileges.
Q. What happens after a diagnosis of MCI is given?
JCM: There is no definitive test for MCI, so we will monitor the person on a regular basis, using information supplied by the patient and informant. If their cognitive status does change for the better, we are happy to revise our diagnosis. In the meantime, we emphasize the early part of the disease. We note that quality of life can really be quite good for people with early AD or MCI of the Alzheimer's type. These people should continue doing all the things they enjoy-as long as they're safe-because accumulating evidence shows that remaining physically, socially, and mentally active is good for a whole host of reasons, including mental enhancement.
People who continue to be mentally engaged might be able to build more connections between brain cells (a process called "plasticity"), which can strengthen a "reserve" against AD. This may help lower the risk of eventually developing AD. All of my patients understand that we are not going to lose ground by waiting for their disease to progress further. We are going to begin treatment with the available AD drugs right away. These medications, even though their benefits are modest at best, may help patients maintain their quality of life in the short term, and, for some, for several years.
Q. When will we be able to separate normal memory changes from more advanced cognition changes evidenced in MCI and Alzheimer's disease?
PVR: It's my hope that brain imaging tests with positron emission tomography (PET) and magnetic resonance imaging (MRI) scans that examine how the brain is functioning (by measuring brain blood flow) will help identify disease early, and let us know if therapies are working. There is currently a large ongoing study-ADNI (Alzheimer's Disease Neuroimaging Initiative)-that is looking to see if brain imaging will be a useful addition to our diagnostic armamentarium.
The National Institute on Aging, in conjunction with other Federal agencies, private companies, and organizations launched ADNI in October 2004. This is a $60 million, five-year public-private partnership that will test whether MRI, PET, other biological markers, and clinical and neuropsychological assessment can be combined to measure the progression of MCI and early Alzheimer's disease. It's hoped that the study will help researchers and clinicians develop new treatments and monitor their effectiveness as well as reduce the length and cost of clinical trials. The project is the most comprehensive effort to date to find neuroimaging and other biomarkers for the cognitive changes associated with MCI and AD.
The study is taking place at approximately 50 sites across the U.S. and Canada. Investigators are recruiting about 800 adults, ages 55 to 90, to participate in the research-approximately 200 cognitively normal older individuals to be followed for three years, 400 people with MCI to be followed for three years, and 200 people with early AD to be followed for two years.
The study will compare neuroimaging, biological, and clinical information from these participants, seeking correlations among the data that will track the progression of memory loss from its earliest stages. Neuroimaging research has suggested that PET or MRI may serve as a more sensitive and consistent measure of disease progression than the neuropsychological and cognitive assessments now typically used in research and clinical practice. As MCI and AD progress, for example, areas of the brain involved with memory, such as the hippocampus, shrink.
Using the high-resolution images produced by MRI, researchers will evaluate the best ways of measuring this volume loss in the hippocampus and other brain structures. PET scans assess brain function by measuring the rate of metabolism of glucose, the brain's fuel. PET scans of people with AD show that glucose in certain parts of the brain is metabolized at lower levels than in healthy people, and previous studies have shown that low glucose metabolism can be seen in some people even before noticeable symptoms of memory loss occur. The ADNI will also seek to identify additional biological factors from blood, cerebrospinal fluid, and urine samples. Johns Hopkins and Washington University are two of the many centers involved in the study.
Other centers, including Washington University and the University of Pittsburgh, are studying a compound called PIB (Pittsburgh compound B) that labels brain amyloid directly. It is possible that a PIB scan, either alone or in combination with a blood or spinal fluid test, will predict who will develop MCI, which individuals with MCI actually have the early AD or Lewy body dementia form, and which individuals with MCI are unlikely to progress to dementia. Undoubtedly, this is one area of dementia research that will bear fruitful results in the near future.
Q. Do people need to be examined by an Alzheimer's expert for suspected MCI?
JCM: You don't need to go to a regional AD center or be examined by a neurologist in order to be tested for MCI. You do need a physician who is interested in dementia and is willing to take the time needed for the examination. This doctor can be your family doctor or an internist.
That said, it's been my experience that the majority of primary care physicians do not have the time, interest, or expertise to make the diagnosis of MCI. In fact, it is likely that many patients who are already past the MCI stage, and now have true AD, are unrecognized by their own family physician.
Here's how that can happen. Due to our standard medical system, patients generally spend very little time in the office with the doctor. Imagine a 75-year-old MCI patient with his doctor in the examination room. When the doctor asks how he's doing, the patient typically says, "fine" because he has little or no insight into his condition. Even if the doctor were to ask an AD patient how his memory is, the patient would probably say, "fine." The doctor will generally not probe any further, nor will he separately query the family, which would be much more revealing but also more time-consuming.
If you suspect MCI in yourself or a loved one, and you are looking for a doctor, start with your local chapter of the Alzheimer's Association and ask for a list of physicians in your area who can assist you. The national office of the Alzheimer's Association (225 N. Michigan Ave., Fl. 17, Chicago, IL 60601; 1-800-272-3900; www.alz.org/findchapter.asp) can help you locate your local chapter.
About the Authors:
John C. Morris, M.D., the Friedman Distinguished Professor of Neurology at Washington University School of Medicine, St. Louis, Missouri, is the Director of the Center for Aging, and the Director of the Alzheimer's Disease Research Center, both at Washington University. Dr. Morris, the editor-in-chief of Alzheimer's Disease and Associated Disorders, was awarded the 2005 Potamkin Prize for Research in Pick's, Alzheimer's, and Related Disease from the American Academy of Neurology. Called the "Nobel Prize of Neurology," the Potamkin Prize honors and rewards researchers for their work in helping advance the understanding of Alzheimer's disease and related disorders.
Peter V. Rabins, M.D., M.P.H., medical editor of The Johns Hopkins Memory Bulletin, is Professor of Psychiatry at the Johns Hopkins School of Medicine. A world-renowned expert in geriatric psychiatry, Dr. Rabins lectures extensively on memory and Alzheimer's disease. He is co-author of the best-selling guide for caregivers, The 36-Hour Day.
The information in this article "Mild Cognitive Impairment" was originally published as part of:
The Johns Hopkins Memory Bulletin, Winter 2006 Issue, January 27, 2006, Published by Johns Hopkins Medicine, Baltimore, Maryland. © Medletter Associates, 2006
