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Memory Check-ups: As Essential as an Oil Change

The most frequent questions asked at Alzheimer's disease conferences and in the Bryan ADRC Memory Disorders Clinic by patients and their loved ones are "Are my current memory problems normal?" and "What do I need to do to fix them?" Clinicians and basic researchers in AD now recognize that the disease begins insidiously and silently 5-10 years or more before onset of obvious changes in memory, behavior/personality or ability to function at home or work.

CIND and MCI Defined

It is natural that, as the population ages, more and more persons are concerned about their memory, especially those in the early stages of AD (which is now often termed mild cognitive impairment (MCI)).

When memory, behavior, or job/home function is reported to be abnormal by history, by observation of others or by clinical examination, it is important to rule out common, almost trivial, causes because they are reversible. These include effects of medications, depression, sleep disorder such as sleep apnea or restless legs, substance use (particularly alcohol), or other medical illness such as poorly controlled diabetes, etc.

Recently, clinicians have coined the phrase CIND (cognitively impaired non-demented) for persons with these mild, but definite syndromes. If causes such as those listed above are excluded, then the person is termed MCI, which implies minimal or no disturbance of ability to function. There are three forms of MCI-amnestic MCI with mostly memory involved (usually early AD); single domain/non-memory MCI (sometimes early frontal lobe dementia or lobar syndromes such as progressive aphasia); and multiple domain/minimal impairment MCI (often small vessel "ministroke" disease). Continued research is needed in early detection.

Why Get a Check-up?

Why would you get your memory checked up at such an early time-point as CIND or MCI? Because many clinicians are now convinced that prompt and early treatment is associated with stabilization or even reversal of dementia syndromes, even those with double copies of the high risk APOE4 gene.

What's Involved?

Proper evaluation includes clinical exam, neuropsychological screens or tests, blood work such as B12, thyroid, glucose, kidney and liver function, and anatomical neuro-imaging such as CT scan or PET scan. Further, blood work in our clinic looks in detail at liver function (vitamin B1 deficiency) and conditions with increased oxidative stress (abnormal cholesterol values, increased homocysteine levels, vitamin E deficiency, iron overload or copper deficiency). Prompt and continued correction of identified abnormalities plus using the established guidelines of acetylcholinesterase inhibitors and vitamin E is changing the course of MCI and AD.

It is perhaps self-evident that correcting the various factors that lead to CIND-meds, alcohol, sleep problems, depression-make sense. Also, correcting the many factors usually associated with MCI and early dementia also makes sense. Since even some persons with high risk APOE4/4 (double copies) can make it to their 80's or older without disease, it is clear that most cases of AD depend on additional adverse genetic or environmental factors. Many of these factors are identifiable and treatable. Memory check-ups: Like an oil change, they will help prolong the life of your brain.

Risk Reduction in Alzheimers and Related Dementias

The risk of dementia in the aging U.S. population is significant: up to 30-50 percent of persons who age into their 70’s, 80’s and beyond will have some form of dementia before they die. For a given person, the over-all figures on risk may help or hinder their approach to risk reduction.

Three large groups exist at present: those at risk, those with already mild cognitive impairment or MCI (greater than expected for age), and those already into dementia syndrome. The most common question that I, as a clinician, hear after evaluating an older person with dementia is one or more of the family, whether siblings or children, asking, “What is my risk?”, “What can I do?”

Since beginning basic science and clinical research into AD 25 years ago, I can now also ask myself personally, “What is my risk?” and “What am I going to do?” My mother was diagnosed with AD at age 75 (14 years into my research career) and died at age 85 in early 2007.

General Principles

My clinical approach to prevention and treatment of AD and related disorders is very aggressive. I firmly believe that risk is ascertainable and that there are definite steps that can reduce risk or modulate MCI or dementia, if already started.

The major hurdles are to understand general findings that apply to risk and prevention/treatment and then to personalize these for a given individual or family, finding solutions that are achievable, realistic, and that ensure compliance.

General principles that relate to risk are obvious: if you have a first degree relative (mother, father, sibling) with dementia, your personal risks are increased.

Likewise, certain other principles have emerged from the many research studies carried out to date: elevated homocysteine in midlife increases risk of eventual dementia by about two times, eating food high in saturated fat and trans fatty acid increases risk by about two times, previous significant head injury increases risk by a variable amount, eating fish or other foods such as almonds and flax high in omega-3 essential fatty acids may decrease risk by two times.

Genetic Factors

In general, the “normal” American diet is most likely a huge culprit in increased risk. In our published series of 1,500 patients with dementia, the large proportion of cases starting after age 65 have mixed etiology—vascular and Alzheimer. Thus, things that are bad for the heart and blood vessels: hypertension, bad cholesterol levels, diabetes, uncontrolled heart or vascular disease are probably also factors that increase risk.

Many of the risk factors above are controllable by medical treatment or life style changes. Genetic factors are not usually directly controllable, but serve as important guides to individualize risk for a given person and to guide to specific regimens that may soften the adverse effect of that gene. In my mother’s case, she is one of the two percent of persons that carry a double copy (E4/4) of the oldest human apolipoprotein E gene, APOE4. Because we inherit one gene from each parent, I and all of my siblings carry at least one E4 gene, increasing our eventual risk of AD.

E4 is a “thrifty” gene, probably ideal for low fat environments particularly for the developing fetus. My mother had a healthy, mostly vegetarian diet in her later years and had onset of AD at age 75, 10 years beyond average age of onset for E4/4 persons.

Moreover, up to 50 percent of E4/4 persons may escape AD dementia altogether. Thus, except for the rare and tragic cases of familial early onset AD, even a genetic factor such as E4 is only a risk factor.

For myself and my family, and for those patients with MCI/dementia suit-able for full testing of E4 status, this is a huge billboard for “Eat Healthy.” While full testing for APOE4 is not recommended for “normals” or persons at risk, there are a number of other biological markers and genes that have specific regimens for treatment and prevention.

Why did my mother not fully escape, as do some, the E4/4 risk? She was a widow, living alone, with some degree of depression, and sometimes not eating well. Her other physical factors that may have led to brain injury and AD included: B12 deficiency, elevated homocysteine, B1 deficiency, and moderate sleep apnea. All of these factors were treated, some later than others.

Reducing the Risk

In summary, there is no reason why risk reduction of AD and other dementias, as much as treatment, itself, should be viewed any differently than treating elevated blood sugar, cholesterol or the like.

Through monitoring of memory and behavior in persons without any obvious risk, or early intervention in persons with clear-cut increased risk, there is the best chance of reducing risk or avoiding these illnesses altogether.

Treatment will always be multifactorial, including diet, healthy sleep, life style modification, and personalized individualized identification of environmental and genetic risk factors.

While we all await the possibility of more specific disease treatment, we had best avail ourselves of the very effect tools already at our disposal. This will reduce fear, inspire compliance, and reduce the burden of this illness on our families and society. If not now, when?

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