Monday, November 15, 2010


ALZHEIMER’S DISEASE (AD) is the most common form of dementia. This incurable, degenerative, and terminal disease was first described by German psychiatrist and neuro-pathologist, Alois Alzheimer in 1906 and was subsequently named after him. Generally, it is diagnosed in people over 65 years of age, although the less-prevalent “early-onset” of Alzheimer's does occur before this age. In 2010, there were 30.6 million sufferers worldwide. Alzheimer's is predicted to affect 1 in 85 people globally by 2050 and after age 80 half will have it. The risk factors for this malady include family history, gluten intolerance, heavy metal excess, fever blisters, high blood sugar, physical and psychological stress, obesity, head trauma, drugs and age. There is a Tsunami of fat-related AD brewing as obese Baby Boomers go from grey to white hair.

The earliest observable symptoms are often mistakenly thought to be “age-related” senior moments. The inability to acquire new memories, the difficulty in recalling recently observed facts are noted first by the individual, then by loved ones and lastly friends. These individuals, particularly those with a high social IQ, cover up these mental lapses with believable excuses. As the disease advances, symptoms include confusion, irritability, aggression, mood swings, language breakdown, long-term memory loss and the general withdrawal of the sufferer as their senses decline. Gradually, bodily functions are lost, ultimately leading to death. AD develops for an indeterminate period of time before becoming fully apparent, and it can progress undiagnosed for years. The mean life expectancy following diagnosis is approximately seven years. Fewer than three percent of individuals live more than fourteen years after diagnosis. When AD is suspected, the diagnosis is usually confirmed with behavioral assessments and cognitive tests, such as a MMSE. A Psychological Inventory Test (see later) that checks 9 different brain areas of function also helps in diagnosis. It is best to pick up the disease in its earliest stages when much can be done to delay or even prevent it. Often I order a MRI to look at the hippocampus volume, and if in real doubt, do a PET scan with a PIB contrast. Individual prognosis is difficult to assess, as the duration and severity of the disease varies much from patient to patient. AD develops for an indeterminate period of time before becoming fully apparent, and it can progress undiagnosed for years.

If Alzheimer’s is in your future, much can be done to greatly delay, or better yet, prevent it. Despite the many ways to determine if you are in harm's way, there is no guarantee that it will arrive until after it is too late. Therefore, an ounce of prevention should be considered before a ton of care. One cannot change their genes (Apo E or Family History), but can certainly amend them in what is termed epigenetic modification. There are at least 7 methods to do this. The research indicates that AD is an inflammatory process and we should quench the continuing fire, rather than what most of us Physicians do, which is to get rid of the smoke or smoky thinking. The 3 drugs that are FDA approved today increase an important chemical in neuro-transmission, Acetyl Choline. They are Aricept, Exelon and Razadyne. The other FDA medication is Nemanda which tries, but unsuccessfully, to put out the fire. Unlike the cardinal signs of acute inflammation in the rest of the body, Calor, Dolor, Tumor, Rubor {Heat, Pain, Swelling and Redness), they are not manifest in the brain in this chronic condition. The Brain is not easily accessed and Alzheimer’s is a slow ongoing oxidative smoldering process with neuronal damage by the slow release of free radicals.

Recently it was determined that a toxic protein found in Alzheimer's patients, (amyloid-beta derived diffusible ligand, or ADDL), removes insulin receptors from nerve cells making them insulin resistant and stopping brain insulin signaling crucial for memory. The binding of ADDLs to synapses somehow prevents insulin receptors from accumulating at the synapses where they are needed. Instead, they are piling up where they are made, in the cell body near the nucleus. Insulin cannot reach receptors there. This finding is the first molecular evidence of why nerve cells become insulin resistant in Alzheimer's disease. This is termed by scientists as Type 3 Diabetes. The pathologic Tangles and Amyloid plaques are the result rather than the cause of the process. That is why the vaccine and recently hopeful drugs have not worked.

The best time to prevent or treat Alzheimer’s is ASAP. The difficulty is to determine who needs therapy. Minimal Cognitive Dysfunction (MCD) was once thought to be a natural part of aging and called, until recently, Benign Forgetfulness of the Age. We now know that as many as 70% of these folks develop AD. To determine these, a Neuro-Cognitive test should be performed. This gives a rapid and valid assessment of a suspects brain function. Abnormal results are sometimes referred to the neuro-psychologist for a full evaluation. These studies bridge the gap between current paper-based testing methods and more expensive clinical options. This assessment provides greater certainty by providing a standardized, precise and objective test. The test that I use is CNS Vital Signs, which gives a specific, tangible measurement of a base line and with serial testing a determination of the rapidity of the onset of AD. It is standardized, objective, valid and reliable with millisecond timing accuracy. It provides measurement of minute changes such as those associated with superimposed drug effects and cognitive impairment. This instrument which is done at the office, or in the patient's home in about 30 minutes, is automatically scored. The scores are then compared to normal standards and are then integrated into clinical domains such as Verbal Memory. It is also paid for by insurances with the CPT code of 96101/02/03 or 96118/19/20. With this information one can decide how aggressive one should be in an intervention.

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