In addition to Alzheimer Disease (AD), clinical medicine currently recognizes the following non-curable syndromes of memory loss, cognitive dysfunction or dementia: Age-Related Cognitive Decline, Mild Cognitive Impairment, Senile Dementia of the Alzheimer Type (SDAT), Pick's Disease, Diffuse Lewy Body Disease, Progressive Supranuclear Palsy (Steele-Richardson Syndrome), Huntington's Disease and others.
1 In some cases the specific syndrome is associated only with progressive dementia (AD, SDAT, Pick's), while others may have additional associated neurologic abnormalities that give them their unique clinical picture. These syndromes are not currently "curable", but commonly referred to as "medically manageable". The true occurrence Alzheimer Disease is uncommon. What most media and non-medical people mean when they refer to Alzheimer Disease is actually Senile Dementia of the Alzheimer Type (SDAT). Statistically speaking, SDAT is much more common than true "Alzheimer Disease".This confusion, which is probably totally unnecessary, comes from a purely academic distinction. The original description of Alzheimer Disease, by Alois Alzheimer himself, limited the application of the term to
"pre-senile dementia", meaning that it begins before the age of 55 years. Although those older than 55 were ultimately recognized as having the identical pathological (clinical, structural and biochemical) abnormalities as Alzheimer originally described, the term
"senile dementia" came to be applied to the syndrome when it began after age 55. In the strange lexicography of academic medicine,
"pre-senile dementia" is still historically recognized as Alzheimer Disease while
"senile dementia" evolved into the academic syndrome of "Senile Dementia of the Alzheimer Type" (SDAT). There is reasonable scientific evidence that the two "syndromes" are actually identical and separated only based on the artificial criteria of age at clinical onset.
1
From a biomedical research standpoint, most syndromes involving memory loss, cognitive decline, cognitive impairment-dysfunction and dementia are currently thought to be multi-factorial in their cause. Among the more prevalent theories and mechanisms regarding the "cause(s)" of memory loss-cognitive decline-dementia are abnormalities involving genetics
1, aging, biochemistry, structure and/or cardiovascular function. These major causative categories can be further subdivided into various potentially causative subcategories within each major category. For example, biochemical mechanisms of various memory loss-cognitive decline-dementia syndromes may involve neuro-transmitter chemical deficiency or excess, such as Acetylcholine, DOPA (Di-hydrOxy-Phenyl-Alanine) or Glutamate toxicity.
1 In addition, biochemical abnormalities involving Oxygen Free Radical injury, inflammation
2-7, hormone imbalances
8, protein abnormalities
9,10, and others have been implicated. Likewise, alterations in brain physical structure, as well as cardiovascular mechanisms, also have a fair amount of scientific evidence in their favor.
11-14 There is also evidence that vascular disease; diabetes and memory loss-dementia syndromes have many risk factors in common.
11-15 Additional factors that may play a part in the development of clinical memory, cognitive or dementia syndromes are silent strokes, gluten (Wheat) toxicity, chronic toxic metal accumulation, non-diabetic
sugar toxicity (gluco-toxicity) , homocystine toxicity, micro-nutrient imbalance and physiological regulation disorders (dys-autonomia).
One of the real clinical problems that clinicians face when investigating and deciding whether treatment is warranted is the dilemma of so-called "mild cognitive impairment". For doctors that actually care for patients, the line from a patient with an occasional memory lapse to mild memory problems (officially labeled "Mild Cognitive Impairment" or MCI) is not always easy to determine. "Evidence based" or "academic (scientific)" medical doctors commonly explain that some loss of memory and cognitive function is "normal" and to be expected as we age.
16 The real point here is to understand whether one is using a
"statistical" or "individual" benchmark to decide if functional changes in mental and cognitive performance are normal, "abnormal" or "pathological." In "scientific" medicine, testing and examining
groups or selected
populations of subjects establish statistical norms. If the variable being investigated (memory loss, for example) is statistically average across the selected population it is usually said to be normal. But statistics
never strictly apply to an individual. So it is true, that like all other parts of the human body, the statistically average brain does undergo "aging". However, it is just as true that the statistically average changes declared "normal" by "scientific" medicine are
not found in populations of healthy aged (the
real normals!). In other words, statistics
should never apply clinically to an individual.
Unfortunately, short of an autopsy or surgical brain biopsy, there is no real "objective" test that can absolutely confirm the diagnosis of Alzheimer Disease or any other form of Memory Loss, Cognitive Impairment or another form of Dementia. And there is no specific treatment for AD or any of the "scientifically defined" syndromes of memory Loss, Cognitive Impairment or named Dementia syndromes. So, is mental decline and/or memory dysfunction really a part of "normal healthy aging"? Curiously, when truly "healthy aged" populations are studied (Okinawans, Hunza, and numerous others selected populations), the statistically "normal" abnormalities accepted by academic scientific medicine (memory loss, increase degenerative diseases like stroke, heart disease and cancer, etc.) and changes in joint X-ray (degenerative arthritis, etc.) or brain MRI scans (patchy or diffuse areas of "unexplained" scaring, also called senile plaque, gliosis, lacunar infarcts or age-related ischemic leuko-encephalopathy) are not seen! Thus, the public confusion over what "scientific normal" really means is quite real, well entrenched and dangerous. Since there is no way to tell if mild memory or cognitive problems will progress to a more serious problem and healthy aged populations do not experience these problems, it should be assumed that any degree of memory loss or cognitive impairment should be, individually, carefully and completely evaluated medically for all risk factors for AD/SDAT-like syndromes.
Although loss of memory can be devastating to the individual, according to "evidence-based" "scientific" medicine, some memory loss may not necessarily be a "pathological" condition. Unfortunately, in those who have this scientifically conjured "statistically normal", age-related dysfunction the condition has now been shown to progress to Mild Cognitive Impairment (MCI).
16 MCI is a known transition stage from normal to Senile Dementia of an Alzheimer Type (SDAT).
17 Since there is no definitive test to tell who will progress from normal, (really a statistical term; meaning that if a high percentage of the aging population has mild memory loss it is considered a "normal occurrence", statistically speaking), how can a clinician tell, if there really is a "problem"? If there is a problem, is there any specific curative treatment for it? If there is no cure or specific treatment, what is the point of making a "specific (named) diagnosis anyway"? Other than for insurance payment, administrative coding or academic purposes, it really makes no difference what name the problem is given if it cannot really be treated!
At Bio Health Center
At Bio Health Center, rather than focusing on academic diagnostic labels (i.e Alzheimer, SDAT, Lewey Body Disease, Mixed Dementia, Multi-Infarct Dementia, etc.), for which there really are no definitive or specific treatments, we have developed a staging process for memory loss, cognitive impairment and/or some dementia patients. Based on the individual patient's clinical presentation, they will be classified into one of four levels of symptomatic expression of memory loss-cognitive dysfunction or actual dementia. In addition, cardiovascular, radiological and laboratory studies are used to rule in or rule out potentially treatable underlying causative mechanisms of memory loss-cognitive dysfunction-dementia. The reasons for this approach are several. First, using specific diagnostic labels can serve mostly to discourage and frighten both the patient and their loved ones unnecessarily. Second, the stratification of the problem based on clinical staging allows more accurate determination of progression or regression of the actual clinical condition undergoing Integrative Medical treatment. Third, the various supportive and interventional therapies used a Bio Health Center can more rationally be combined according to the actual clinical and/or laboratory level of the problem. Fourth, for those in the earlier stages of clinical symptoms the various stages can act as a goal to be achieved in reversing or stabilizing (i.e. regressing from stage 3 to stage 2, progression of clinical symptoms.
The staging system currently used at Bio Health Center for memory impairment, cognitive dysfunction and dementia consists of the following four clinical stages:
Stage I:
Mild or occasional memory problems, noticeable primarily by the patient or possibly a close loved one, such as a spouse or child, but the patient is able to effectively conduct their activities of daily living (bathing, dressing, food preparation, shopping, paying bills, etc.) without difficulty. All or most testing is normal or "non-diagnostic", except for possible evidence of
Micro-Vascular disease (see below) and/or accelerated
protein glycation
Stage II:
Mild to moderate memory or intellectual problems significant enough to mention them to others, including family members or a health care practitioner. The patient is able to effectively conduct some activities of daily living (bathing, dressing, food preparation, shopping, paying bills, etc.), but with noticeable difficulty and may require occasional assistance. Lab, cardiovascular and/or radiographic testing demonstrating abnormalities may be consistent clinical with symptoms. This stage could also be comparable to so-called "mild" cognitive impairment of aging described in "evidence-based" scientific medical literature, but more advanced;
Stage III:
Moderate memory loss or disturbed executive brain function problems that clearly and regularly interfere with activities of daily living (bathing, dressing, food preparation, shopping, paying bills, etc.) and require assistance regularly, but not full time. Lab, cardiovascular and/or radiographic testing demonstrating abnormalities are consistent clinical with symptoms;
Stage IV
Clinical dementia requiring a majority or full time supervisory care for all or most activities of daily living (bathing, dressing, food preparation, shopping, paying bills, etc.). Clear evidence of laboratory, vascular testing and/or CT/MRI/PET scans abnormalities
Prior to clinical staging, each patient should undergo a thorough clinical, laboratory, cardiovascular and radiological evaluation looking for confirmatory diagnostic evidence, and also to rule out potentially reversible causes of memory loss, cognitive dysfunction or dementia.
REFERENCES
1. Beal MF, Richardson EP Jr, Martin J. Alzheimer's Disease and Other Dementias. In [eds: Isselbacher AB, Braunwald E, Wilson JD, et al] Harrison's Principles of Internal Medicine. 1994;1:2269-2272.
2. Nissen SE, Tuzcu EM, Schoenhagen P, et al. For the REVARSAL Investigators. Effect of Intensive Compared With Moderate Lipid-Lowering Therapy on Progression of Coronary Atherosclerosis: a Randomized Controlled Trial. JAMA. 2004;291:1071-1080.
7. Feron O, Dessy C, Moniotte S, et al. Hypercholesterolemia Decreases Nitric Oxide Production by Promoting the Interaction of Caveolin and Endothelial Nitric Oxide Synthase. J Clin Invest. 1999;103:897-905
8. Rosario ER Chang L, Stancyzk FZ, et al. Age-Related Testosterone Depletion and the Development of Alzheimer Disease. JAMA. 2004;292:1431-1432.
9. Bustos C, Hernandez-Presa MA, Ortego M, et al. HMG-Co A Reductase Inhibition by Atorvastatin Reduced Neointimal Inflammation in a Rabbit Model of Atherosclerosis. J Am Coll Cardiol. 1998;32:2057-2064.
10. Jen s, Wall U, Bergbrant A, et al. Endothelium-Dependent Vasodilation and Tissue-Type Plasminogen Activator Release in Borderline Hypertension. Arterio Scler Throm Vasc Biolo. 1997;17:3376-3388.
11.van Boven AJ, Jukema JW, Zwinderman AH, et al. Reduction of Transient Myocardial Ischemia With Pravastatin in Addition to the Conventional Treatment in Patients With Angina Pectoris. Circulation. 1996;94:1503-1505.
12. Libby P. Molecular Basis of the Acute Coronary Syndromes. Circulation. 1995;91:2844-2850.
13. Libby P. Current Concepts of the Pathogenesis of the Acute Coronary Syndromes. Circulation. 1995;104:365-372.
14. Aikawa M, Rabkin E Okada Y, et al. Lipid Lowering By Diet Reduces Matrix Metalloproteinace Activity and Increases Collagen Content of Rabbit Atheroma: A Potential Mechanism of Lesion Stabilization. Circulation. 1998;97:2433-2444.
15. Boucier T, Libby P. HMG CoA Reductase Inhibitors Reduce Plasminogen Activator Inhibitor-1 Expression by Human Vascular Smooth Muscle and Endothelial Cells. Atheroscler Thromb Vasc Biol. 2000;20:556-562.
16.
www.familydoctor.org Memory Loss With Aging: What's Normal, What's Not.
http://familydoctor.org/124.xml? 1/14/06.
17.
www.MayoClinic.com Mild Cognitive Impairment. http://www.mayoclinic.com/health/mild-cognitive-impairment/DS00533 1/14/06.
