Alzheimer’s Disease: A Prequel-Part XXIV

(1/3/15)- The following is considered the latest definition of Alzheimer's disease. However, there are still other researchers who believe that other concomitant or some upstream event may start the slow process toward AD.

"AD has been conceptualized as a progressive pathophysiological process in which Amyloid beta (Aβ) toxicity is believed to result in sequence of dynamic changes, including the accumulation of intracellular neurofibrillary tangles (NFTs), synaptic loss, neuroinflammatory processes and disrupted neurotransmission. Importantly, these changes are thought to accumulate during a protracted preclinical phase, with the acceleration of such changes marking the transition to MCI, the symptomatic predementia phase of AD

(4/27/09)-Alzheimer's Death Rate per 100,000

United States 22.9

Alabama 33.2; Alaska 21.3; Arizona 31.3; Arkansas 22.6; California 23.2; Colorado 28.5; Connecticut 16.1; Delaware 20.0 ; District of Columbia 19.1; Florida 18.4; Georgia 27.0; Hawaii 11.4; Idaho 29.4; Illinois 20.8; Indiana 24.7; Iowa 25.4; Kansas 27.2; Kentucky 28.9; Louisiana 34.2; Maine 29.1; Maryland 17.5; Massachusetts 19.8; Michigan 21.2; Minnesota 22.5; Mississippi 26.7; Missouri 25.4; Montana 23.9; Nebraska 21.8; Nevada 17.1; New Hampshire 26.1; New Jersey 17.1; New Mexico 8.3; New York 9.2; North Carolina 29.5; North Dakota 29.8; Ohio 26.0; Oklahoma 28.1; Oregon 28.9; Pennsylvania 18.9; Rhode Island 18.8; South Carolina 32.4; South Dakota 27.3; Tennessee 36.2; Texas 27.2; Utah 21.5; Vermont 25.7; Virginia 22.5; Washington 35.9; West Virginia 23.2; Wisconsin 22.4; Wyoming 22.7;

Guam NSD 2; Puerto Rico 38.5 2; Virgin Islands NSD 2;

Notes: Age-adjusted rates per 100,000 U.S. standard population. Populations used for computing death rates are postcensal estimates based on the 2000 Census estimated as of July 1, 2005. Since death rates are affected by the population composition of a given area, age-adjusted death rates should be used for comparisons between areas because they control for differences in population composition. Data are for 2005.

Sources: The Centers for Disease Control and Prevention (CDC), National Center for Health

Statistics, Division of Vital Statistics, National Vital Statistics: Report Volume 56, Number 10, April, 2008, Table 29.

Definitions: NSD: Not Sufficient Data.

(6/13/04)- This prequel is being written as a reflection following completion of 23 articles on Alzheimer’s disease and poignantly following the death of former President Ronald Reagan after a 10 year battle with Alzheimer’s disease. It is a reflection on the ethical principles of pharmaceutical treatment of Alzheimer’s disease and should not be viewed as a criticism of any of the articles written in this series. It reflects more on the dilemma of treating dementia. We believe the questions asked below need to be answered in all fairness to the people being treated for the disease.

It seems reasonable to assume that any pharmaceutical treatment should not be begun until there is evidence-based medical research that an individual will benefit from the prescribed treatment. Here, we are not talking about standard research protocols, where there are controlled research guidelines for use of drugs on humans, though even here there are ethical considerations that need clarification. Clinical treatment ethically necessitates an acceptable benefit-cost ratio prior to starting the pharmaceutical treatment, especially in those cases that involve long-term drug treatment. There is no question that drug studies look at the safety and efficacy of the pharmaceutical treatment. What is the personal cost of being on a drug for ten years etc.? What are the negative implications of long term therapy?

In dementia, we are faced with a clear dilemma. To date (June 11, 2004), there is no rational based on supposed pathophysiology for early treatment of Alzheimer’s disease. However, there are four drugs approved for treatment of mild to moderate Alzheimer’s disease and one drug for moderate to severe Alzheimer’s. For the most part, these drugs treat symptoms of AD, rather than modifying the effects of the disease. They do nothing to prevent the disease. They are based on a depletion of choline acetyltranferase, which may be a downstream result of the disease. This theory is based for the most part on post-mortem studies of individuals with a late stage of the disease. Newer techniques (PET scan, MRI etc.) hold promise for clearer earlier understanding of the disease process. As far as this author can determine, there is much less data concerning changes in choline acetyltranferase activity at the early stages of the disease. Yet, there are attempts to apply this type of treatment to not only the early stages of AD but also to possible precursors of Alzheimer’s i. e. mild cognitive impairment,. Aside from early onset Alzheimer’s that appears to be genetic in origin, most cases of AD have a range of symptoms that is suggestive not only of genetic origin, but also environmental infarcts. But what are the evolutionary implications of such a disease? If it is more common the older one gets, could this be a meta form of apoptosis?

In some cases the drugs used in treatment of AD retard the progress of certain symptoms/behaviors associated with Alzheimer’s. But what are the effects on those who are not helped, and what price does a person pay biopsychosocially by being on the drug for an extended period of time?

It also seems safe to assume that treatment onset may be different for the targeted goal of the drug therapy, as in general medicine where you may have a vaccine for prevention of the disease given in childhood or drugs given to target symptoms of the disease at the onset of the overt expression of the disease or a different regimen when the disease becomes more serious. Could the same be true of Alzheimer’s disease? Or does one size fit all in this case?

Now to look at another face of this disease: one is faced with a disease that has a 100% mortality rate in the long run. We would assume most of the readers of this prequel are familiar with the effects of AD on the individual. But what of the existential pain felt by the individual and the pain of the caregivers? Do we opt for any kind of treatment, even if we do not know the long-term implications of the treatment or if the downside risks are high? Hope is an essential component of our existence. People want to believe there are pharmaceutical therapies that can prevent their dying a perceived painful death. Medications help in this aspect and should not be sold short. But what of alternative treatments that face an uphill battle in face of the Pharmaceutical Industry?

The story of the treatment of AD is still unfolding. This author hopes that this continuing series of articles will help individuals understand a devastating disease and provide information for them or their caregivers to make informed decisions about their treatment.

For some other articles on Alzheimer's Disease Please see:

See: Alzheimer's Disease Part I-Medications for Alzheimer's.
See: Alzheimer’s Disease Part II- Selegiline and AD.
See: Alzheimer's Disease Part III- Use of Gingko Biloba in memory problems of Alzheimer patients
See: Part IV-Alternative Treatments for AD
See: Part V-Possible New Drugs for Alzheimer's Disease
See: Part VI-Early Diagnosis
See: Part VII-Metrifonate

 Disease PartVIII

- Implications of Longer Life Expectancies
See: Alzheimer's Part IX-Ethical Care Principles
See: Alzheimer's Disease-Part X-Estrogen and Alzheimer's Disease
See: Alzheimer's Disease Part XI-Pocket Smell Test (PST)
See: Alzheimer's Disease Part XII-MAO-B
See: Alzheimer's Disease Part XIII -Critical Flicker Fusion Threshold Test
See: Alzheimer's Disease Part XIV-Donepezil
See: Alzheimer's Disease Part XV-Cerebrolysin
See: Alzheimer's Disease Part XVI-MCI
See: Alzheimer's Disease Part XVII-Summary
See: Alzheimer's Disease Part XVIII-NO Releasing NSAIDs
See: Alzheimer's Disease Part XIX-Vitamin E
See: Alzheimer's Disease-Part XX-Clinical Trials
See: Alzheimer's Disease-Part XXI- AD and the Brain
See: Alzhemer's Disease-Part XXII-Lewy Bodies Disease
See: Alzheimer's Disease-Part XXIII-HMG
See: Alzheimer's Disease-Part XXV-Psychosis
See: Alzheimer's Disease-Part XXVI-Amyloid-beta Hypothesis Controversy 
See: Alzheimer's Disease-Part XXVII- AD and Diabetes
See: Alzhemeir's Disease-Part XXVIII - Insulin and AD


Harold Rubin, MS, ABD, CRC, Guest Lecturer
updated January 3, 2015

To e-mail: or  

Return to Home