Alzheimer's Disease: A Treatment Strategy

Kimmo Hatanpaa hatanpaa at helix
Mon Jan 16 23:37:56 EST 1995


I like your attitude! A few comments follow.

I don't think the eye test is worth the trouble until  1) the
preliminary experiment published in Science has been
replicated by other groups, and 2) it has been shown that the
test is specific for Alzheimer's disease (AD) and doesn't give
false positives in other dementias. 

The Science paper was about finding AD patients among
normal controls. That is not a big challenge as such: a simple
Mini Mental Test would do as well. The real problem is making
sure that the dementia is caused by AD. There are many other
causes of dementia, and for some of those, an effective
treatment is available once the condition has been correctly
diagnosed. Pernicious anemia is an example of a condition
that often causes AD-like symptoms and that can be
diagnosed by a simple blood test. The diagnosis of AD has to
be based on careful exclusion of other diseases causing
dementia. The eye test is of little value until its specificity has
been proven. 

You say the medical literature has proven that effective
treatment for AD is available. Sorry, but I just can't share your
enthusiasm in this matter. In my opinion, so far no drug has
been proven to slow the course of AD. The only possible
exception to this is acetyl-carnitine, as long as you are willing
to overlook the fact that the studies showing dramatic effects
have been done by Italian groups who are sponsored by the
Italian drug company that makes acetyl-carnitine, while other
groups tend to get negative results or report very little benefit. 

In the light of the latest data, Deprenyl has been a
disappointment considering the initial encouraging findings and
all the animal data supporting its general neuroprotective and
antiaging potential. There has been some behavioral
improvement in some patients, but very little or no cognitive
improvement. My guess is that all the positive findings are
caused by Deprenyl's antidepressive effects. It is actually a
very good antidepressant, possibly as good as any of the
highly publicized modern antidepressants.  Incidentally, another
so called smart-drug, Hydergine, is also an antidepressant and
has shown a similar pattern of slight behavioral changes in AD
patients. I hope that future Deprenyl studies with larger patient
numbers will prove me wrong and show that there is a
subgroup of AD patients whose disease will be actually slowed
down by Deprenyl. 

By this I don't mean that people with AD shouldn't take the
drugs that you recommend. If there is even the slightest
possibility that something might work, why not try it? After all,
most of the drugs you listed are relatively safe, and AD
patients couldn't end up much worse anyway.

One general remark: in the medical sciences, you shouldn't
believe any dramatic or revolutionary results until the studies
have been replicated by at least one other group. Not
everything you find in Medline is true. One example is a study
you cite in your paper, the study by a Japanese group that
claimed that AD could be not only halted but also almost
reversed by a combination of iron, vitamin B-6, and Coenzyme
Q10. This was published as a letter to the editor in Lancet in
1992. Why do you think nothing has been heard of this
miraculous cure for AD ever since?

I think the most promising group of drugs for AD is the one
that you dismiss as ineffective: AchE inhibitors. The problem
with physostigmine and tacrine is not efficacy, the problem is
the side effects. However, there are some very promising new
AchE inhibitors undergoing animal studies. These new drugs
are specific to the brain type of AchE and therefore shouldn't
cause systemic side effects. 

K. Hatanpaa, M.D.





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