Page 231 - The Memory Program How to Prevent Memory Loss and Enhance Memory Power

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from dopamine deficiency. In the early work, human fetal cells that produced dopamine were
transplanted, because such cells are more likely to retain the capacity to reproduce than adult cells.
Later, the abortion controversy led to a U.S. ban on the use of fetal tissue in medical research or
procedures. This political detour submerged the revolutionary impact of the finding that cells from
outside the body can actually survive and reproduce after being placed inside the brain. A Mexican
neurosurgeon reported the initial successful transplants in Parkinson's disease, but Scandinavian and
American doctors could not replicate the results, and the jury is still out on this issue. But note that
long-term follow-up of these transplanted Parkinson's patients has revealed a disturbing side effect:
involuntary jerks and movements caused by the transplanted dopamine cells continuing to reproduce,
because the normal regulatory mechanisms that suppress their action within the brain don't work well
on transplanted cells.

Memory loss involves the hippocampus and surrounding areas, which are relatively small regions,
but also the frontal cortex, which occupies a huge portion of the brain's surface. This wide
representation of memory in the brain makes transplantation an unlikely candidate for the next
memory “cure.” Nonetheless, if a method can be developed to transplant cells that reproduce and
differentiate into hippocampal nerve cells, preferably cholinergic nerve cells, the field would truly be
revolutionized. My prediction, however, is that highly effective promemory medications will be
developed long before implantation of cells into the brain can be used to solve the problem of
memory loss.
TEAMFLY

Blocking Formation of Toxic Compounds

Most of the existing therapies, and those in research development, focus on stimulating natural
promemory factors— the good guys— in the brain, or by blocking destruction of the good guys (e.g.,
cholinesterase inhibitors). But what about the opposite strategy: blocking the bad guys— the toxic
enzymes, the destructive genes and neurotransmitters that trigger and mediate cell death?
Antioxidants represent one such approach. But in recent years, the focus has shifted to more
sophisticated techniques that attempt to block the formation of deposits in the brain that damage
nerve cells. These deposits, which are called amyloid plaques and neurofibrillary tangles, typically
occur in Alzheimer's disease. The same plaques are present, though to a much lesser extent, in
elderly people with age-related memory loss. So the question naturally arises: what if we could block
the formation of plaques and tangles in the first place?

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Team-Fly