Transplantation
A more direct human application is transplantation, which has been tried with dopamine-producing cells in Parkinson’s patients who suffer 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.
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?
Preventing Amyloid Formation
Many drug companies are now in hot pursuit of compounds (Beta-block is the name of one such drug in development) that can block the enzymes that trigger the formation of Beta-amyloid, which is the main protein component of the amyloid plaque. Recently, an experimental vaccine has also been developed for this purpose. Many of these compounds are toxic, and we are still a long way from translating these concepts into a clinically useful treatment. But if it does occur, millions of patients and families with dementia, particularly Alzheimer’s disease, will be eternally grateful.
Taken From: The Memory Program How to Prevent Memory Loss
and Enhance Memory Power
