The questions of interest to most of us are whether Alzheimer's can be prevented, whether it can be arrested once it starts, and whether the damage it has caused can be reversed. Prevention is theoretically possible, once we understand how the disease comes about, and this understanding may also make it possible to stop the disease at any point. But reversing the damage once it has occurred is not even theoretically possible. There is a great deal of discussion at present of cures for other diseases of or injuries to the nervous system, such as Parkinson's disease or spinal cord injuries, but it seems to me that none of these cures would be able to reverse the damage in Alzheimer's once it has occurred.
Until very recently the accepted wisdom in biology was that nerves in the central nervous system, which includes the brain and the spinal cord, can never regenerate. That is, once they are damaged, the damage is permanent - the damaged cells cannot repair themselves, and the undamaged cells cannot divide to provide new cells.
Our skin, for example, repairs itself after injury in that the undamaged cells divide rapidly to provide new healthy cells that take the place of the damaged ones. In cases where so much skin is damaged that this process cannot provide enough new cells, skin can be taken from another part of the body to cover the injured area, and the cells in this graft will divide in their new home and connect up with the ones already there. This is a relatively easy process because skin cells are connected to their neighbors very simply - all they have to do is touch each other snugly, as their main function is to protect the body parts underneath them.
Nerve cells, in contrast, generally stop dividing around the time of birth. Learning, as we have seen, takes place through the selective strengthening of connections between neurons, and does not require the growth of new cells. And until very recently it was believed that the neurons cannot be stimulated to divide again, even in the case of injury.
In the past few years, however, there have been hints that a way can be found to make the neurons in the spinal cord start dividing again after an injury. This technique is still in the laboratory stage, and has not yet been refined enough to start using it in injured people, but let us assume that it will someday be used in patients. Such an advance might be possible because the nerve cells in the spinal cord are connected to one another in fairly fixed ways. These neurons are merely messengers that allow the brain to tell the muscles what to do. They normally form connections with one another before birth, and these connections are not changed by the learning process. When we learn to walk, say, changes occur in neural connections in the motor networks of the brain and in the cerebellum, the area at the base of the brain responsible for fine-tuning our movements. The connections between the neurons in the spinal cord, however, remain fixed. Thus if there is some way to get these neurons to regenerate after they have been damaged, it is plausible that they might be able to reconnect to one another in the way they did when they were first developing, and this may be enough to allow the patient to walk once again.
The situation in the brain, though, as we have seen throughout the book, is far more complex. The connections between the neurons are changed by everything we learn during our lives, and these changed connections actually constitute our knowledge. Thus if they become tangled up, there is no way to untangle them. Even if the remaining healthy neurons could be made to divide by some spectacular medical breakthrough, the odds would be astronomical against any new connections they made being the right ones. Since these connections were all established by a slow learning process in the first place, any reconnection would require a similar slow learning process.
Indeed, the evidence of occasional recovery from serious brain damage offers strong support for this claim. Some people who have been in a coma for a long time, generally after suffering brain damage due to the brain being starved of oxygen for too many minutes, do eventually regain near-normal functioning. But this requires a lengthy learning period, in which the patient must learn to walk, talk, feed and dress himself, all over again. In such cases many of the connections have apparently remained intact while others were damaged, so that the patient's expert knowledge in a particular field may be preserved and become available once again when the patient becomes able to access it.
Thus if some way were found of making the neurons in the brain divide, the most that could be hoped for in the case of Alzheimer's patients would be that they could start the process of learning all over again. But since in the case of Alzheimer's, unlike the case of oxygen starvation, the patient's knowledge about the world is often one of the first casualties of the disease, it would probably take as many years to relearn all this knowledge as it took to learn it in the first place. And since even the brains of normally aging individuals have trouble making the changes that are required for learning a great deal of new material, the prospect of restoring Alzheimer's patients to their former situation seems extremely remote.
Our only hope, then, is prevention, which remains possible even if a cure may not be. But this is not a forlorn hope. Mankind has practically eradicated many incurable viral diseases, such as smallpox, through prevention, so we may hope that a preventive measure will be found in the case of Alzheimer's as well.
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