served in Parkinson's disease. According to this rationale, methods of treatment that increase acetylcholine to normal levels should halt the degeneration and loss of neurons. (Acetylcholine can be increased by administering precursors of the neurotransmitter, which the patient's system then breaks down in a normal way, or by blocking the destruction of acetylcholine so that it is active longer.) In addition, several other neurotransmitters clearly suffer some deficit in Alzheimer's disease, so that multiple replacement of neurotransmitters, or the use of drugs that act like transmitters, are options for treatment that should be examined.

The administration of nerve growth factor has been a news-worthy step in laboratory attempts to prevent degeneration of the nerve fiber tracts known as the cholinergic pathways. In animals, nerve growth factor successfully protects the neurons of the hippocampus from dying, which should in turn preserve the workings of short-term memory. But applying such a therapy to humans raises several practical questions: how might a large molecule like nerve growth factor be made to cross the blood-brain barrier, and how would it then be directed to the specific region of the brain where it is needed? Two proposed solutions are a form of reservoir or pump implanted in the brain to give a continuous infusion of the compound, and the use of smaller molecules—analogues of nerve growth factor— that might pass more easily throughout the brain to the required sites. Preliminary reports of the use of nerve growth factor in a small trial, which have appeared recently, are exciting, but they have not yet been confirmed.

Meanwhile, stepping back to the perspective of epidemiology, researchers have posed a fruitful question by turning the usual query about dementia into its opposite. In other words, who does not get dementia? What are the factors that allow someone to reach an advanced age and continue to function successfully? For now, both this angle of investigation and the straightforward inquiry into agents of disease call for more and better understood study populations. In long-lived Americans it is especially difficult to sort out the factors that may have affected health over the course of, say, 80 years; however, studies in some regions of the world that have changed less rapidly than this country may be able to assemble populations



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