Abstract
Trials of cholinergic-enhancing agents in patients with Alzheimer’s disease have shown that modest benefits are produced in some patients, but that not all patients respond to such treatment. Alzheimer’s disease is not merely the result of a cholinergic deficit, and deficiencies of other neurotransmitters have been demonstrated. Findings implicating the noradrenergic system in AD have prompted the search for combinations of drugs that will address the combined cholinergic-noradrenergic deficits; a number of clinical trials of combination therapy are under way. At the same time, continuing research focuses on therapeutic approaches aimed at either preventing Alzheimer’s disease or slowing its progression. Potential approaches to slow disease progression include intervention in β-amyloid production, prevention of excitatory amino acid-mediated toxicity, and use of nerve growth factor. Identification of an Alzheimer’s disease gene would permit identification of the at-risk population long before onset and might constitute a first step toward disease eradication.
| Original language | English |
|---|---|
| Pages (from-to) | S52-S55 |
| Journal | Neurology |
| Volume | 43 |
| Issue number | 8 |
| State | Published - Aug 1993 |
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