This Article  • References  • Full text PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citing articles on HighWire  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

Arch Neurol. 1989;46(1):13.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—The development of an effective agent to increase brain levels of acetylcholine in patients with the memory disorder of Alzheimer's disease, who are known to be deficient in brain acetylcholine, is of utmost importance. Clinical trials with immediate-release physostigmine salicylate, which inhibits enzymatic degradation of acetylcholine, have been reported to be beneficial,^1,2 equivocal,³ or negative⁴ in Alzheimer's disease. Immediate-release physostigmine salicylate has an extremely short plasma half-life of approximately 30 minutes,^5,6 which limits bioavailability of physostigmine for uptake into the brain. Many of the re

Mean plasma physostigmine concentrations in five young healthy male volunteers after oral physostigmine salicylate administration: closed circles indicate 2-mg immediate-release physostigmine salicylate; open circles, 9-mg controlled-release (CR) physostigmine salicylate; open rectangle, 12-mg CR physostigmine salicylate; and open triangle, 15-mg CR physostigmine salicylate. ported studies failed to monitor the bioavailability of this compound. The development of a controlled-release formulation . . . [Full Text PDF of this Article]

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?