Several investigators have documented olfac,o tory deficits in Alzheimer's diz~ase (AD) (Serby et al. 1985; Warner et al. 11986, Knupfer and Speigel 1986; Koss et al. 1987; Doty et al. 1987). Preliminary studies have examined the chemical (Serby 1986) and pathological (Averbach 198~; Esid and Wilcock 1984) correlates of hyposrnia in AD. Acetylcholine (ACh), which has particular relevance to the pathophysiology of AD (Bartus e;~ al. 1982), is an abundant olfactory bulb (OB) neurotransmitter. Furthermore, ACh and bethanechol enhance odor detection when applied to the nasal mucosa in humans (Skouby and ZilstofffPede~en 1954). Thus, it is possible that the olfactory deficits in AD are related to reduced ACh tra~mission. One means of learning more about the neurochemistry of olfaction and of AD is to observe the consequences of pharmacological manipulations. We therefore evaluated the effects of the cholinergic aatagonist scopolamine ~a ~ t h odor detection and odor identification, initially in young normal volunteers.
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Serby et al. (1990) studied this question.
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