“…More recently, studies of other pathways linked to AD, including those involving amyloid proteins (Selkoe, 1994), Tau protein (Hellstrom-Lindahl, 2000), and inflammation (Breitner, 1996), have supplanted the cholinergic hypothesis; however, loss of high affinity nicotine binding sites, measured in postmortem tissue or by PET imaging, remains a consistent marker of AD (Nordberg et al, , 1997Kasa et al, 1997;Rusted et al, 2000). A comparable decrease in the binding of other nicotinic agonists has been seen in the brains of patients with AD, including acetylcholine in the presence of atropine, methyl-carbamylcholine, cytisine, epibatidine, and ABT418 (Warpman and Nordberg, 1995;Gotti et al, 1997;Kasa et al, 1997). Studies in rodents suggest that nicotine and the other nicotinic agonists used to date recognize the same populations of nAChRs in the cerebral cortex (Zoli et al, 1998).…”