Effects of Acute Nicotine Administration on Cognitive Event-Related Potentials in Tacrine-Treated and Non-Treated Patients with Alzheimer’s Disease

Abstract

Earlier studies of cognitive event-related brain potentials (ERPs) reporting diminished amplitudes and delayed latencies of the P300 potential in dementia of the Alzheimer type (DAT), together with independent findings of the P300- and performance-enhancing properties of nicotine in normal adults, stimulated this study to explore the single-dose effects of nicotine on auditory and visual P300s in DAT. Thirteen patients, 6 currently receiving treatment with the cholinesterase inhibitor tacrine (tetrahydroaminoacridine; THA) and the remaining being medication free, were administered 2 mg of nicotine polacrilex under double-blind, randomized, placebo-controlled conditions. Prior to nicotine administration, THA-treated patients exhibited shorter auditory P300 latencies than non-treated patients. Acutely administered nicotine failed to alter auditory P300, but increased the amplitudes of visual P300s in both DAT patient groups. Neither THA treatment nor single-dose nicotine altered behavioural performance in the visual and auditory task paradigms. The results are discussed in relation to nicotinic cholinergic, attentional and cognitive processes in DAT.

Chronic Nicotine Treatment Impacts the Regulation of Opioid and Non-opioid Peptides in the Rat Dorsal Striatum

“…This suggests that the increase of these peptides may reflect elevated precursor synthesis, consistent with the elevated preproenkephalin mRNA levels in the striatum after chronic nicotine application (15). Another class of opioid peptides, dynorphins derived from PDYN including dynorphin (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17) and dynorphin(1-8), was not modulated by chronic nicotine. This is consistent with previous literature linking PDYN peptides to aversive states associated with drug withdrawal (47), which were not induced in our experiment.…”

“…various aspects of neurochemical transmission and has a strong impact on diverse physiological processes (2), resulting in drug-seeking and drug-taking behaviors for normal smokers and for a considerable number of patients suffering from schizophrenia and Alzheimer disease, who use nicotine for self-medication (3,4). The dorsal striatum (DS) 1 is one of the key brain regions that has been associated with neural regulation during chronic nicotine exposure (5).…”

Effects of nicotine and smoking on event‐related potentials: A review

“…As with amplitude, several studies reported no effect on N100 latency (Ilan & Polich, 1999Knott et al, 1999a;Knott et al, 2002;Le Houezec et al, 1994;Michel et al, 1988). Houlihan et al (2001) reported that smoking/ nicotine shortened N100 latency to both memory-set and probe stimuli in a Sternberg-type task.…”

“…Regarding effects for imperative stimuli (either with or without a warning stimulus), several studies reported no effects of nicotine on either exogenous ERP components or performance (Ilan & Polich, 1999Knott, 1985;Knott et al, 2002;Le Houezec et al, 1994;Michel at al., 1988). Others reported that smoking/nicotine facilitated performance in the absence of effects on exogenous ERP components (Knott, 1986;Knott et al, 1999a).…”

“…For an RT memory task, Pineda, Herrera, Kang, and Sandler (1998) reported that smoking/ nicotine increased P300 amplitude without affecting RT. Similarly, Knott et al (2002) tested Alzheimer's subjects in an oddball task and reported that nicotine gum increased P300 amplitude without affecting RT. In contrast, Ilan and Polich (2001) tested participants using a Stroop-type color/word interference task.…”