Glucose regulation and face recognition deficits in older adults: the role of attention

The present study investigated the perceptual, attentional, and memory processes underlying face recognition deficits observed in older adults with impaired glucoregulation. Participants were categorized as good glucoregulators or poor glucoregulators on the basis of an oral glucose tolerance test. Using event-related potential (ERP) methodology, 23 participants (62–88 years) performed a 2-stimulus oddball task. Participants were asked to rate and memorize 10 “target” faces, which were then presented amongst 120 unfamiliar foils. Behavioral results indicated that good glucoregulators were significantly more accurate at recognizing target faces. ERP markers of early visual perception (P1 and N170 components) and memory formation (P3 component) were unaffected by glucoregulatory efficiency. The P2 component, an index of attentional processing, was larger and delayed in the poor glucoregulators. To the best of our knowledge, this study is the first to suggest that face recognition deficits in poor glucoregulators may be due to impairments in attentional processing.     

AF-DX 116, a Presynaptic Muscarinic Receptor Antagonist, Potentiates the Effects of Glucose and Reverses the Effects of Insulin on Memory

Male Swiss mice were tested 24 h after training in a one-trial step-through inhibitory avoidance task. Low subeffective doses of -(+)-glucose (10 mg/kg, ip), but not its stereoisomer -(−)-glucose (30 mg/kg, ip), administered immediately after training, and AF-DX 116 (0.3 mg/kg, ip), a presynaptic muscarinic receptor antagonist, given 10 min after training, interact to improve retention. Insulin (8 IU/kg, ip) impaired retention when injected immediately after training, and the effects were reversed, in a dose-related manner, by AF-DX 116 (0.3, 1.0, or 3.0 mg/kg, ip) administered 10 min following insulin. Since AF-DX 116 possibly blocks autoreceptors mediating the inhibition of acetylcholine release from cholinergic nerve terminals, the present data support the view that changes in the central nervous system glucose availability, subsequent to modification of circulating glucose levels, influence the activity of central cholinergic mechanisms involved in memory storage of an inhibitory avoidance response in mice.