PET imaging of cortical 11C-nicotine binding correlates with the cognitive function of attention in Alzheimer´s disease.
2006 (English)In: Psychopharmacology, ISSN 0033-3158, Vol. 188, no 4, 509-520 p.Article in journal (Refereed) Published
Rationale: Patients suffering from Alzheimer's disease (AD) experience a marked reduction in cortical nicotinic acetylcholine receptors (nAChRs). In particular, selective loss of the α-sub-4β-sub-2 nAChR subtype was observed in postmortem AD brain tissue. The α-sub-4 and α-sub-7 nAChR subunits were suggested to play an important role in cognitive function. Positron emission tomography (PET) has so far been used to visualize neuronal nAChRs in vivo by 11C-nicotine binding. Objectives: To investigate the relationship between measures of cognitive function and in vivo 11C-nicotine binding in mild AD brain as assessed by PET. Materials and methods: Twenty-seven patients with mild AD were recruited in this study. A dual tracer model with administration of 1-sup-5O-water for regional cerebral blood flow and (S)(-)11C-nicotine was used to assess nicotine binding sites in the brain by PET. Cognitive function was assessed using neuropsychological tests of global cognition, episodic memory, attention, and visuospatial ability. Results: Mean cortical 11C-nicotine binding significantly correlated with the results of attention tests (r = -0.44 and p = 0.02) and Trail Making Test A (TMT-A) (r = 0.42 and p = 0.03)]. No significant correlation was observed between 11C-nicotine binding and the results of tests of episodic memory or visuospatial ability. Regional analysis showed that 11C-nicotine binding in the frontal and parietal cortex, which are the main areas for attention, correlated significantly with the Digit Symbol test and TMT-A results. Conclusion: Cortical nicotinic receptors in vivo in mild AD patients are robustly associated with the cognitive function of attention.
Place, publisher, year, edition, pages
2006. Vol. 188, no 4, 509-520 p.
PET, Alzheimer’s disease, attention, cognition, nicotine, brain, tomography
IdentifiersURN: urn:nbn:se:su:diva-19423DOI: doi:10.1007/s00213-006-0447-7OAI: oai:DiVA.org:su-19423DiVA: diva2:185947
This research was supported by the Swedish Research Council (project no. 05817), Stiftelsen for Gamla Tjanarinnor, Stohne's Foundation, and Swedish Brain Power.2007-11-122007-11-122011-01-11Bibliographically approved