Failure to modulate neural response to increased task demand in mild Alzheimer's disease: fMRI study of visuospatial processing
2008 (English)In: Neurobiology of Disease, ISSN 0969-9961, Vol. 31, no 3, 287-297 p.Article in journal (Refereed) Published
Alzheimer's disease (AD) is characterized by disturbances of visuospatial cognition. Given that these impairments are closely related to metabolic and neuropathological changes, our study aimed to investigate the functional competency of brain regions in the visuospatial networks responsible for early clinical symptoms in AD using event-related functional magnetic resonance imaging (fMRI). Participants (13AD patients with mild symptoms and 13 age- and education-matched controls) performed an angle discrimination task with varying task demand. Using a novel approach that modeled the dependency of the blood oxygenation level-dependent (BOLD) signal on the subject's reaction time allowed us to investigate task demand-dependent signal changes between the groups. Both groups demonstrated overlapping neural networks engaged in angle discrimination, including the parieto-occipital and frontal regions. In several network regions, AD patients showed a significantly weaker and sometimes no BOLD signal due to increased task demand compared with controls, demonstrating failure to modulate the neural response to increased task demand. A general task demand-independent increase of activation in AD patients compared with controls was found in right middle temporal gyrus. This latter finding may indicate an attempt to compensate for dysfunctional areas in the dorsal visual pathway. These results confirm deficits in visuospatial abilities, which occur early in AD, and offer new insights into the neural mechanisms underlying this impairment.
Place, publisher, year, edition, pages
2008. Vol. 31, no 3, 287-297 p.
neurodegenerative disease, behavior, reaction time, parametric design, neuroimaging, dorsal stream
IdentifiersURN: urn:nbn:se:su:diva-17363DOI: doi:10.1016/j.nbd.2008.04.013ISI: 000258862000001PubMedID: 18619845OAI: oai:DiVA.org:su-17363DiVA: diva2:183884
This work was supported by the Swedish Brain Power, the Swedish Research Council (O.A.), the Ragnhild och Einar Lundströms Minne, Stockholm Odd Fellow Logers Minnes och Hyllningsfond, the Lions Club International, the Gun and Bertil Stohnes Foundation, the Foundation for Gamla Tjänarinnor, and the Swedish Dementia Foundation (to P.V).2009-01-142009-01-142011-01-10Bibliographically approved