title: Effects of brain amyloid deposition and reduced glucose metabolism on the default mode of brain function in normal aging.
abstract: Brain β-amyloid (Aβ) deposition during normal aging is highlighted as an initial pathogenetic event in the development of Alzheimer's disease. Many recent brain imaging studies have focused on areas deactivated during cognitive tasks [the default mode network (DMN), i.e., medial frontal gyrus/anterior cingulate cortex and precuneus/posterior cingulate cortex], where the strength of functional coordination was more or less affected by cerebral Aβ deposits. In the present positron emission tomography study, to investigate whether regional glucose metabolic alterations and Aβ deposits seen in nondemented elderly human subjects (n = 22) are of pathophysiological importance in changes of brain hemodynamic coordination in DMN during normal aging, we measured cerebral glucose metabolism with [(18)F]FDG, Aβ deposits with [(11)C]PIB, and regional cerebral blood flow during control and working memory tasks by H(2)(15)O on the same day. Data were analyzed using both region of interest and statistical parametric mapping. Our results indicated that the amount of Aβ deposits was negatively correlated with hemodynamic similarity between medial frontal and medial posterior regions, and the lower similarity was associated with poorer working memory performance. In contrast, brain glucose metabolism was not related to this medial hemodynamic similarity. These findings suggest that traceable Aβ deposition, but not glucose hypometabolism, in the brain plays an important role in occurrence of neuronal discoordination in DMN along with poor working memory in healthy elderly people.
authors.affiliation: Research Center for Child Mental Development, Graduate School of Medical Science, Kanazawa University, Kanazawa 920-8641, Japan.
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Kikuchi
authors.forename: Tetsu
authors.initials: T
authors.lastname: Hirosawa
authors.forename: Masamichi
authors.initials: M
authors.lastname: Yokokura
authors.forename: Shunsuke
authors.initials: S
authors.lastname: Yagi
authors.forename: Norio
authors.initials: N
authors.lastname: Mori
authors.forename: Etsuji
authors.initials: E
authors.lastname: Yoshikawa
authors.forename: Yujiro
authors.initials: Y
authors.lastname: Yoshihara
authors.forename: Genichi
authors.initials: G
authors.lastname: Sugihara
authors.forename: Kiyokazu
authors.initials: K
authors.lastname: Takebayashi
authors.forename: Yasuhide
authors.initials: Y
authors.lastname: Iwata
authors.forename: Katsuaki
authors.initials: K
authors.lastname: Suzuki
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Nakamura
authors.forename: Takatoshi
authors.initials: T
authors.lastname: Ueki
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Minabe
authors.forename: Yasuomi
authors.initials: Y
authors.lastname: Ouchi
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000473:pathology*; D000682:Amyloid / Q000378:metabolism*; D000704:Analysis of Variance; D000814:Aniline Compounds; D052160:Benzothiazoles; D001921:Brain / Q000098:blood supply* / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000502:physiology; D001931:Brain Mapping; D005260:Female; D019788:Fluorodeoxyglucose F18; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D007091:Image Processing, Computer-Assisted; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D008570:Memory, Short-Term / Q000502:physiology; D008875:Middle Aged; D009483:Neuropsychological Tests; D010775:Photic Stimulation / Q000379:methods; D049268:Positron-Emission Tomography / Q000379:methods; D019275:Radiopharmaceuticals; D012039:Regional Blood Flow / Q000502:physiology; D013844:Thiazoles
chemical_list: C475519:2-(4'-(methylamino)phenyl)-6-hydroxybenzothiazole; D000682:Amyloid; D000814:Aniline Compounds; D052160:Benzothiazoles; D019275:Radiopharmaceuticals; D013844:Thiazoles; D019788:Fluorodeoxyglucose F18; D005947:Glucose