Regular paperCognition, glucose metabolism and amyloid burden in Alzheimer's disease
Section snippets
Subject selection
Patients were recruited from an AD research cohort followed at the University of California, San Francisco Memory and Aging Center (UCSF-MAC). The clinical evaluation included a history and physical examination by a neurologist, a structured caregiver interview administered by a nurse, and a comprehensive battery of neuropsychological tests (Kramer et al., 2003). Clinical diagnoses were assigned by consensus at a multidisciplinary conference using standard research criteria (McKhann et al., 1984
Results
The patient cohort consisted of 39 AD patients (24 males) with a mean age of 68.3 ± 10.5 and 16.8 ± 2.8 years of education. Patients' mean scores for MMSE and CDRSB were 21.8 ± 5.7 and 5.5 ± 3.0, respectively. CDRSB data were only available for 34 patients. The cohort had an estimated average disease duration of 5.4 ± 2.8 years (Table 1) and a mean global PIB uptake of 1.67 with a range of 0.92–2.33.
Separate voxel-wise multiple regressions of FDG uptake with each of the cognitive/functional
Discussion
This study investigated in vivo relationships between Aβ plaque load, dementia severity and glucose metabolism in a cohort of 39 patients with probable AD. Consistent with the existing literature, we found cognitive decline to be strongly associated with decreased glucose metabolism in frontal and temporo-parietal regions (Heiss et al., 1991a, Heiss et al., 1991b, Herholz et al., 2002, Langbaum et al., 2009, Mielke et al., 1994, Minoshima et al., 1995b). The observed effects were not driven by
Disclosure statement
The authors have nothing to disclose.
Acknowledgements
This work was supported by National Institute on Aging grants NIA K23-AG031861 (GDR), NIA AG027859 (WJJ), NIA P01-AG1972403 and P50-AG023501 (BLM), Alzheimer's Association NIRG-07-59422 (GDR) and ZEN-08-87090 (WJJ), John Douglas French Alzheimer's Foundation (GDR).
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