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Regional Cerebral Metabolic Alterations in Dementia of the Alzheimer Type
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1983
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Alzheimer disease is the leading cause of dementia, yet its pathogenesis, physiology, diagnosis, and treatment remain poorly understood despite recent advances. The study used dynamic FDG‑PET on a Donner 280‑crystal ring to scan 10 Alzheimer patients and six healthy controls. Alzheimer patients showed significantly reduced FDG uptake in the temporoparietal cortex, indicating localized metabolic deficits, while PET provides a powerful noninvasive method to assess cerebral pathophysiology.
Alzheimer disease is the most common cause of dementia in adults. Despite recent advances in our understanding of its anatomy and chemistry, we remain largely ignorant of its pathogenesis, physiology, diagnosis, and treatment. Dynamic positron emission tomography using [18F] fluorodeoxyglucose (FDG) was performed on the Donner 280-crystal ring in 10 subjects with dementia of the Alzheimer type and six healthy age-matched controls. Ratios comparing mean counts per resolution element in frontal, temporoparietal, and entire cortex regions in brain sections 10 mm thick obtained 40–70 min following FDG injection showed relatively less FDG uptake in the temporoparietal cortex bilaterally in all the Alzheimer subjects (p < 0.01). Left-right alterations were less prominent than the anteroposterior changes. This diminished uptake was due to lowered rates of FDG use and suggests that the metabolic effects of Alzheimer disease are most concentrated in the temporoparietal cortex. Positron emission tomography is a most powerful tool for the noninvasive in vivo assessment of cerebral pathophysiology in dementia.