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Neural Correlates of Memory Encoding in Subtypes of Mild Cognitive Impairment /

  • Author(s): Clark, Lindsay R.
  • et al.
Abstract

Alzheimer's disease (AD) affects approximately 5 million adults over age 65 in the U.S. Examining brain function in individuals at risk for AD, such as those with Mild Cognitive Impairment (MCI), may improve identification of potential markers of AD prior to the onset of significant clinical symptoms, which will be important to prevention efforts and extending quality of life. Subtypes of MCI with primary memory (amnestic) or non-memory (non- amnestic) impairments may reflect different neuropathologic etiologies. However, evidence to support this notion is mixed, possibly due to a lack of comprehensive neuropsychological definitions of MCI or examination of cerebrovascular dysfunction that may contribute to cognitive decline. In the current study, functional cerebral blood flow (CBF) and blood-oxygenation level dependent (BOLD) responses were simultaneously acquired in an MRI scanner while older adults with amnestic MCI (aMCI; n = 14), non-amnestic MCI (naMCI; n = 13), and normal cognitive functioning (CN; n = 20) completed a face-name associative encoding paradigm. Region of interest analyses were conducted in the hippocampus, parahippocampal gyrus (PHG), precuneus, and anterior cingulate cortex (ACC). At rest, reduced CBF within medial temporal regions (MTL) was observed in aMCI, but there were no differences between the CN and naMCI group. During face-name encoding, the aMCI group exhibited greater percent change BOLD in the MTL, whereas the naMCI group exhibited significantly greater percent change CBF in the left precuneus. Relationships between MTL BOLD/CBF and memory performance (e.g., list learning, face-name recognition) were observed in the MCI groups only. There were no significant group differences in stroke risk, and the relationships among stroke risk, resting CBF, and CBF/ BOLD during encoding were not significant. Overall, the current findings support distinct patterns in CBF at rest and in BOLD/CBF during encoding between aMCI and naMCI groups, and suggest that these individuals - although all diagnosed with mild cognitive impairment - exhibit distinct alterations in neurovascular function that may underlie their varied cognitive deficits on neuropsychological tests and may be associated with a unique trajectory of cognitive decline. Further research using CBF/BOLD to predict disease progression in individuals with MCI may be indicated

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