Journal of Alzheimer's disease : JAD · 2024
Memory consolidation, temporal and parietal atrophy, and metabolism in amyloid-β positive and negative mild cognitive impairment.
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Keith Cierra M, Haut Marc W, Vieira Ligo Teixeira Camila, Mehta Rashi I, Phelps Holly, Ward Melanie, Miller Mark, Navia R Osvaldo, Coleman Michelle M, Marano Gary, Wang Xiaofei, Pockl Stephanie, Rajabalee Nafiisah, Scarisbrick David M, McCuddy William T, D'Haese Pierre-François, Rezai Ali, Wilhelmsen Kirk
Аннотация
BACKGROUND: Alzheimer's disease (AD) is classically characterized by alterations in memory consolidation. With the advent of diagnostic biomarkers, some patients clinically diagnosed with AD display biomarkers inconsistent with the diagnosis.
OBJECTIVE: We aimed to explore differences in memory consolidation and neurodegeneration of the temporal and parietal lobes as a function of amyloid-β status in amnestic mild cognitive impairment (aMCI).
METHODS: We examined differences in memory consolidation and neurodegeneration between patients diagnosed with amyloid-β positive aMCI (Aβ+ N = 78), amyloid-β negative aMCI (Aβ- N = 48), and healthy participants (HP; N = 41), within a well-characterized clinical cohort.
RESULTS: Aβ+ exhibited more pronounced consolidation impairments compared to Aβ-, while Aβ- faced more consolidation challenges than HP. Both Aβ+ and Aβ- were similar in hippocampal volume and entorhinal thickness, but Aβ+ had thinner inferior parietal cortex than Aβ-. Using 18F-fluoro-deoxyglucose-positron emission tomography, metabolism in both temporal and parietal regions was lower in Aβ+ relative to Aβ-.
CONCLUSIONS: These findings suggest pathologies other than AD likely contribute to memory consolidation difficulties in aMCI, and neurodegeneration of the parietal cortex in combination with hypometabolism may contribute to more pronounced consolidation problems in Aβ+.
OBJECTIVE: We aimed to explore differences in memory consolidation and neurodegeneration of the temporal and parietal lobes as a function of amyloid-β status in amnestic mild cognitive impairment (aMCI).
METHODS: We examined differences in memory consolidation and neurodegeneration between patients diagnosed with amyloid-β positive aMCI (Aβ+ N = 78), amyloid-β negative aMCI (Aβ- N = 48), and healthy participants (HP; N = 41), within a well-characterized clinical cohort.
RESULTS: Aβ+ exhibited more pronounced consolidation impairments compared to Aβ-, while Aβ- faced more consolidation challenges than HP. Both Aβ+ and Aβ- were similar in hippocampal volume and entorhinal thickness, but Aβ+ had thinner inferior parietal cortex than Aβ-. Using 18F-fluoro-deoxyglucose-positron emission tomography, metabolism in both temporal and parietal regions was lower in Aβ+ relative to Aβ-.
CONCLUSIONS: These findings suggest pathologies other than AD likely contribute to memory consolidation difficulties in aMCI, and neurodegeneration of the parietal cortex in combination with hypometabolism may contribute to more pronounced consolidation problems in Aβ+.