Abstract

We investigated the relationship between hippocampal subfield volumes and cortical amyloid-beta (Aβ) deposition in Alzheimer’s disease (AD). Fifty participants (11 cognitively unimpaired [CU], 10 with mild cognitive impairment [MCI], and 29 with AD) who underwent 18F-florbetaben positron emission tomography, magnetic resonance imaging, and neuropsychological tests were enrolled. The hippocampal subfield volumes were obtained using an automated brain volumetry system with the Winterburn atlas and were compared among the diagnostic groups, and the correlations with the Aβ deposition and AD risk factors were determined. Patients with MCI and AD showed decreased volume in the stratum radiatum/lacunosum/moleculare (SRLM) of the cornu ammonis (CA)1 and CA4-dentate gyrus (DG) compared with the CU. Decreased SRLM and CA4-DG volumes were associated with an increased Aβ deposition in the global cortex (R = −0.459, p = 0.001; R = −0.393, p = 0.005, respectively). The SRLM and CA4-DG volumes aided in the distinction of AD from CU (areas under the receiver operating characteristic [AUROC] curve = 0.994 and 0.981, respectively, p < 0.001), and Aβ+ from Aβ− individuals (AUROC curve = 0.949 and 0.958, respectively, p < 0.001). Hippocampal subfield volumes demonstrated potential as imaging biomarkers in the diagnosis and detection of AD and Aβ deposition, respectively.

Highlights

  • APOE ε4 carriers were more frequent in patients with Alzheimer’s disease (AD) and mild cognitive impairment (MCI) than in cognitively unimpaired (CU) individuals

  • standardized uptake value ratio (SUVR) for 18 F-florbetaben in the global cortex was greater in patients with AD and MCI than in the CU individuals

  • Our study suggests that the stratum radiatum/lacunosum/moleculare (SRLM) and CA4-dentate gyrus (DG) are specific hippocampal subfields that are associated with cortical Aβ deposition

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Summary

Introduction

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. The hippocampus plays a critical role in episodic and long-term memory through its extensive afferent and efferent connections with the cortical and subcortical structures [1,2]. Atrophy of the hippocampus is reportedly related to the clinical severity and progression of Alzheimer’s disease (AD), which typically presents as severe progressive memory impairment [3–5]. Hippocampal atrophy visualized using structural imaging has been used as one of the in vivo neuroimaging biomarkers in AD, together with the hallmark pathologic biomarkers, such as amyloid-beta (Aβ) and tau proteins [6,7]

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