Hippocampal formation alterations differently contribute to autobiographic memory deficits in mild cognitive impairment and Alzheimer's disease. Issue 6 (4th April 2017)

• Record Type: Journal Article
• Authors: Hirjak, Dusan; Wolf, Robert C.; Remmele, Barbara; Seidl, Ulrich; Thomann, Anne K.; Kubera, Katharina M.; Schröder, Johannes; Maier‐Hein, Klaus H.; Thomann, Philipp A.
• Is Part Of: Hippocampus. Volume 27:Issue 6(2017)
• Page Start: 702
• Page End: 715
• Publication Date: 2017-04-04
• Subjects: Alzheimer's disease -- autobiographical memory -- Freesurfer -- hippocampus -- mild cognitive impairment -- MRI; Hippocampus (Brain) -- Periodicals; 612.825
• DOI: 10.1002/hipo.22726
• Languages: English
• ISSNs: 1050-9631

Abstract

Abstract: Autobiographical memory (AM) is part of declarative memory and includes both semantic and episodic aspects. AM deficits are among the major complaints of patients with Alzheimer's disease (AD) even in early or preclinical stages. Previous MRI studies in AD patients have showed that deficits in semantic and episodic AM are associated with hippocampal alterations. However, the question which specific hippocampal subfields and adjacent extrahippocampal structures contribute to deficits of AM in individuals with mild cognitive impairment (MCI) and AD patients has not been investigated so far. Hundred and seven participants (38 AD patients, 38 MCI individuals and 31 healthy controls [HC]) underwent MRI at 3 Tesla. AM was assessed with a semi‐structured interview (E‐AGI). FreeSurfer 5.3 was used for hippocampal parcellation. Semantic and episodic AM scores were related to the volume of 5 hippocampal subfields and cortical thickness in the parahippocampal and entorhinal cortex. Both semantic and episodic AM deficits were associated with bilateral hippocampal alterations. These associations referred mainly to CA1, CA2‐3, presubiculum, and subiculum atrophy. Episodic, but not semantic AM loss was associated with cortical thickness reduction of the bilateral parahippocampal and enthorinal cortex. In MCI individuals, episodic, but not semantic AM deficits were associated with alterations of the CA1, presubiculum and subiculum. Our findings support the crucial role of CA1, presubiculum, and subiculum in episodic memory. The present results implicate that in MCI individuals, semantic and episodic AM deficits are subserved by distinct neuronal systems.