Diminution of context association memory structure in subjects with subjective cognitive decline
Alzheimer's disease (AD) progresses insidiously from the preclinical stage to dementia. While people with subjective cognitive decline (SCD) have normal cognitive performance, some may be in the preclinical stage of AD. Neurofibrillary tangles appear first in the transentorhinal cortex, followe...
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Published in | Human brain mapping Vol. 39; no. 6; pp. 2549 - 2562 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
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United States
John Wiley & Sons, Inc
01.06.2018
John Wiley and Sons Inc |
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Abstract | Alzheimer's disease (AD) progresses insidiously from the preclinical stage to dementia. While people with subjective cognitive decline (SCD) have normal cognitive performance, some may be in the preclinical stage of AD. Neurofibrillary tangles appear first in the transentorhinal cortex, followed by the entorhinal cortex in the clinically silent stage of AD. We expected the earliest changes in subjects with SCD to occur in medial temporal subfields other than the hippocampal proper. These selective structural changes would affect specific memory subcomponents. We used the Family Picture subtest of the Wechsler Memory Scale‐III, which was modified to separately compute character, activity, and location subscores for episodic memory subcomponents. We recruited 43 subjects with SCD, 44 subjects with amnesic mild cognitive impairment, and 34 normal controls. MRI was used to assess cortical thickness, subcortical gray matter volume, and fractional anisotropy. The results demonstrated that SCD subjects showed significant cortical atrophy in their bilateral parahippocampus and perirhinal and the left entorhinal cortices but not in their hippocampal regions. SCD subjects also exhibited significantly decreased mean fractional anisotropy in their bilateral uncinate fasciculi. The diminution of cortical thickness over the mesial temporal subfields corresponded to brain areas with early tangle deposition, and early degradation of the uncinate fasciculus was in accordance with the retrogenesis hypothesis. The parahippocampus and perirhinal cortex contribute mainly to context association memory while the entorhinal cortex, along with the uncinate fasciculus, contributes to content‐related contextual memory. We proposed that context association and related memory structures are vulnerable in the SCD stage. |
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AbstractList | Alzheimer's disease (AD) progresses insidiously from the preclinical stage to dementia. While people with subjective cognitive decline (SCD) have normal cognitive performance, some may be in the preclinical stage of AD. Neurofibrillary tangles appear first in the transentorhinal cortex, followed by the entorhinal cortex in the clinically silent stage of AD. We expected the earliest changes in subjects with SCD to occur in medial temporal subfields other than the hippocampal proper. These selective structural changes would affect specific memory subcomponents. We used the Family Picture subtest of the Wechsler Memory Scale-III, which was modified to separately compute character, activity, and location subscores for episodic memory subcomponents. We recruited 43 subjects with SCD, 44 subjects with amnesic mild cognitive impairment, and 34 normal controls. MRI was used to assess cortical thickness, subcortical gray matter volume, and fractional anisotropy. The results demonstrated that SCD subjects showed significant cortical atrophy in their bilateral parahippocampus and perirhinal and the left entorhinal cortices but not in their hippocampal regions. SCD subjects also exhibited significantly decreased mean fractional anisotropy in their bilateral uncinate fasciculi. The diminution of cortical thickness over the mesial temporal subfields corresponded to brain areas with early tangle deposition, and early degradation of the uncinate fasciculus was in accordance with the retrogenesis hypothesis. The parahippocampus and perirhinal cortex contribute mainly to context association memory while the entorhinal cortex, along with the uncinate fasciculus, contributes to content-related contextual memory. We proposed that context association and related memory structures are vulnerable in the SCD stage.Alzheimer's disease (AD) progresses insidiously from the preclinical stage to dementia. While people with subjective cognitive decline (SCD) have normal cognitive performance, some may be in the preclinical stage of AD. Neurofibrillary tangles appear first in the transentorhinal cortex, followed by the entorhinal cortex in the clinically silent stage of AD. We expected the earliest changes in subjects with SCD to occur in medial temporal subfields other than the hippocampal proper. These selective structural changes would affect specific memory subcomponents. We used the Family Picture subtest of the Wechsler Memory Scale-III, which was modified to separately compute character, activity, and location subscores for episodic memory subcomponents. We recruited 43 subjects with SCD, 44 subjects with amnesic mild cognitive impairment, and 34 normal controls. MRI was used to assess cortical thickness, subcortical gray matter volume, and fractional anisotropy. The results demonstrated that SCD subjects showed significant cortical atrophy in their bilateral parahippocampus and perirhinal and the left entorhinal cortices but not in their hippocampal regions. SCD subjects also exhibited significantly decreased mean fractional anisotropy in their bilateral uncinate fasciculi. The diminution of cortical thickness over the mesial temporal subfields corresponded to brain areas with early tangle deposition, and early degradation of the uncinate fasciculus was in accordance with the retrogenesis hypothesis. The parahippocampus and perirhinal cortex contribute mainly to context association memory while the entorhinal cortex, along with the uncinate fasciculus, contributes to content-related contextual memory. We proposed that context association and related memory structures are vulnerable in the SCD stage. Alzheimer's disease (AD) progresses insidiously from the preclinical stage to dementia. While people with subjective cognitive decline (SCD) have normal cognitive performance, some may be in the preclinical stage of AD. Neurofibrillary tangles appear first in the transentorhinal cortex, followed by the entorhinal cortex in the clinically silent stage of AD. We expected the earliest changes in subjects with SCD to occur in medial temporal subfields other than the hippocampal proper. These selective structural changes would affect specific memory subcomponents. We used the Family Picture subtest of the Wechsler Memory Scale‐III, which was modified to separately compute character, activity, and location subscores for episodic memory subcomponents. We recruited 43 subjects with SCD, 44 subjects with amnesic mild cognitive impairment, and 34 normal controls. MRI was used to assess cortical thickness, subcortical gray matter volume, and fractional anisotropy. The results demonstrated that SCD subjects showed significant cortical atrophy in their bilateral parahippocampus and perirhinal and the left entorhinal cortices but not in their hippocampal regions. SCD subjects also exhibited significantly decreased mean fractional anisotropy in their bilateral uncinate fasciculi. The diminution of cortical thickness over the mesial temporal subfields corresponded to brain areas with early tangle deposition, and early degradation of the uncinate fasciculus was in accordance with the retrogenesis hypothesis. The parahippocampus and perirhinal cortex contribute mainly to context association memory while the entorhinal cortex, along with the uncinate fasciculus, contributes to content‐related contextual memory. We proposed that context association and related memory structures are vulnerable in the SCD stage. |
Author | Chen, Pin‐Yu Lai, Ya‐Mei Chen, Ya‐Fang Chiu, Ming‐Jang Chen, Ta‐Fu Huang, Kuo‐Zhou Hua, Mau‐Sun Hsu, Yung‐Chin Tseng, Wen‐Yi Isaac Fan, Ling‐Yun Cheng, Ting‐Wen |
AuthorAffiliation | 6 Department of Psychology Asia University Taichung Taiwan 5 Department of Medical Imaging National Taiwan University Hospital, College of Medicine, National Taiwan University Taipei Taiwan 7 Department of Psychology, College of Science National Taiwan University Taipei Taiwan 3 Center for Clinical Psychology, National Taiwan University Hospital Taipei Taiwan 4 Graduate Institute of Medical Device and Imaging, College of Medicine, National Taiwan University Taipei Taiwan 1 Graduate Institute of Brain and Mind Sciences, College of Medicine, National Taiwan University Taipei Taiwan 2 Department of Neurology National Taiwan University Hospital, College of Medicine, National Taiwan University Taipei Taiwan 8 Graduate Institute of Biomedical Engineering and Bioinformatics National Taiwan University Taipei Taiwan |
AuthorAffiliation_xml | – name: 4 Graduate Institute of Medical Device and Imaging, College of Medicine, National Taiwan University Taipei Taiwan – name: 2 Department of Neurology National Taiwan University Hospital, College of Medicine, National Taiwan University Taipei Taiwan – name: 7 Department of Psychology, College of Science National Taiwan University Taipei Taiwan – name: 1 Graduate Institute of Brain and Mind Sciences, College of Medicine, National Taiwan University Taipei Taiwan – name: 3 Center for Clinical Psychology, National Taiwan University Hospital Taipei Taiwan – name: 5 Department of Medical Imaging National Taiwan University Hospital, College of Medicine, National Taiwan University Taipei Taiwan – name: 8 Graduate Institute of Biomedical Engineering and Bioinformatics National Taiwan University Taipei Taiwan – name: 6 Department of Psychology Asia University Taichung Taiwan |
Author_xml | – sequence: 1 givenname: Ling‐Yun surname: Fan fullname: Fan, Ling‐Yun organization: National Taiwan University Hospital, College of Medicine, National Taiwan University – sequence: 2 givenname: Ya‐Mei surname: Lai fullname: Lai, Ya‐Mei organization: Center for Clinical Psychology, National Taiwan University Hospital – sequence: 3 givenname: Ta‐Fu surname: Chen fullname: Chen, Ta‐Fu organization: National Taiwan University Hospital, College of Medicine, National Taiwan University – sequence: 4 givenname: Yung‐Chin surname: Hsu fullname: Hsu, Yung‐Chin organization: Graduate Institute of Medical Device and Imaging, College of Medicine, National Taiwan University – sequence: 5 givenname: Pin‐Yu surname: Chen fullname: Chen, Pin‐Yu organization: Graduate Institute of Medical Device and Imaging, College of Medicine, National Taiwan University – sequence: 6 givenname: Kuo‐Zhou surname: Huang fullname: Huang, Kuo‐Zhou organization: National Taiwan University Hospital, College of Medicine, National Taiwan University – sequence: 7 givenname: Ting‐Wen surname: Cheng fullname: Cheng, Ting‐Wen organization: National Taiwan University Hospital, College of Medicine, National Taiwan University – sequence: 8 givenname: Wen‐Yi Isaac orcidid: 0000-0002-2314-6868 surname: Tseng fullname: Tseng, Wen‐Yi Isaac organization: National Taiwan University Hospital, College of Medicine, National Taiwan University – sequence: 9 givenname: Mau‐Sun surname: Hua fullname: Hua, Mau‐Sun organization: National Taiwan University – sequence: 10 givenname: Ya‐Fang surname: Chen fullname: Chen, Ya‐Fang email: joannayfc@gmail.com organization: National Taiwan University Hospital, College of Medicine, National Taiwan University – sequence: 11 givenname: Ming‐Jang orcidid: 0000-0002-4158-4423 surname: Chiu fullname: Chiu, Ming‐Jang email: mjchiu@ntu.edu.tw organization: National Taiwan University |
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Keywords | uncinate fasciculus subjective cognitive decline cortical thickness parahippocampus context memory entorhinal cortex perirhinal cortex |
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Notes | Funding information Ministry of Science and Technology, Taiwan, Grant/Award Number: 105‐2314‐B‐002039; National Health Research Institutes, Taiwan, Grant/Award Number: 05A1‐PHSP03‐028; National Taiwan University, Grant/Award Number: 105R8954‐2 Ya‐Mei Lai and Ta‐Fu Chen contributed equally to this work. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Funding information Ministry of Science and Technology, Taiwan, Grant/Award Number: 105‐2314‐B‐002039; National Health Research Institutes, Taiwan, Grant/Award Number: 05A1‐PHSP03‐028; National Taiwan University, Grant/Award Number: 105R8954‐2 |
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Snippet | Alzheimer's disease (AD) progresses insidiously from the preclinical stage to dementia. While people with subjective cognitive decline (SCD) have normal... |
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SubjectTerms | Aged Aged, 80 and over Alzheimer's disease Analysis of Variance Anisotropy Atrophy Atrophy - pathology Brain Brain - diagnostic imaging Brain - physiopathology Brain Mapping Case-Control Studies Cognitive ability Cognitive Dysfunction - complications Cognitive Dysfunction - diagnostic imaging Cognitive tasks Computer memory context memory Cortex (entorhinal) Cortex (perirhinal) Cortex (temporal) cortical thickness Decision Making, Computer-Assisted Dementia disorders Disease Progression entorhinal cortex Female Hippocampus Humans Magnetic Resonance Imaging Male Memory Memory Disorders - diagnostic imaging Memory Disorders - etiology Memory, Episodic Middle Aged Neurodegenerative diseases Neurofibrillary tangles Neuropsychological Tests Parahippocampal gyrus parahippocampus perirhinal cortex Regression Analysis Retrospective Studies subjective cognitive decline Substantia grisea uncinate fasciculus White Matter - diagnostic imaging White Matter - pathology |
Title | Diminution of context association memory structure in subjects with subjective cognitive decline |
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