Medial temporal lobe function and structure in mild cognitive impairment
Functional magnetic resonance imaging (fMRI) was used to study memory‐associated activation of medial temporal lobe (MTL) regions in 32 nondemented elderly individuals with mild cognitive impairment (MCI). Subjects performed a visual encoding task during fMRI scanning and were tested for recognition...
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| Published in | Annals of neurology Vol. 56; no. 1; pp. 27 - 35 |
|---|---|
| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.07.2004
Willey-Liss |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Functional magnetic resonance imaging (fMRI) was used to study memory‐associated activation of medial temporal lobe (MTL) regions in 32 nondemented elderly individuals with mild cognitive impairment (MCI). Subjects performed a visual encoding task during fMRI scanning and were tested for recognition of stimuli afterward. MTL regions of interest were identified from each individual's structural MRI, and activation was quantified within each region. Greater extent of activation within the hippocampal formation and parahippocampal gyrus (PHG) was correlated with better memory performance. There was, however, a paradoxical relationship between extent of activation and clinical status at both baseline and follow‐up evaluations. Subjects with greater clinical impairment, based on the Clinical Dementia Rating Sum of Boxes, recruited a larger extent of the right PHG during encoding, even after accounting for atrophy. Moreover, those who subsequently declined over the 2.5 years of clinical follow‐up (44% of the subjects) activated a significantly greater extent of the right PHG during encoding, despite equivalent memory performance. We hypothesize that increased activation in MTL regions reflects a compensatory response to accumulating AD pathology and may serve as a marker for impending clinical decline. Ann Neurol 2004;56:27–35 |
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| AbstractList | Functional magnetic resonance imaging (fMRI) was used to study memory-associated activation of medial temporal lobe (MTL) regions in 32 nondemented elderly individuals with mild cognitive impairment (MCI). Subjects performed a visual encoding task during fMRI scanning and were tested for recognition of stimuli afterward. MTL regions of interest were identified from each individual's structural MRI, and activation was quantified within each region. Greater extent of activation within the hippocampal formation and parahippocampal gyrus (PHG) was correlated with better memory performance. There was, however, a paradoxical relationship between extent of activation and clinical status at both baseline and follow-up evaluations. Subjects with greater clinical impairment, based on the Clinical Dementia Rating Sum of Boxes, recruited a larger extent of the right PHG during encoding, even after accounting for atrophy. Moreover, those who subsequently declined over the 2.5 years of clinical follow-up (44% of the subjects) activated a significantly greater extent of the right PHG during encoding, despite equivalent memory performance. We hypothesize that increased activation in MTL regions reflects a compensatory response to accumulating AD pathology and may serve as a marker for impending clinical decline. Functional magnetic resonance imaging (fMRI) was used to study memory-associated activation of medial temporal lobe (MTL) regions in 32 nondemented elderly individuals with mild cognitive impairment (MCI). Subjects performed a visual encoding task during fMRI scanning and were tested for recognition of stimuli afterward. MTL regions of interest were identified from each individual's structural MRI, and activation was quantified within each region. Greater extent of activation within the hippocampal formation and parahippocampal gyrus (PHG) was correlated with better memory performance. There was, however, a paradoxical relationship between extent of activation and clinical status at both baseline and follow-up evaluations. Subjects with greater clinical impairment, based on the Clinical Dementia Rating Sum of Boxes, recruited a larger extent of the right PHG during encoding, even after accounting for atrophy. Moreover, those who subsequently declined over the 2.5 years of clinical follow-up (44% of the subjects) activated a significantly greater extent of the right PHG during encoding, despite equivalent memory performance. We hypothesize that increased activation in MTL regions reflects a compensatory response to accumulating AD pathology and may serve as a marker for impending clinical decline.Functional magnetic resonance imaging (fMRI) was used to study memory-associated activation of medial temporal lobe (MTL) regions in 32 nondemented elderly individuals with mild cognitive impairment (MCI). Subjects performed a visual encoding task during fMRI scanning and were tested for recognition of stimuli afterward. MTL regions of interest were identified from each individual's structural MRI, and activation was quantified within each region. Greater extent of activation within the hippocampal formation and parahippocampal gyrus (PHG) was correlated with better memory performance. There was, however, a paradoxical relationship between extent of activation and clinical status at both baseline and follow-up evaluations. Subjects with greater clinical impairment, based on the Clinical Dementia Rating Sum of Boxes, recruited a larger extent of the right PHG during encoding, even after accounting for atrophy. Moreover, those who subsequently declined over the 2.5 years of clinical follow-up (44% of the subjects) activated a significantly greater extent of the right PHG during encoding, despite equivalent memory performance. We hypothesize that increased activation in MTL regions reflects a compensatory response to accumulating AD pathology and may serve as a marker for impending clinical decline. Functional magnetic resonance imaging (fMRI) was used to study memory‐associated activation of medial temporal lobe (MTL) regions in 32 nondemented elderly individuals with mild cognitive impairment (MCI). Subjects performed a visual encoding task during fMRI scanning and were tested for recognition of stimuli afterward. MTL regions of interest were identified from each individual's structural MRI, and activation was quantified within each region. Greater extent of activation within the hippocampal formation and parahippocampal gyrus (PHG) was correlated with better memory performance. There was, however, a paradoxical relationship between extent of activation and clinical status at both baseline and follow‐up evaluations. Subjects with greater clinical impairment, based on the Clinical Dementia Rating Sum of Boxes, recruited a larger extent of the right PHG during encoding, even after accounting for atrophy. Moreover, those who subsequently declined over the 2.5 years of clinical follow‐up (44% of the subjects) activated a significantly greater extent of the right PHG during encoding, despite equivalent memory performance. We hypothesize that increased activation in MTL regions reflects a compensatory response to accumulating AD pathology and may serve as a marker for impending clinical decline. Ann Neurol 2004;56:27–35 |
| Author | Atiya, Monika Greve, Douglas N. Albert, Marilyn S. Sperling, Reisa A. Salat, David H. Bates, Julianna F. Dale, Anders M. Blacker, Deborah Killiany, Ronald J. Dickerson, Bradford C. Stern, Chantal E. |
| AuthorAffiliation | 4 Harvard Medical School, Boston, MA 5 Department of Radiology, Massachusetts General Hospital, Charlestown, MA 6 Department of Psychiatry, Massachusetts General Hospital, Charlestown, MA 7 Max Planck Institute for Psychiatry, Munich, Germany 8 Departments of Anatomy and Neurobiology, Boston University of Medicine 10 Department of Neurology, Division of Cognitive Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 2 Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA 9 Center for Memory and Brain, Boston University, Boston, MA 3 Department of Neurology, Brigham and Women’s Hospital 1 Department of Neurology, Massachusetts General Hospital |
| AuthorAffiliation_xml | – name: 7 Max Planck Institute for Psychiatry, Munich, Germany – name: 9 Center for Memory and Brain, Boston University, Boston, MA – name: 1 Department of Neurology, Massachusetts General Hospital – name: 2 Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA – name: 6 Department of Psychiatry, Massachusetts General Hospital, Charlestown, MA – name: 5 Department of Radiology, Massachusetts General Hospital, Charlestown, MA – name: 8 Departments of Anatomy and Neurobiology, Boston University of Medicine – name: 3 Department of Neurology, Brigham and Women’s Hospital – name: 4 Harvard Medical School, Boston, MA – name: 10 Department of Neurology, Division of Cognitive Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD |
| Author_xml | – sequence: 1 givenname: Bradford C. surname: Dickerson fullname: Dickerson, Bradford C. email: bradd@nmr.mgh.harvard.edu organization: Department of Neurology, Massachusetts General Hospital – sequence: 2 givenname: David H. surname: Salat fullname: Salat, David H. organization: Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA – sequence: 3 givenname: Julianna F. surname: Bates fullname: Bates, Julianna F. organization: Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA – sequence: 4 givenname: Monika surname: Atiya fullname: Atiya, Monika organization: Department of Psychiatry, Massachusetts General Hospital, Charlestown, MA – sequence: 5 givenname: Ronald J. surname: Killiany fullname: Killiany, Ronald J. organization: Departments of Anatomy and Neurobiology, Boston University of Medicine – sequence: 6 givenname: Douglas N. surname: Greve fullname: Greve, Douglas N. organization: Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA – sequence: 7 givenname: Anders M. surname: Dale fullname: Dale, Anders M. organization: Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA – sequence: 8 givenname: Chantal E. surname: Stern fullname: Stern, Chantal E. organization: Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA – sequence: 9 givenname: Deborah surname: Blacker fullname: Blacker, Deborah organization: Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA – sequence: 10 givenname: Marilyn S. surname: Albert fullname: Albert, Marilyn S. organization: Department of Neurology, Massachusetts General Hospital – sequence: 11 givenname: Reisa A. surname: Sperling fullname: Sperling, Reisa A. organization: Department of Neurology, Massachusetts General Hospital |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15918156$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/15236399$$D View this record in MEDLINE/PubMed |
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| CODEN | ANNED3 |
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| SubjectTerms | Aged Aged, 80 and over Alzheimer Disease - pathology Alzheimer Disease - physiopathology Biological and medical sciences Cognition Disorders - diagnosis Cognition Disorders - pathology Cognition Disorders - physiopathology Disease Progression Female Hippocampus - anatomy & histology Hippocampus - physiology Humans Magnetic Resonance Imaging Male Medical sciences Memory - physiology Neurology Neuropsychological Tests Pattern Recognition, Visual Temporal Lobe - pathology Temporal Lobe - physiology |
| Title | Medial temporal lobe function and structure in mild cognitive impairment |
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