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Dementia, asymmetry of temporal lobe structures, and Apolipoprotein E genotype: Relationships to cerebral atrophy and neuropsychological impairment

Published online by Cambridge University Press:  13 November 2002

ERIN D. BIGLER
Affiliation:
Departments of Psychology and Neuroscience, Brigham Young University, Provo, Utah Departments of Psychiatry and Radiology, University of Utah, Salt Lake City, Utah
DAVID F. TATE
Affiliation:
Departments of Psychology and Neuroscience, Brigham Young University, Provo, Utah
MICHAEL J. MILLER
Affiliation:
Departments of Psychology and Neuroscience, Brigham Young University, Provo, Utah
SARA A. RICE
Affiliation:
Departments of Psychology and Neuroscience, Brigham Young University, Provo, Utah
CORY D. HESSEL
Affiliation:
Departments of Psychology and Neuroscience, Brigham Young University, Provo, Utah
HEATH D. EARL
Affiliation:
Departments of Psychology and Neuroscience, Brigham Young University, Provo, Utah
JOANN T. TSCHANZ
Affiliation:
Department of Psychology, Utah State University, Logan, Utah
BRENDA PLASSMAN
Affiliation:
Department of Psychiatry, Duke University, Durham, North Carolina
KATHLEEN A. WELSH-BOHMER
Affiliation:
Department of Psychiatry, Duke University, Durham, North Carolina

Abstract

We examined asymmetry of hippocampal volume as well as other temporal lobe structures (temporal lobe, temporal horn of the lateral ventricular system, parahippocampal and fusiform gyri) in 194 subjects from the Cache County, Utah study, with varying disorders [85 with Alzheimer's disease (AD), 59 with some cognitive or neuropsychiatric disorder—referenced as a Mixed Neuropsychiatric group, 30 with mild ambiguous/mild cognitive impairment (MA/MCI) and 20 controls] and APOE genotypes. Asymmetry was determined by subtracting left-side volume from the right corrected by total intracranial volume. No significant asymmetry was observed to be associated with presence of the ε4 allele. Since the AD-ε4 allele risk effect may be expressed early in the course of the disorder, we also examined asymmetry indices in AD, MA/MCI and Mixed Neuropsychiatric subjects early in the course of their disorder (2 years or less) to those with longer duration illness (greater than 2 years). We observed a leftward asymmetry (i.e., left side larger) regardless of APOE genotype in hippocampal volume where both AD and MCI subjects demonstrated a leftward shift in hippocampal size when length of disease (LOD) was less but not more than 2 years. Leftward asymmetry was not associated with LOD in the Mixed Neuropsychiatric group. These findings do not support an association between ε4 and hippocampal asymmetry in dementia. We also examined whether asymmetry influenced neuropsychological performance, but minimal effects were observed. Where significance or strong trends were observed, better neuropsychological performance was associated with larger parenchymal volume of temporal lobe structures. These findings were interpreted as representing cognitive reserve effects where larger volume was protective against impairment. The role of asymmetry research in understanding neuropsychological performance in dementia is discussed. (JINS, 2002, 8, 925–933.)

Type
Research Article
Copyright
© 2002 The International Neuropsychological Society

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