Longitudinal changes of cortical thickness in early- versus late-onset Alzheimer's disease

Early-onset Alzheimer's disease (EOAD) has been shown to progress more rapidly than late-onset Alzheimer's disease (LOAD). However, no studies have compared the topography of brain volume reduction over time. The purpose of this 3-year longitudinal study was to compare EOAD and LOAD in terms of their rates of decline in cognitive testing and topography of cortical thinning. We prospectively recruited 36 patients with AD (14 EOAD and 22 LOAD) and 14 normal controls. All subjects were assessed with neuropsychological tests and with magnetic resonance imaging at baseline, Year 1, and Year 3. The EOAD group showed more rapid decline than the LOAD group in attention, language, and frontal-executive tests. The EOAD group also showed more rapid cortical thinning in widespread association cortices. In contrast, the LOAD group presented more rapid cortical thinning than the EOAD group only in the left parahippocampal gyrus. Our study suggests that patients with EOAD show more rapid cortical atrophy than patients with LOAD, which accounts for faster cognitive decline on neuropsychological tests.

[1]  T J Rosen,et al.  Age at Onset and Rate of Progression of Alzheimer's Disease , 1987, Journal of the American Geriatrics Society.

[2]  M. Albert,et al.  A standardized technique for establishing onset and duration of symptoms of Alzheimer's disease. , 1995, Archives of neurology.

[3]  Julie S. Snowden,et al.  Cognitive Phenotypes in Alzheimer's Disease and Genetic Risk , 2007, Cortex.

[4]  B. O’Donnell,et al.  The prognosis in Alzheimer's disease. 'How far' rather than 'how fast' best predicts the course. , 1990, Archives of neurology.

[5]  E. Mori,et al.  Age at onset and language disturbances in Alzheimer’s disease , 1998, Neuropsychologia.

[6]  B. Seltzer,et al.  A comparison of clinical features in early- and late-onset primary degenerative dementia. One entity or two? , 1983, Archives of neurology.

[7]  H. Crystal,et al.  Rate of Progression of Alzheimer's Disease , 1989, Journal of the American Geriatrics Society.

[8]  David A Wolk,et al.  Apolipoprotein E (APOE) genotype has dissociable effects on memory and attentional–executive network function in Alzheimer’s disease , 2010, Proceedings of the National Academy of Sciences.

[9]  Janet B W Williams.  Diagnostic and Statistical Manual of Mental Disorders , 2013 .

[10]  Nick C Fox,et al.  Whole-brain atrophy rate in Alzheimer disease , 2008, Neurology.

[11]  M. Albert,et al.  Age at onset of Alzheimer's disease , 1994, Neurology.

[12]  KJ Worsley,et al.  SurfStat: A Matlab toolbox for the statistical analysis of univariate and multivariate surface and volumetric data using linear mixed effects models and random field theory , 2009, NeuroImage.

[13]  G. Frisoni,et al.  Structural correlates of early and late onset Alzheimer’s disease: voxel based morphometric study , 2004, Journal of Neurology, Neurosurgery & Psychiatry.

[14]  M. Folstein,et al.  Clinical diagnosis of Alzheimer's disease , 1984, Neurology.

[15]  Tetsuya Mori,et al.  Differences in cerebral metabolic impairment between early and late onset types of Alzheimer's disease , 2002, Journal of the Neurological Sciences.

[16]  Karl J. Friston,et al.  A unified statistical approach for determining significant signals in images of cerebral activation , 1996, Human brain mapping.

[17]  K. Ishii,et al.  Voxel-based morphometric comparison between early- and late-onset mild Alzheimer's disease and assessment of diagnostic performance of z score images. , 2005, AJNR. American journal of neuroradiology.

[18]  S. Cappa,et al.  Neuropsychological heterogeneity in mild Alzheimer's disease. , 1993, Dementia.

[19]  L. Gwyther,et al.  Early‐onset Alzheimer's disease , 1987, Neurology.

[20]  Sue J. Kang,et al.  Glucose metabolism in early onset versus late onset Alzheimer's disease: an SPM analysis of 120 patients. , 2005, Brain : a journal of neurology.

[21]  Sang Won Seo,et al.  Effects of demographic factors on cortical thickness in Alzheimer's disease , 2011, Neurobiology of Aging.

[22]  A. Alavi,et al.  MR signal abnormalities at 1.5 T in Alzheimer's dementia and normal aging. , 1987, AJR. American journal of roentgenology.

[23]  C. Pozzilli,et al.  Factors affecting course and survival in Alzheimer's disease. A 9-year longitudinal study. , 1994, Archives of neurology.

[24]  B. Hyman,et al.  The impact of different presenilin 1 andpresenilin 2 mutations on amyloid deposition, neurofibrillary changes and neuronal loss in the familial Alzheimer's disease brain: evidence for other phenotype-modifying factors. , 1999, Brain : a journal of neurology.

[25]  Alan C. Evans,et al.  Cortical thickness analysis examined through power analysis and a population simulation , 2005, NeuroImage.

[26]  Sang Won Seo,et al.  Seoul Neuropsychological Screening Battery-Dementia Version (SNSB-D): A Useful Tool for Assessing and Monitoring Cognitive Impairments in Dementia Patients , 2010, Journal of Korean medical science.

[27]  Kiralee M. Hayashi,et al.  The topography of grey matter involvement in early and late onset Alzheimer's disease. , 2007, Brain : a journal of neurology.

[28]  C. Holmes,et al.  Alzheimer’s disease: differences in technetium-99m HMPAO SPECT scan findings between early onset and late onset dementia , 2003, Journal of neurology, neurosurgery, and psychiatry.

[29]  Wiesje M van der Flier,et al.  Early-versus late-onset Alzheimer's disease: more than age alone. , 2010, Journal of Alzheimer's disease : JAD.

[30]  Nick C Fox,et al.  Change in rates of cerebral atrophy over time in early-onset Alzheimer's disease: longitudinal MRI study , 2003, The Lancet.

[31]  E. Mori,et al.  Age at Onset and Visuocognitive Disturbances in Alzheimer Disease , 1998, Alzheimer disease and associated disorders.

[32]  K Herholz,et al.  Metabolic interaction between ApoE genotype and onset age in Alzheimer’s disease: implications for brain reserve , 2004, Journal of Neurology, Neurosurgery & Psychiatry.

[33]  E. Rogaeva.  The solved and unsolved mysteries of the genetics of early-onset Alzheimer’s disease , 2007, NeuroMolecular Medicine.

[34]  Emma J. Burton,et al.  A comprehensive study of gray matter loss in patients with Alzheimer’s disease using optimized voxel-based morphometry , 2003, NeuroImage.

[35]  R P Lesser,et al.  Basal temporal language area demonstrated by electrical stimulation , 1986, Neurology.

[36]  R. Mohs,et al.  Clinical and neuropsychological differences between patients with earlier and later onset of Alzheimer's disease , 1996, Neurology.