Abstract
The density of Lewy bodies or the concurrent β-amyloid pathology would act as modulators in the relative timing of dementia during the course of Parkinson’s disease. Depending on the temporal relationship between the onset of parkinsonism and that of cognitive impairment, patients with Parkinson’s disease with mild cognitive impairment were divided into two groups of earlier (<1 year) and later (≥1 year) cognitive decline, and cortical atrophy patterns and correlation of gray matter and timing of cognitive decline were analyzed using voxel-based morphometry. The morphometric analysis showed that patients with earlier cognitive decline demonstrated greater cortical atrophy in the inferior parietal and orbitofrontal areas than did those with later cognitive decline. Additionally, the anatomical bases of the timing of their cognitive decline differed in terms of correlation patterns. These data suggest that the pathological burden in Parkinson’s disease with mild cognitive impairment may be more severe in patients with earlier cognitive decline than in those with later cognitive decline, and that the neural basis corresponding to the timing of cognitive decline may differ in these patients.
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References
Hurtig HI, Trojanowski JQ, Galvin J et al (2000) Alpha-synuclein cortical Lewy bodies correlate with dementia in Parkinson’s disease. Neurology 54:1916–1921
Aarsland D, Perry R, Brown A, Larsen JP, Ballard C (2005) Neuropathology of dementia in Parkinson’s disease: a prospective, community-based study. Ann Neurol 58:773–776
Ballard C, Ziabreva I, Perry R et al (2006) Differences in neuropathologic characteristics across the Lewy body dementia spectrum. Neurology 67:1931–1934
Caviness JN, Driver-Dunckley E, Connor DJ et al (2007) Defining mild cognitive impairment in Parkinson’s disease. Mov Disord 22:1272–1277
Aarsland D, Bronnick K, Larsen JP, Tysnes OB, Alves G (2009) Cognitive impairment in incident, untreated Parkinson disease: the Norwegian ParkWest study. Neurology 72:1121–1126
Adler CH, Caviness JN, Sabbagh MN et al (2010) Heterogeneous neuropathological findings in Parkinson’s disease with mild cognitive impairment. Acta Neuropathol 120:827–828
Jellinger KA (2010) Neuropathology in Parkinson’s disease with mild cognitive impairment. Acta Neuropathol 120:829–830 (author reply 831)
Alves G, Bronnick K, Aarsland D et al (2010) CSF amyloid-beta and tau proteins, and cognitive performance, in early and untreated Parkinson’s disease: the Norwegian ParkWest study. J Neurol Neurosurg Psychiatry 81:1080–1086
Montine TJ, Shi M, Quinn JF et al (2010) CSF Abeta(42) and tau in Parkinson’s disease with cognitive impairment. Mov Disord 25:2682–2685
Hughes AJ, Daniel SE, Kilford L, Lees AJ (1992) Accuracy of clinical diagnosis of idiopathic Parkinson’s disease: a clinico-pathological study of 100 cases. J Neurol Neurosurg Psychiatry 55:181–184
Lee JE, Park B, Song SK, Sohn YH, Park HJ, Lee PH (2010) A comparison of gray and white matter density in patients with Parkinson’s disease dementia and dementia with Lewy bodies using voxel-based morphometry. Mov Disord 25:28–34
Lee JE, Park HJ, Song SK, Sohn YH, Lee JD, Lee PH (2010) Neuroanatomic basis of amnestic MCI differs in patients with and without Parkinson disease. Neurology 75:2009–2016
Kim H, Na DL (1999) Normative data on the Korean version of the Boston naming test. J Clin Exp Neuropsychol 21:127–133
Ashburner J (2007) A fast diffeomorphic image registration algorithm. Neuroimage 38:95–113
Good CD, Johnsrude IS, Ashburner J, Henson RN, Friston KJ, Frackowiak RS (2001) A voxel-based morphometric study of ageing in 465 normal adult human brains. Neuroimage 14:21–36
Masliah E, Rockenstein E, Veinbergs I et al (2001) beta-amyloid peptides enhance alpha-synuclein accumulation and neuronal deficits in a transgenic mouse model linking Alzheimer’s disease and Parkinson’s disease. Proc Natl Acad Sci USA 98:12245–12250
Tsigelny IF, Crews L, Desplats P et al (2008) Mechanisms of hybrid oligomer formation in the pathogenesis of combined Alzheimer’s and Parkinson’s diseases. PLoS One 3:e3135
Rowe CC, Ng S, Ackermann U et al (2007) Imaging beta-amyloid burden in aging and dementia. Neurology 68:1718–1725
Song SK, Lee JE, Park HJ, Sohn YH, Lee JD, Lee PH (2011) The pattern of cortical atrophy in patients with Parkinson’s disease according to cognitive status. Mov Disord 26:289–296
Jicha GA, Schmitt FA, Abner E et al (2010) Prodromal clinical manifestations of neuropathologically confirmed Lewy body disease. Neurobiol Aging 31:1805–1813
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This study was supported by the Mid-career Researcher Program through an NRF grant funded by MEST (2010-0007749).
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J.E. Lee and K.H. Cho contributed equally to this work.
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Lee, J.E., Cho, K.H., Kim, M. et al. The pattern of cortical atrophy in Parkinson’s disease with mild cognitive impairment according to the timing of cognitive dysfunction. J Neurol 259, 469–473 (2012). https://doi.org/10.1007/s00415-011-6203-x
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DOI: https://doi.org/10.1007/s00415-011-6203-x