[18F]THK5351 PET Imaging in Patients with Mild Cognitive Impairment
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Background and Purpose Mild cognitive impairment (MCI) is a condition with diverse clinical outcomes and subgroups. Here we investigated the topographic distribution of tau in vivo using the positron emission tomography (PET) tracer [18F]THK5351 in MCI subgroups. Methods This study included 96 participants comprising 38 with amnestic MCI (aMCI), 21 with nonamnestic MCI (naMCI), and 37 with normal cognition (NC) who underwent 3.0-T MRI, [18F]THK5351 PET, and detailed neuropsychological tests. [18F]flutemetamol PET was also performed in 62 participants. The aMCI patients were further divided into three groups: 1) verbal-aMCI, only verbal memory impairment; 2) visual-aMCI, only visual memory impairment; and 3) both-aMCI, both visual and verbal memory impairment. Voxel-wise statistical analysis and region-of-interest -based analyses were performed to evaluate the retention of [18F]THK5351 in the MCI subgroups. Subgroup analysis of amyloid-positive and -negative MCI patients was also performed. Correlations between [18F]THK5351 retention and different neuropsychological tests were evaluated using statistical parametric mapping analyses. Results [18F]THK5351 retention in the lateral temporal, mesial temporal, parietal, frontal, posterior cingulate cortices and precuneus was significantly greater in aMCI patients than in NC subjects, whereas it did not differ significantly between naMCI and NC participants. [18F] THK5351 retention was greater in the both-aMCI group than in the verbal-aMCI and visualaMCI groups, and greater in amyloid-positive than amyloid-negative MCI patients. The cognitive function scores were significantly correlated with cortical [18F]THK5351 retention. Conclusions [18F]THK5351 PET might be useful for identifying distinct topographic patterns of [18F]THK5351 retention in subgroups of MCI patients who are at greater risk of the progression to Alzheimer’s dementia.
Abstract
Background and Purpose Mild cognitive impairment (MCI) is a condition with diverse clinical outcomes and subgroups. Here we investigated the topographic distribution of tau in vivo using the positron emission tomography (PET) tracer [18F]THK5351 in MCI subgroups. Methods This study included 96 participants comprising 38 with amnestic MCI (aMCI), 21 with nonamnestic MCI (naMCI), and 37 with normal cognition (NC) who underwent 3.0-T MRI, [18F]THK5351 PET, and detailed neuropsychological tests. [18F]flutemetamol PET was also performed in 62 participants. The aMCI patients were further divided into three groups: 1) verbal-aMCI, only verbal memory impairment; 2) visual-aMCI, only visual memory impairment; and 3) both-aMCI, both visual and verbal memory impairment. Voxel-wise statistical analysis and region-of-interest -based analyses were performed to evaluate the retention of [18F]THK5351 in the MCI subgroups. Subgroup analysis of amyloid-positive and -negative MCI patients was also performed. Correlations between [18F]THK5351 retention and different neuropsychological tests were evaluated using statistical parametric mapping analyses. Results [18F]THK5351 retention in the lateral temporal, mesial temporal, parietal, frontal, posterior cingulate cortices and precuneus was significantly greater in aMCI patients than in NC subjects, whereas it did not differ significantly between naMCI and NC participants. [18F] THK5351 retention was greater in the both-aMCI group than in the verbal-aMCI and visualaMCI groups, and greater in amyloid-positive than amyloid-negative MCI patients. The cognitive function scores were significantly correlated with cortical [18F]THK5351 retention. Conclusions [18F]THK5351 PET might be useful for identifying distinct topographic patterns of [18F]THK5351 retention in subgroups of MCI patients who are at greater risk of the progression to Alzheimer’s dementia.
참고문헌 (74)
- Brooks LG, "Assessing the progression of mild cognitive impairment to Alzheimer’s disease : current trends and future directions", Alzheimers Res Ther, 2, pp.28~ (2010)
- Petersen RC, "Mild cognitive impairment : clinical characterization and outcome", Arch Neurol, 56, pp.303~308 (1999)
- Cummings JL, "Disease-modifying therapies for Alzheimer disease : challenges to early intervention", Neurology, 69, pp.1622~1634 (2007)
- Petersen RC, "Mild cognitive impairment as a diagnostic entity", J Intern Med, 256, pp.183~194 (2004)
- Grundman M, "Mild cognitive impairment can be distinguished from Alzheimer disease and normal aging for clinical trials", Arch Neurol, 61, pp.59~66 (2004)
- Guillozet AL, "Neurofibrillary tangles, amyloid, and memory in aging and mild cognitive impairment", Arch Neurol, 60, pp.729~736 (2003)
- Dugger BN, "Neuropathological comparisons of amnestic and nonamnestic mild cognitive impairment", BMC Neurol, 15, pp.146~ (2015)
- Ferman TJ, "Nonamnestic mild cognitive impairment progresses to dementia with Lewy bodies", Neurology, 81, pp.2032~2038 (2013)
- Schneider JA, "The neuropathology of probable Alzheimer disease and mild cognitive impairment", Ann Neurol, 66, pp.200~208 (2009)
- Geslani DM, "Mild cognitive impairment : an operational definition and its conversion rate to Alzheimer’s disease", Dement Geriatr Cogn Disord, 19, pp.383~389 (2005)
- Larrieu S, "Incidence and outcome of mild cognitive impairment in a population-based prospective cohort", Neurology, 59, pp.1594~1599 (2002)
- Ye BS, "The heterogeneity and natural history of mild cognitive impairment of visual memory predominant type", J Alzheimers Dis, 43, pp.143~152 (2015)
- Tabert MH, "Neuropsychological prediction of conversion to Alzheimer disease in patients with mild cognitive impairment", Arch Gen Psychiatry, 63, pp.916~924 (2006)
- McGuinness B, "Predicting conversion to dementia in a memory clinic: a standard clinical approach compared with an empirically defined clustering method (latent profile analysis) for mild cognitive impairment subtyping", Alzheimers Dement (Amst), 1, pp.447~454 (2015)
- Michaud TL, "The risk of incident mild cognitive impairment and progression to dementia considering mild cognitive impairment subtypes", Dement Geriatr Cogn Dis Extra, 7, pp.15~29 (2017)
- Braak H, "Neuropathological stageing of Alzheimer-related changes", Acta Neuropathol, 82, pp.239~259 (1991)
- Thal DR, "Phases of Aβ-deposition in the human brain and its relevance for the development of AD", Neurology, 58, pp.1791~1800 (2002)
- Riemenschneider M, "Cerebrospinal fluid tau and beta-amyloid 42 proteins identify Alzheimer disease in subjects with mild cognitive impairment", Arch Neurol, 59, pp.1729~1734 (2002)
- Bouwman FH, "Longitudinal changes of CSF biomarkers in memory clinic patients", Neurology, 69, pp.1006~1011 (2007)
- Brys M, "Prediction and longitudinal study of CSF biomarkers in mild cognitive impairment", Neurobiol Aging, 30, pp.682~690 (2009)
- Villemagne VL, "Imaging tau and amyloid-β proteinopathies in Alzheimer disease and other conditions", Nat Rev Neurol, 14, pp.225~236 (2018)
- Landau SM, "Amyloid negativity in patients with clinically diagnosed Alzheimer disease and MCI", Neurology, 86, pp.1377~1385 (2016)
- Arriagada PV, "Neurofibrillary tangles but not senile plaques parallel duration and severity of Alzheimer’s disease", Neurology, 42, pp.631~639 (1992)
- Kadir A, "Dynamic changes in PET amyloid and FDG imaging at different stages of Alzheimer’s disease", Neurobiol Aging, 33, pp.198.e1~198.e14 (2012)
- Landau SM, "Amyloid deposition, hypometabolism, and longitudinal cognitive decline", Ann Neurol, 72, pp.578~586 (2012)
- Nelson PT, "Correlation of Alzheimer disease neuropathologic changes with cognitive status : a review of the literature", J Neuropathol Exp Neurol, 71, pp.362~381 (2012)
- Serrano-Pozo A, "Neuropathological alterations in Alzheimer disease", Cold Spring Harb Perspect Med, 1, pp.a006189~ (2011)
- Villemagne VL, "Tau imaging : early progress and future directions", Lancet Neurol, 14, pp.114~124 (2015)
- Harada R, "18F-THK5351 : a novel PET radiotracer for imaging neurofibrillary pathology in Alzheimer disease", J Nucl Med, 57, pp.208~214 (2016)
- T807, a novel tau positron emission tomography imaging agent for Alzheimer’s disease, "Alzheimers Dement", 2013, 666~676
- Villemagne VL, "In vivo evaluation of a novel tau imaging tracer for Alzheimer’s disease", Eur J Nucl Med Mol Imaging, 41, pp.816~826 (2014)
- Cho H, "In vivo cortical spreading pattern of tau and amyloid in the Alzheimer disease spectrum", Ann Neurol, 80, pp.247~258 (2016)
- Ng KP, "Monoamine oxidase B inhibitor, selegiline, reduces 18FTHK5351 uptake in the human brain", Alzheimers Res Ther, 9, pp.25~ (2017)
- Cho H, "Tau PET in Alzheimer disease and mild cognitive impairment", Neurology, 87, pp.375~383 (2016)
- THK5351 and cerebral glucose hypometabolism in Alzheimer’s disease, "Neurobiol Aging", 2017, 210~219
- Chiotis K, "Imaging in-vivo tau pathology in Alzheimer’s disease with THK5317 PET in a multimodal paradigm", Eur J Nucl Med Mol Imaging, 43, pp.1686~1699 (2016)
- Johnson KA, "Tau positron emission tomographic imaging in aging and early Alzheimer disease", Ann Neurol, 79, pp.110~119 (2016)
- Petersen RC, "Clinical practice. Mild cognitive impairment", N Engl J Med, 364, pp.2227~2234 (2011)
- Kim MJ, "Cortical thinning in verbal, visual, and both memory-predominant mild cognitive impairment", Alzheimer Dis Assoc Disord, 25, pp.242~249 (2011)
- Greve DN, "Cortical surface-based analysis reduces bias and variance in kinetic modeling of brain PET data", Neuroimage, 92, pp.225~236 (2014)
- Greve DN, "Different partial volume correction methods lead to different conclusions : an(18)F-FDG-PET study of aging", Neuroimage, 132, pp.334~343 (2016)
- Okamura N, "Non-invasive assessment of Alzheimer’s disease neurofibrillary pathology using 18F-THK5105 PET", Brain, 137(Pt 6), pp.1762~1771 (2014)
- THK-5351, "PLoS One", 2016, e0158460~
- Thurfjell L, "Automated quantification of 18F-flutemetamol PET activity for categorizing scans as negative or positive for brain amyloid : concordance with visual image reads", J Nucl Med, 55, pp.1623~1628 (2014)
- Benjamini Y, "Controlling the false discovery rate : a practical and powerful approach to multiple testing", J R Stat Soc Series B Stat Methodol, 57, pp.289~300 (1995)
- Maass A, "Comparison of multiple tau-PET measures as biomarkers in aging and Alzheimer’s disease", Neuroimage, 157, pp.448~463 (2017)
- Morris JC, "Mild cognitive impairment represents early-stage Alzheimer disease", Arch Neurol, 58, pp.397~405 (2001)
- Espinosa A, "A longitudinal follow-up of 550 mild cognitive impairment patients: evidence for large conversion to dementia rates and detection of major risk factors involved", J Alzheimers Dis, 34, pp.769~780 (2013)
- Markesbery WR, "Neuropathologic substrate of mild cognitive impairment", Arch Neurol, 63, pp.38~46 (2006)
- Petersen RC, "Neuropathologic features of amnestic mild cognitive impairment", Arch Neurol, 63, pp.665~672 (2006)
- Reinlieb M, "The patterns of cognitive and functional impairment in amnestic and non-amnestic mild cognitive impairment in geriatric depression", Am J Geriatr Psychiatry, 22, pp.1487~1495 (2014)
- Weakley A, "Analysis of verbal fluency ability in amnestic and non-amnestic mild cognitive impairment", Arch Clin Neuropsychol, 28, pp.721~731 (2013)
- Sabbagh MN, "Correlations between SPECT regional cerebral blood flow and psychometric testing in patients with Alzheimer’s disease", J Neuropsychiatry Clin Neurosci, 9, pp.68~74 (1997)
- Hayashi S, "Verbal or visual memory score and regional cerebral blood flow in Alzheimer disease", Dement Geriatr Cogn Dis Extra, 8, pp.1~11 (2018)
- Han JY, "Functional neural correlates of figure copy and recall task performances in cognitively impaired individuals : an 18F-FDG-PET study", Neuroreport, 26, pp.1077~1082 (2015)
- Smith EE, "Spatial versus object working memory : PET investigations", J Cogn Neurosci, 7, pp.337~356 (1995)
- Damasio H, "Neural correlates of naming actions and of naming spatial relations", Neuroimage, 13, pp.1053~1064 (2001)
- Ventre-Dominey J, "Double dissociation in neural correlates of visual working memory : a PET study", Brain Res Cogn Brain Res, 25, pp.747~759 (2005)
- Kneebone AC, "Rey Complex Figure : figural and spatial memory before and after temporal lobectomy for intractable epilepsy", J Int Neuropsychol Soc, 13, pp.664~671 (2007)
- Fowler JS, "Age-related increases in brain monoamine oxidase B in living healthy human subjects", Neurobiol Aging, 18, pp.431~435 (1997)
- -L-deprenyl using whole hemisphere autoradiography, "Neurochem Int", 2011, 60~68
- Mormino EC, "Synergistic effect of β-amyloid and neurodegeneration on cognitive decline in clinically normal individuals", JAMA Neurol, 71, pp.1379~1385 (2014)
- Rowe CC, "Brain amyloid imaging", J Nucl Med, 52, pp.1733~1740 (2011)
- Coutinho AM, "Brain metabolism and cerebrospinal fluid biomarkers profile of non-amnestic mild cognitive impairment in comparison to amnestic mild cognitive impairment and normal older subjects", Alzheimers Res Ther, 7, pp.58~ (2015)
- Villemagne VL, "Longitudinal assessment of Aβ and cognition in aging and Alzheimer disease", Ann Neurol, 69, pp.181~192 (2011)
- Hanseeuw B, "Patients with amyloid-negative mild cognitive impairment have cortical hypometabolism but the hippocampus is preserved", J Alzheimers Dis, 53, pp.651~660 (2016)
- Baron JC, "In vivo mapping of gray matter loss with voxel-based morphometry in mild Alzheimer’s disease", Neuroimage, 14, pp.298~309 (2001)
- Karas GB, "A comprehensive study of gray matter loss in patients with Alzheimer’s disease using optimized voxel-based morphometry", Neuroimage, 18, pp.895~907 (2003)
- Thompson PM, "Dynamics of gray matter loss in Alzheimer’s disease", J Neurosci, 23, pp.994~1005 (2003)
- Tong J, "Distribution of monoamine oxidase proteins in human brain : implications for brain imaging studies", J Cereb Blood Flow Metab, 33, pp.863~871 (2013)
- Harada R, "Correlations of 18F-THK5351 PET with postmortem burden of tau and astrogliosis in Alzheimer disease", J Nucl Med, 59, pp.671~674 (2018)
- Vermeiren C, "The tau positron-emission tomography tracer AV-1451 binds with similar affinities to tau fibrils and monoamine oxidases", Mov Disord, 33, pp.273~281 (2018)
- Sidoryk-Wegrzynowicz M, "Role of astrocytes in brain function and disease", Toxicol Pathol, 39, pp.115~123 (2011)
- Carter SF, "Evidence for astrocytosis in prodromal Alzheimer disease provided by 11C-deuterium-L-deprenyl: a multitracer PET paradigm combining 11C-Pittsburgh compound B and 18F-FDG", J Nucl Med, 53, pp.37~46 (2012)