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11 results on '"Schmansky, Nicholas J."'

1. Shared genetic risk between corticobasal degeneration, progressive supranuclear palsy, and frontotemporal dementia

Author

Yokoyama, Jennifer S, Karch, Celeste M, Fan, Chun C, Bonham, Luke W, Kouri, Naomi, Ross, Owen A, Rademakers, Rosa, Kim, Jungsu, Wang, Yunpeng, Höglinger, Günter U, Müller, Ulrich, Ferrari, Raffaele, Hardy, John, International FTD-Genomics Consortium (IFGC), Momeni, Parastoo, Sugrue, Leo P, Hess, Christopher P, James Barkovich, A, Boxer, Adam L, Seeley, William W, Rabinovici, Gil D, Rosen, Howard J, Miller, Bruce L, Schmansky, Nicholas J, Fischl, Bruce, Hyman, Bradley T, Dickson, Dennis W, Schellenberg, Gerard D, Andreassen, Ole A, Dale, Anders M, and Desikan, Rahul S

Subjects
Biomedical and Clinical Sciences, Neurosciences, Rare Diseases, Frontotemporal Dementia (FTD), Brain Disorders, Aging, Dementia, Acquired Cognitive Impairment, Neurodegenerative, Pick's Disease, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Alzheimer's Disease Related Dementias (ADRD), Genetics, Human Genome, 2.1 Biological and endogenous factors, Neurological, Basal Ganglia Diseases, Frontotemporal Dementia, Humans, Inclusion Bodies, Neurons, Risk Factors, Supranuclear Palsy, Progressive, Tauopathies, tau Proteins, International FTD-Genomics Consortium, Clinical Sciences, Neurology & Neurosurgery
Abstract

Corticobasal degeneration (CBD), progressive supranuclear palsy (PSP) and a subset of frontotemporal dementia (FTD) are neurodegenerative disorders characterized by tau inclusions in neurons and glia (tauopathies). Although clinical, pathological and genetic evidence suggests overlapping pathobiology between CBD, PSP, and FTD, the relationship between these disorders is still not well understood. Using summary statistics (odds ratios and p values) from large genome-wide association studies (total n = 14,286 cases and controls) and recently established genetic methods, we investigated the genetic overlap between CBD and PSP and CBD and FTD. We found up to 800-fold enrichment of genetic risk in CBD across different levels of significance for PSP or FTD. In addition to NSF (tagging the MAPT H1 haplotype), we observed that SNPs in or near MOBP, CXCR4, EGFR, and GLDC showed significant genetic overlap between CBD and PSP, whereas only SNPs tagging the MAPT haplotype overlapped between CBD and FTD. The risk alleles of the shared SNPs were associated with expression changes in cis-genes. Evaluating transcriptome levels across adult human brains, we found a unique neuroanatomic gene expression signature for each of the five overlapping gene loci (omnibus ANOVA p

Published
2017

2. Selective disruption of the cerebral neocortex in Alzheimer's disease.

Author

Desikan, Rahul S, Sabuncu, Mert R, Schmansky, Nicholas J, Reuter, Martin, Cabral, Howard J, Hess, Christopher P, Weiner, Michael W, Biffi, Alessandro, Anderson, Christopher D, Rosand, Jonathan, Salat, David H, Kemper, Thomas L, Dale, Anders M, Sperling, Reisa A, Fischl, Bruce, and Alzheimer's Disease Neuroimaging Initiative

Subjects
Alzheimer's Disease Neuroimaging Initiative, Hippocampus, Neocortex, Humans, Alzheimer Disease, tau Proteins, Magnetic Resonance Imaging, Radiography, Aged, Aged, 80 and over, Female, Male, Amyloid beta-Peptides, and over, Neurodegenerative, Alzheimer's Disease, Neurosciences, Acquired Cognitive Impairment, Brain Disorders, Aging, Alzheimer's Disease including Alzheimer's Disease Related Dementias, Dementia, 2.1 Biological and endogenous factors, Neurological, General Science & Technology
Abstract

BackgroundAlzheimer's disease (AD) and its transitional state mild cognitive impairment (MCI) are characterized by amyloid plaque and tau neurofibrillary tangle (NFT) deposition within the cerebral neocortex and neuronal loss within the hippocampal formation. However, the precise relationship between pathologic changes in neocortical regions and hippocampal atrophy is largely unknown.Methodology/principal findingsIn this study, combining structural MRI scans and automated image analysis tools with reduced cerebrospinal fluid (CSF) Aβ levels, a surrogate for intra-cranial amyloid plaques and elevated CSF phosphorylated tau (p-tau) levels, a surrogate for neocortical NFTs, we examined the relationship between the presence of Alzheimer's pathology, gray matter thickness of select neocortical regions, and hippocampal volume in cognitively normal older participants and individuals with MCI and AD (n = 724). Amongst all 3 groups, only select heteromodal cortical regions significantly correlated with hippocampal volume. Amongst MCI and AD individuals, gray matter thickness of the entorhinal cortex and inferior temporal gyrus significantly predicted longitudinal hippocampal volume loss in both amyloid positive and p-tau positive individuals. Amongst cognitively normal older adults, thinning only within the medial portion of the orbital frontal cortex significantly differentiated amyloid positive from amyloid negative individuals whereas thinning only within the entorhinal cortex significantly discriminated p-tau positive from p-tau negative individuals.Conclusions/significanceCortical Aβ and tau pathology affects gray matter thinning within select neocortical regions and potentially contributes to downstream hippocampal degeneration. Neocortical Alzheimer's pathology is evident even amongst older asymptomatic individuals suggesting the existence of a preclinical phase of dementia.

Published
2010

3. Automated MRI measures identify individuals with mild cognitive impairment and Alzheimer's disease*

Author

Desikan, Rahul S, Cabral, Howard J, Hess, Christopher P, Dillon, William P, Glastonbury, Christine M, Weiner, Michael W, Schmansky, Nicholas J, Greve, Douglas N, Salat, David H, Buckner, Randy L, Fischl, Bruce, and Initiative, Alzheimer's Disease Neuroimaging

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Neurosciences, Dementia, Behavioral and Social Science, Alzheimer's Disease, Acquired Cognitive Impairment, Biomedical Imaging, Bioengineering, Aging, Brain Disorders, Neurodegenerative, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Clinical Research, 4.2 Evaluation of markers and technologies, 4.1 Discovery and preclinical testing of markers and technologies, Detection, screening and diagnosis, Neurological, Adolescent, Adult, Aged, Aged, 80 and over, Alzheimer Disease, Biomarkers, Brain Mapping, Cerebral Cortex, Cognition Disorders, Disease Progression, Early Diagnosis, Epidemiologic Methods, Female, Humans, Image Interpretation, Computer-Assisted, Magnetic Resonance Imaging, Male, Middle Aged, Neuropsychological Tests, Prognosis, Young Adult, MRI, mild cognitive impairment, Alzheimers disease, diagnostic marker, Alzheimer's Disease Neuroimaging Initiative, Medical and Health Sciences, Psychology and Cognitive Sciences, Neurology & Neurosurgery, Biomedical and clinical sciences, Health sciences, Psychology
Abstract

Mild cognitive impairment can represent a transitional state between normal ageing and Alzheimer's disease. Non-invasive diagnostic methods are needed to identify mild cognitive impairment individuals for early therapeutic interventions. Our objective was to determine whether automated magnetic resonance imaging-based measures could identify mild cognitive impairment individuals with a high degree of accuracy. Baseline volumetric T1-weighted magnetic resonance imaging scans of 313 individuals from two independent cohorts were examined using automated software tools to identify the volume and mean thickness of 34 neuroanatomic regions. The first cohort included 49 older controls and 48 individuals with mild cognitive impairment, while the second cohort included 94 older controls and 57 mild cognitive impairment individuals. Sixty-five patients with probable Alzheimer's disease were also included for comparison. For the discrimination of mild cognitive impairment, entorhinal cortex thickness, hippocampal volume and supramarginal gyrus thickness demonstrated an area under the curve of 0.91 (specificity 94%, sensitivity 74%, positive likelihood ratio 12.12, negative likelihood ratio 0.29) for the first cohort and an area under the curve of 0.95 (specificity 91%, sensitivity 90%, positive likelihood ratio 10.0, negative likelihood ratio 0.11) for the second cohort. For the discrimination of Alzheimer's disease, these three measures demonstrated an area under the curve of 1.0. The three magnetic resonance imaging measures demonstrated significant correlations with clinical and neuropsychological assessments as well as with cerebrospinal fluid levels of tau, hyperphosphorylated tau and abeta 42 proteins. These results demonstrate that automated magnetic resonance imaging measures can serve as an in vivo surrogate for disease severity, underlying neuropathology and as a non-invasive diagnostic method for mild cognitive impairment and Alzheimer's disease.

Published
2009

7. Shared genetic risk between corticobasal degeneration, progressive supranuclear palsy, and frontotemporal dementia

Author

Yokoyama, Jennifer S., Karch, Celeste M., Fan, Chun C., Bonham, Luke W., Naomi, Kouri, Ross, Owen A., Rosa, Rademakers, Jungsu, Kim, Yunpeng, Wang, Höglinger, Günter U., Ulrich, Muller, Raffaele, Ferrari, John, Hardy, International FTD-Genomics Consortium (IFGC Ferrari, R, Hernandez, Dg, Nalls, Ma, Rohrer, Jd, Ramasamy, A, Kwok, Jbj, Dobson-Stone, C, Schofield, Pr, Halliday, Gm, Hodges, Jr, Piguet, O, Bartley, L, Thompson, E, Haan, E, Hernández, I, Ruiz, A, Boada, M, Borroni, B, Padovani, A, Cruchaga, C, Cairns, Nj, Benussi, L, Binetti, G, Ghidoni, R, Forloni, G, Albani, D, Galimberti, D, Fenoglio, C, Serpente, M, Scarpini, E, Clarimón, J, Lleó, A, Blesa, R, Landqvist Waldö, M, Nilsson, C, Mackenzie, Ira, Hsiung, Gyr, Mann, Dma, Grafman, J, Morris, Cm, Attems, J, Griffiths, Td, Mckeith, Ig, Thomas, Aj, Pietrini, P, Huey, Ed, Wassermann, Em, Baborie, A, Jaros, E, Tierney, Mc, Pastor, P, Razquin, C, Ortega-Cubero, S, Alonso, E, Perneczky, R, Diehl-Schmid, J, Alexopoulos, P, Kurz, A, Rainero, I, Rubino, E, Pinessi, L, Rogaeva, E, St George-Hyslop, P, Rossi, G, Tagliavini, F, Giaccone, G, Rowe, Jb, Schlachetzki, Jcm, Uphill, J, Collinge, J, Mead, S, Danek, A, Van Deerlin VM, Grossman, M, Trojanowski, Jq, van der Zee, J, Cruts, M, Van Broeckhoven, C, Cappa, Sf, Leber, I, Hannequin, D, Golfier, V, Vercelletto, M, Brice, A, Nacmias, B, Sorbi, S, Bagnoli, S, Piaceri, I, Nielsen, Je, Hjermind, Le, Riemenschneider, M, Mayhaus, M, Ibach, B, Gasparoni, G, Pichler, S, Gu, W, Rossor, Mn, Fox, Nc, Warren, Jd, Spillantini, Mg, Morris, Hr, Rizzu, P, Heutink, P, Snowden, Js, Rollinson, S, Richardson, A, Gerhard, A, Bruni, Ac, Maletta, R, Frangipane, F, Cupidi, C, Bernardi, L, Anfossi, M, Gallo, M, Conidi, Me, Smirne, N, Rademakers, R, Baker, M, Dickson, Dw, Graff-Radford, Nr, Petersen, Rc, Knopman, D, Josephs, Ka, Boeve, Bf, Parisi, Je, Seeley, Ww, Miller, Bl, Karydas, Am, Rosen, H, van Swieten JC, Dopper, Eg, Seelaar, H, Pijnenburg, Yal, Scheltens, P, Logroscino, G, Capozzo, R, Novelli, V, Puca, Aa, Franceschi, M, Postiglione, A, Milan, G, Sorrentino, P, Kristiansen, M, Chiang, Hh, Graff, C, Pasquier, F, Rollin, A, Deramecourt, V, Lebouvier, T, Kapogiannis, D, Ferrucci, L, Pickering-Brown, S, Singleton, Ab, Hardy, J, Momeni, P. )., Parastoo, Momeni, Sugrue, Leo P., Hess, Christopher P., James Barkovich, A., Boxer, Adam L., Seele, William W., Rabinovici, Gil D., Rosen, Howard J., Miller, Bruce L., Schmansky, Nicholas J., Bruce, Fischl, Hyman, Bradley T., Dickson, Dennis W., Schellenberg, Gerard D., Andreassen, Ole A., Dale, Anders M., Desikan, and Rahul S., and Int FTD-Genomics Consortium

Subjects
pathology [Tauopathies], 0301 basic medicine, Pathology, Aging, genetics [Basal Ganglia Diseases], Genome-wide association study, Neurodegenerative, diagnosis [Supranuclear Palsy, Progressive], diagnosis [Frontotemporal Dementia], pathology [Inclusion Bodies], 0302 clinical medicine, Neurology (clinical), Cellular and Molecular Neuroscience, Risk Factors, pathology [Neurons], Corticobasal degeneration, Supranuclear Palsy, 2.1 Biological and endogenous factors, Aetiology, genetics [Frontotemporal Dementia], Alzheimer's Disease Related Dementias (ADRD), Genetics, Inclusion Bodies, Neurons, genetics [Supranuclear Palsy, Progressive], Frontotemporal Dementia (FTD), Tauopathies, Frontotemporal Dementia, Neurological, Supranuclear Palsy, Progressive, Frontotemporal dementia, medicine.medical_specialty, pathology [Supranuclear Palsy, Progressive], Clinical Sciences, MAPT protein, human, Locus (genetics), Single-nucleotide polymorphism, tau Proteins, Biology, Article, Pathology and Forensic Medicine, Progressive supranuclear palsy, 03 medical and health sciences, Rare Diseases, Progressive, Basal Ganglia Diseases, mental disorders, medicine, Acquired Cognitive Impairment, Humans, ddc:610, Genetic association, Neurology & Neurosurgery, International FTD-Genomics Consortium, Prevention, Haplotype, Human Genome, Neurosciences, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), medicine.disease, metabolism [tau Proteins], digestive system diseases, Brain Disorders, 030104 developmental biology, pathology [Frontotemporal Dementia], Dementia, Human medicine, pathology [Basal Ganglia Diseases], 030217 neurology & neurosurgery
Abstract

Corticobasal degeneration (CBD), progressive supranuclear palsy (PSP) and a subset of frontotemporal dementia (FTD) are neurodegenerative disorders characterized by tau inclusions in neurons and glia (tauopathies). Although clinical, pathological and genetic evidence suggests overlapping pathobiology between CBD, PSP, and FTD, the relationship between these disorders is still not well understood. Using summary statistics (odds ratios and p values) from large genome-wide association studies (total n=14,286 cases and controls) and recently established genetic methods, we investigated the genetic overlap between CBD and PSP and CBD and FTD. We found up to 800-fold enrichment of genetic risk in CBD across different levels of significance for PSP or FTD. In addition to NSF (tagging the MAPT H1 haplotype), we observed that SNPs in or near MOBP, CXCR4, EGFR, and GLDC showed significant genetic overlap between CBD and PSP, whereas only SNPs tagging the MAPT haplotype overlapped between CBD and FTD. The risk alleles of the shared SNPs were associated with expression changes in cis-genes. Evaluating transcriptome levels across adult human brains, we found a unique neuroanatomic gene expression signature for each of the five overlapping gene loci (omnibus ANOVA p&nbsp

Published
2017

8. Automated MRI measures identify individuals with mild cognitive impairment and Alzheimer's disease

Author

move to dc.description.sponsorship, Harvard University--MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology. Computer Science and Artificial Intelligence Laboratory, Fischl, Bruce, Buckner, Randy L., Desikan, Rahul S., Cabral, Howard J., Hess, Christopher P., Dillon, William P., Glastonbury, Christine M., Weiner, Michael W., Schmansky, Nicholas J., Greve, Douglas N., Salat, David H., move to dc.description.sponsorship, Harvard University--MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology. Computer Science and Artificial Intelligence Laboratory, Fischl, Bruce, Buckner, Randy L., Desikan, Rahul S., Cabral, Howard J., Hess, Christopher P., Dillon, William P., Glastonbury, Christine M., Weiner, Michael W., Schmansky, Nicholas J., Greve, Douglas N., and Salat, David H.

Abstract

Mild cognitive impairment can represent a transitional state between normal ageing and Alzheimer's disease. Non-invasive diagnostic methods are needed to identify mild cognitive impairment individuals for early therapeutic interventions. Our objective was to determine whether automated magnetic resonance imaging-based measures could identify mild cognitive impairment individuals with a high degree of accuracy. Baseline volumetric T1-weighted magnetic resonance imaging scans of 313 individuals from two independent cohorts were examined using automated software tools to identify the volume and mean thickness of 34 neuroanatomic regions. The first cohort included 49 older controls and 48 individuals with mild cognitive impairment, while the second cohort included 94 older controls and 57 mild cognitive impairment individuals. Sixty-five patients with probable Alzheimer's disease were also included for comparison. For the discrimination of mild cognitive impairment, entorhinal cortex thickness, hippocampal volume and supramarginal gyrus thickness demonstrated an area under the curve of 0.91 (specificity 94%, sensitivity 74%, positive likelihood ratio 12.12, negative likelihood ratio 0.29) for the first cohort and an area under the curve of 0.95 (specificity 91%, sensitivity 90%, positive likelihood ratio 10.0, negative likelihood ratio 0.11) for the second cohort. For the discrimination of Alzheimer's disease, these three measures demonstrated an area under the curve of 1.0. The three magnetic resonance imaging measures demonstrated significant correlations with clinical and neuropsychological assessments as well as with cerebrospinal fluid levels of tau, hyperphosphorylated tau and abeta 42 proteins. These results demonstrate that automated magnetic resonance imaging measures can serve as an in vivo surrogate for disease severity, underlying neuropathology and as a non-invasive diagnostic method for mild cognitive impairment and Alzheimer's disease., American Federation for Aging Research. Medical Student Training in Aging Research Program, National Center for Research Resources (U.S.) (grant P41-RR14075), National Center for Research Resources (U.S.) (grant R01 RR 16594-01A1), National Center for Research Resources (U.S.) (BIRN Morphometric Project BIRN002, U24 RR021382), National Institute of Biomedical Imaging and Bioengineering (U.S.) (R01 EB001550), Mental Illness and Neuroscience Discovery (MIND) Institute, National Institute on Aging (P50 AG05681), National Institute on Aging (P01 AG03991), National Institute on Aging (AG021910)

Published
2012

9. Selective Disruption of the Cerebral Neocortex in Alzheimer's Disease

Author

Harvard University--MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology. Computer Science and Artificial Intelligence Laboratory, Fischl, Bruce, Sabuncu, Mert R., Desikan, Rahul S., Schmansky, Nicholas J., Reuter, Martin, Cabral, Howard J., Hess, Christopher P., Weiner, Michael W., Biffi, Alessandro, Anderson, Christopher D., Rosand, Jonathan, Salat, David H., Kemper, Thomas L., Dale, Anders M., Sperling, Reisa A., Harvard University--MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology. Computer Science and Artificial Intelligence Laboratory, Fischl, Bruce, Sabuncu, Mert R., Desikan, Rahul S., Schmansky, Nicholas J., Reuter, Martin, Cabral, Howard J., Hess, Christopher P., Weiner, Michael W., Biffi, Alessandro, Anderson, Christopher D., Rosand, Jonathan, Salat, David H., Kemper, Thomas L., Dale, Anders M., and Sperling, Reisa A.

Abstract

Background: Alzheimer's disease (AD) and its transitional state mild cognitive impairment (MCI) are characterized by amyloid plaque and tau neurofibrillary tangle (NFT) deposition within the cerebral neocortex and neuronal loss within the hippocampal formation. However, the precise relationship between pathologic changes in neocortical regions and hippocampal atrophy is largely unknown. Methodology/Principal Findings: In this study, combining structural MRI scans and automated image analysis tools with reduced cerebrospinal fluid (CSF) Aß levels, a surrogate for intra-cranial amyloid plaques and elevated CSF phosphorylated tau (p-tau) levels, a surrogate for neocortical NFTs, we examined the relationship between the presence of Alzheimer's pathology, gray matter thickness of select neocortical regions, and hippocampal volume in cognitively normal older participants and individuals with MCI and AD (n = 724). Amongst all 3 groups, only select heteromodal cortical regions significantly correlated with hippocampal volume. Amongst MCI and AD individuals, gray matter thickness of the entorhinal cortex and inferior temporal gyrus significantly predicted longitudinal hippocampal volume loss in both amyloid positive and p-tau positive individuals. Amongst cognitively normal older adults, thinning only within the medial portion of the orbital frontal cortex significantly differentiated amyloid positive from amyloid negative individuals whereas thinning only within the entorhinal cortex significantly discriminated p-tau positive from p-tau negative individuals. Conclusions/Significance: Cortical Aβ and tau pathology affects gray matter thinning within select neocortical regions and potentially contributes to downstream hippocampal degeneration. Neocortical Alzheimer's pathology is evident even amongst older asymptomatic individuals suggesting the existence of a preclinical phase of dementia., National Center for Research Resources (U.S.) (P41-RR14075, R01 RR 16594-01A1 and the NCRR BIRN Morphometric Project BIRN002, U24 RR021382), National Institute of Biomedical Imaging and Bioengineering (U.S.) (R01 EB001550, R01EB006758), National Institute of Neurological Disorders and Stroke (U.S.) (R01 NS052585-01), Mental Illness and Neuroscience Discovery (MIND) Institute, National Institute of Aging (P50 AG05681, P01 AG03991, AG02238 and AG021910), National Institutes of Health (U.S) (P30 AG010129), National Institutes of Health (U.S) (K01 AG030514)

Published
2010

10. Selective Disruption of the Cerebral Neocortex in Alzheimer's Disease

Author

Desikan, Rahul S., Schmansky, Nicholas J., Cabral, Howard J., Hess, Christopher P., Weiner, Michael W., Kemper, Thomas L., Dale, Anders M., Sabuncu, Mert R, the Alzheimer’s Disease Neuroimaging Initiative, Reuter, Martin, Biffi, Alessandro, Anderson, Christopher David, Rosand, Jonathan, Salat, David H., Sperling, Reisa Anne, and Fischl, Bruce R.

Subjects
neurological disorders, neuroscience, neurology of disease and regeneration, Alzheimer disease, cognitive neurology and dementia
Abstract

Background: Alzheimer's disease (AD) and its transitional state mild cognitive impairment (MCI) are characterized by amyloid plaque and tau neurofibrillary tangle (NFT) deposition within the cerebral neocortex and neuronal loss within the hippocampal formation. However, the precise relationship between pathologic changes in neocortical regions and hippocampal atrophy is largely unknown. Methodology/Principal Findings: In this study, combining structural MRI scans and automated image analysis tools with reduced cerebrospinal fluid (CSF) Aß levels, a surrogate for intra-cranial amyloid plaques and elevated CSF phosphorylated tau (p-tau) levels, a surrogate for neocortical NFTs, we examined the relationship between the presence of Alzheimer's pathology, gray matter thickness of select neocortical regions, and hippocampal volume in cognitively normal older participants and individuals with MCI and AD (n = 724). Amongst all 3 groups, only select heteromodal cortical regions significantly correlated with hippocampal volume. Amongst MCI and AD individuals, gray matter thickness of the entorhinal cortex and inferior temporal gyrus significantly predicted longitudinal hippocampal volume loss in both amyloid positive and p-tau positive individuals. Amongst cognitively normal older adults, thinning only within the medial portion of the orbital frontal cortex significantly differentiated amyloid positive from amyloid negative individuals whereas thinning only within the entorhinal cortex significantly discriminated p-tau positive from p-tau negative individuals. Conclusions/Significance: Cortical Aβ and tau pathology affects gray matter thinning within select neocortical regions and potentially contributes to downstream hippocampal degeneration. Neocortical Alzheimer's pathology is evident even amongst older asymptomatic individuals suggesting the existence of a preclinical phase of dementia.

Published
2010
Full Text
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11. Automated MRI Measures Identify Individuals with Mild Cognitive Impairment and Alzheimer's Disease

Author

Desikan, Rahul S., Cabral, Howard J., Hess, Christopher P., Dillon, William P., Glastonbury, Christine M., Weiner, Michael W., Schmansky, Nicholas J., Salat, David H., Greve, Douglas N., Buckner, Randy Lee, Fischl, Bruce R., and Alzheimer’s Disease Neuroimaging Initiative

Subjects
MRI, mild cognitive impairment, Alzheimer’s disease, diagnostic marker
Abstract

Mild cognitive impairment can represent a transitional state between normal ageing and Alzheimer's disease. Non-invasive diagnostic methods are needed to identify mild cognitive impairment individuals for early therapeutic interventions. Our objective was to determine whether automated magnetic resonance imaging-based measures could identify mild cognitive impairment individuals with a high degree of accuracy. Baseline volumetric T1-weighted magnetic resonance imaging scans of 313 individuals from two independent cohorts were examined using automated software tools to identify the volume and mean thickness of 34 neuroanatomic regions. The first cohort included 49 older controls and 48 individuals with mild cognitive impairment, while the second cohort included 94 older controls and 57 mild cognitive impairment individuals. Sixty-five patients with probable Alzheimer's disease were also included for comparison. For the discrimination of mild cognitive impairment, entorhinal cortex thickness, hippocampal volume and supramarginal gyrus thickness demonstrated an area under the curve of 0.91 (specificity 94%, sensitivity 74%, positive likelihood ratio 12.12, negative likelihood ratio 0.29) for the first cohort and an area under the curve of 0.95 (specificity 91%, sensitivity 90%, positive likelihood ratio 10.0, negative likelihood ratio 0.11) for the second cohort. For the discrimination of Alzheimer's disease, these three measures demonstrated an area under the curve of 1.0. The three magnetic resonance imaging measures demonstrated significant correlations with clinical and neuropsychological assessments as well as with cerebrospinal fluid levels of tau, hyperphosphorylated tau and abeta 42 proteins. These results demonstrate that automated magnetic resonance imaging measures can serve as an in vivo surrogate for disease severity, underlying neuropathology and as a non-invasive diagnostic method for mild cognitive impairment and Alzheimer's disease., Psychology

Published
2009
Full Text
View/download PDF

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