Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature
ABSTRACTClinicopathologic correlation studies are critically important for the field of Alzheimer disease (AD) research. Studies on human subjects with autopsy confirmation entail numerous potential biases that affect both their general applicability and the validity of the correlations. Many source...
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| Published in | Journal of neuropathology and experimental neurology Vol. 71; no. 5; pp. 362 - 381 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hagerstown, MD
American Association of Neuropathologists, Inc
01.05.2012
Lippincott Williams & Wilkins Oxford University Press |
| Subjects | |
| Online Access | Get full text |
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| Abstract | ABSTRACTClinicopathologic correlation studies are critically important for the field of Alzheimer disease (AD) research. Studies on human subjects with autopsy confirmation entail numerous potential biases that affect both their general applicability and the validity of the correlations. Many sources of data variability can weaken the apparent correlation between cognitive status and AD neuropathologic changes. Indeed, most persons in advanced old age have significant non-AD brain lesions that may alter cognition independently of AD. Worldwide research efforts have evaluated thousands of human subjects to assess the causes of cognitive impairment in the elderly, and these studies have been interpreted in different ways. We review the literature focusing on the correlation of AD neuropathologic changes (i.e. β-amyloid plaques and neurofibrillary tangles) with cognitive impairment. We discuss the various patterns of brain changes that have been observed in elderly individuals to provide a perspective forunderstanding AD clinicopathologic correlation and conclude that evidence from many independent research centers strongly supports the existence of a specific disease, as defined by the presence of Aβ plaques and neurofibrillary tangles. Although Aβ plaques may play a key role in AD pathogenesis, the severity of cognitive impairment correlates best with the burden of neocortical neurofibrillary tangles. |
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| AbstractList | Clinicopathologic correlation studies are critically important for the field of Alzheimer disease (AD) research. Studies on human subjects with autopsy confirmation entail numerous potential biases that affect both their general applicability and the validity of the correlations. Many sources of data variability can weaken the apparent correlation between cognitive status and AD neuropathologic changes. Indeed, most persons in advanced old age have significant non-AD brain lesions that may alter cognition independently of AD. Worldwide research efforts have evaluated thousands of human subjects to assess the causes of cognitive impairment in the elderly, and these studies have been interpreted in different ways. We review the literature focusing on the correlation of AD neuropathologic changes (i.e. β-amyloid plaques and neurofibrillary tangles) with cognitive impairment. We discuss the various patterns of brain changes that have been observed in elderly individuals to provide a perspective for understanding AD clinicopathologic correlation and conclude that evidence from many independent research centers strongly supports the existence of a specific disease, as defined by the presence of Aβ plaques and neurofibrillary tangles. Although Aβ plaques may play a key role in AD pathogenesis, the severity of cognitive impairment correlates best with the burden of neocortical neurofibrillary tangles. Clinicopathologic correlation studies are critically important for the field of Alzheimer disease (AD) research. Studies on human subjects with autopsy confirmation entail numerous potential biases that affect both their general applicability and the validity of the correlations. Many sources of data variability can weaken the apparent correlation between cognitive status and AD neuropathologic changes. Indeed, most persons in advanced old age have significant non-AD brain lesions that may alter cognition independently of AD. Worldwide research efforts have evaluated thousands of human subjects to assess the causes of cognitive impairment in the elderly, and these studies have been interpreted in different ways. We review the literature focusing on the correlation of AD neuropathologic changes (i.e. β-amyloid plaques and neurofibrillary tangles) with cognitive impairment. We discuss the various patterns of brain changes that have been observed in elderly individuals to provide a perspective for understanding AD clinicopathologic correlation and conclude that evidence from many independent research centers strongly supports the existence of a specific disease, as defined by the presence of Aβ plaques and neurofibrillary tangles. Although Aβ plaques may play a key role in AD pathogenesis, the severity of cognitive impairment correlates best with the burden of neocortical neurofibrillary tangles.Clinicopathologic correlation studies are critically important for the field of Alzheimer disease (AD) research. Studies on human subjects with autopsy confirmation entail numerous potential biases that affect both their general applicability and the validity of the correlations. Many sources of data variability can weaken the apparent correlation between cognitive status and AD neuropathologic changes. Indeed, most persons in advanced old age have significant non-AD brain lesions that may alter cognition independently of AD. Worldwide research efforts have evaluated thousands of human subjects to assess the causes of cognitive impairment in the elderly, and these studies have been interpreted in different ways. We review the literature focusing on the correlation of AD neuropathologic changes (i.e. β-amyloid plaques and neurofibrillary tangles) with cognitive impairment. We discuss the various patterns of brain changes that have been observed in elderly individuals to provide a perspective for understanding AD clinicopathologic correlation and conclude that evidence from many independent research centers strongly supports the existence of a specific disease, as defined by the presence of Aβ plaques and neurofibrillary tangles. Although Aβ plaques may play a key role in AD pathogenesis, the severity of cognitive impairment correlates best with the burden of neocortical neurofibrillary tangles. Clinicopathologic correlation studies are critically important for the field of Alzheimer disease (AD) research. Studies on human subjects with autopsy confirmation entail numerous potential biases that affect both their general applicability and the validity of the correlations. Many sources of data variability can weaken the apparent correlation between cognitive status and AD neuropathologic changes. Indeed, most persons in advanced old age have significant non-AD brain lesions that may alter cognition independently of AD. Worldwide research efforts have evaluated thousands of human subjects to assess the causes of cognitive impairment in the elderly, and these studies have been interpreted in different ways. We review the literature focusing on the correlation of AD neuropathologic changes (i.e. β-amyloid plaques and neurofibrillary tangles) with cognitive impairment. We discuss the various patterns of brain changes that have been observed in elderly individuals to provide a perspective for understanding AD Clinicopathologic correlation and conclude that evidence from many independent research centers strongly supports the existence of a specific disease, as defined by the presence of Aβ plaques and neurofibrillary tangles. Although Aβ plaques may play a key role in AD pathogenesis, the severity of cognitive impairment correlates best with the burden of neocortical neurofibrillary tangles. [PUBLICATION ABSTRACT] Clinicopathologic correlation studies are critically important for the field of Alzheimer disease (AD) research. Studies on human subjects with autopsy confirmation entail numerous potential biases that affect both their general applicability and the validity of the correlations. Many sources of data variability can weaken the apparent correlation between cognitive status and AD neuropathologic changes. Indeed, most persons in advanced old age have significant non-AD brain lesions that may alter cognition independently of AD. Worldwide research efforts have evaluated thousands of human subjects to assess the causes of cognitive impairment in the elderly, and these studies have been interpreted in different ways. We review the literature focusing on the correlation of AD neuropathologic changes (i.e. beta-amyloid plaques and neurofibrillary tangles) with cognitive impairment. We discuss the various patterns of brain changes that have been observed in elderly individuals to provide a perspective for understanding AD clinicopathologic correlation and conclude that evidence from many independent research centers strongly supports the existence of a specific disease, as defined by the presence of AA plaques and neurofibrillary tangles. Although AA plaques may play a key role in AD pathogenesis, the severity of cognitive impairment correlates best with the burden of neocortical neurofibrillary tangles. ABSTRACTClinicopathologic correlation studies are critically important for the field of Alzheimer disease (AD) research. Studies on human subjects with autopsy confirmation entail numerous potential biases that affect both their general applicability and the validity of the correlations. Many sources of data variability can weaken the apparent correlation between cognitive status and AD neuropathologic changes. Indeed, most persons in advanced old age have significant non-AD brain lesions that may alter cognition independently of AD. Worldwide research efforts have evaluated thousands of human subjects to assess the causes of cognitive impairment in the elderly, and these studies have been interpreted in different ways. We review the literature focusing on the correlation of AD neuropathologic changes (i.e. β-amyloid plaques and neurofibrillary tangles) with cognitive impairment. We discuss the various patterns of brain changes that have been observed in elderly individuals to provide a perspective forunderstanding AD clinicopathologic correlation and conclude that evidence from many independent research centers strongly supports the existence of a specific disease, as defined by the presence of Aβ plaques and neurofibrillary tangles. Although Aβ plaques may play a key role in AD pathogenesis, the severity of cognitive impairment correlates best with the burden of neocortical neurofibrillary tangles. |
| Author | Schneider, Julie A. Alafuzoff, Irina Trojanowski, John Q. Bigio, Eileen H. Mackenzie, Ian R. Hulette, Christine M. Leverenz, James B. McKee, Ann C. Masliah, Eliezer Thal, Dietmar R. Montine, Thomas J. Frosch, Matthew P. Iwatsubo, Takeshi Hof, Patrick R. Woltjer, Randall L. Cairns, Nigel J. Castellani, Rudolph J. Haroutunian, Vahram Crain, Barbara J. Kukull, Walter A. Davies, Peter Duyckaerts, Charles Jicha, Gregory A. Nelson, Peter T. Tredici, Kelly Del Bouras, Constantin Jellinger, Kurt A. Wisniewski, Thomas Kövari, Enikö Morris, John C. Troncoso, Juan C. Love, Seth Mann, David M. Braak, Heiko Sonnen, Joshua A. Beach, Thomas G. Hyman, Bradley T. |
| AuthorAffiliation | From the Sanders-Brown Center on Aging (PTN, GAJ) and Departments of Pathology (PTN) and Neurology (GAJ), University of Kentucky, Lexington, Kentucky; Department of Genetics and Pathology (IA), Rudbeck Laboratory, Uppsala University, Uppsala, Sweden; Department of Pathology (EHB), Northwestern Alzheimer Disease Center, Northwestern University Feinberg School of Medicine, Chicago, Illinois; Department of Psychiatry (CB, EK), Geneva University School of Medicine, Geneva, Switzerland; Section of Clinical Neuroanatomy, Department of Neurology (HB, KDT) and Institute of Pathology - Laboratory of Neuropathology (DRT), University of Ulm, Ulm, Germany; Departments of Neurology (NJC, JCM) and Pathology and Immunology (NJC), Washington University School of Medicine, St. Louis, Missouri; Department of Pathology (RJC), University of Maryland School of Medicine; Departments of Pathology (BJC, JCT), Oncology (BJC), and Neurology (JCT), Johns Hopkins School of Medicine, Baltimore, Maryland; Departmen |
| AuthorAffiliation_xml | – name: From the Sanders-Brown Center on Aging (PTN, GAJ) and Departments of Pathology (PTN) and Neurology (GAJ), University of Kentucky, Lexington, Kentucky; Department of Genetics and Pathology (IA), Rudbeck Laboratory, Uppsala University, Uppsala, Sweden; Department of Pathology (EHB), Northwestern Alzheimer Disease Center, Northwestern University Feinberg School of Medicine, Chicago, Illinois; Department of Psychiatry (CB, EK), Geneva University School of Medicine, Geneva, Switzerland; Section of Clinical Neuroanatomy, Department of Neurology (HB, KDT) and Institute of Pathology - Laboratory of Neuropathology (DRT), University of Ulm, Ulm, Germany; Departments of Neurology (NJC, JCM) and Pathology and Immunology (NJC), Washington University School of Medicine, St. Louis, Missouri; Department of Pathology (RJC), University of Maryland School of Medicine; Departments of Pathology (BJC, JCT), Oncology (BJC), and Neurology (JCT), Johns Hopkins School of Medicine, Baltimore, Maryland; Department of Pathology (PD) and Dominick P. Purpura Department of Neurosciencey (PD), Feinstein Institute of Medical Research, Albert Einstein University, Manhasset, New York; Service de Neuropathologie Raymond Escourolle (CD), Hopital de la Salpêtriére, Paris, France; C.S. Kubik Laboratory for Neuropathology (MPF) and Department of Neurology (BTH), Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; Departments of Psychiatry (VH) and Neuroscience (PRH), The Mount Sinai School of Medicine, New York, New York; Departments of Pathology (CMH) and Neurology (CMH), Duke University School of Medicine, Durham, North Carolina; Department of Neuropathology (TI), Graduate School of Medicine at the University of Tokyo, Tokyo, Japan; Institute of Clinical Neurobiology (KAJ), Vienna, Austria; VA-Puget Sound Health Care System (JBL) and Department of Epidemiology (WAK), School of Public Health and Departments of Neurology (JBL) and Pathology (JBL, TJM, JAS), School of Medicine, University of Washington, Seattle, Washington; Department of Neuropathology (SL), Institute of Clinical Neurosciences, Frenchay Hospital and School of Clinical Sciences (SL), University of Bristol, Bristol, United Kingdom; Department of Pathology (IRM), University of British Columbia, Vancouver, British Columbia, Canada; Department of Neuropathology at Hope Hospital (DMM), University of Manchester, Salford, United Kingdom; Departments of Neurosciences (EM) and Pathology (EM), School of Medicine, University of California, San Diego, La Jolla, California; Department of Pathology (ACM) and Bedford Veterans Administration Medical Center (ACM), Boston University, Bedford, Massachusetts; Departments of Pathology and Neurological Sciences and Rush University Alzheimer’s Disease Center (JAS), Rush University Medical Center, Chicago, Illinois; Department of Pathology and Laboratory Medicine (JQT), Institute on Aging, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania; Departments of Neurology, Pathology, and Psychiatry and NYU Alzheimer’s Disease Center (TW), NYU Langone Medical Center, New York; Department of Pathology (RLW), Oregon Health and Science University, Portland, Oregon; and Civin Laboratory for Neuropathology (TGB), Banner Sun Health Research Institute, Sun City, Arizona |
| Author_xml | – sequence: 1 givenname: Peter surname: Nelson middlename: T. fullname: Nelson, Peter T. organization: From the Sanders-Brown Center on Aging (PTN, GAJ) and Departments of Pathology (PTN) and Neurology (GAJ), University of Kentucky, Lexington, Kentucky; Department of Genetics and Pathology (IA), Rudbeck Laboratory, Uppsala University, Uppsala, Sweden; Department of Pathology (EHB), Northwestern Alzheimer Disease Center, Northwestern University Feinberg School of Medicine, Chicago, Illinois; Department of Psychiatry (CB, EK), Geneva University School of Medicine, Geneva, Switzerland; Section of Clinical Neuroanatomy, Department of Neurology (HB, KDT) and Institute of Pathology - Laboratory of Neuropathology (DRT), University of Ulm, Ulm, Germany; Departments of Neurology (NJC, JCM) and Pathology and Immunology (NJC), Washington University School of Medicine, St. Louis, Missouri; Department of Pathology (RJC), University of Maryland School of Medicine; Departments of Pathology (BJC, JCT), Oncology (BJC), and Neurology (JCT), Johns Hopkins School of Medicine, Baltimore, Maryland; Department of Pathology (PD) and Dominick P. Purpura Department of Neurosciencey (PD), Feinstein Institute of Medical Research, Albert Einstein University, Manhasset, New York; Service de Neuropathologie Raymond Escourolle (CD), Hopital de la Salpêtriére, Paris, France; C.S. Kubik Laboratory for Neuropathology (MPF) and Department of Neurology (BTH), Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; Departments of Psychiatry (VH) and Neuroscience (PRH), The Mount Sinai School of Medicine, New York, New York; Departments of Pathology (CMH) and Neurology (CMH), Duke University School of Medicine, Durham, North Carolina; Department of Neuropathology (TI), Graduate School of Medicine at the University of Tokyo, Tokyo, Japan; Institute of Clinical Neurobiology (KAJ), Vienna, Austria; VA-Puget Sound Health Care System (JBL) and Department of Epidemiology (WAK), School of Public Health and Departments of Neurology (JBL) and Pathology (JBL, TJM, JAS), School of Medicine, University of Washington, Seattle, Washington; Department of Neuropathology (SL), Institute of Clinical Neurosciences, Frenchay Hospital and School of Clinical Sciences (SL), University of Bristol, Bristol, United Kingdom; Department of Pathology (IRM), University of British Columbia, Vancouver, British Columbia, Canada; Department of Neuropathology at Hope Hospital (DMM), University of Manchester, Salford, United Kingdom; Departments of Neurosciences (EM) and Pathology (EM), School of Medicine, University of California, San Diego, La Jolla, California; Department of Pathology (ACM) and Bedford Veterans Administration Medical Center (ACM), Boston University, Bedford, Massachusetts; Departments of Pathology and Neurological Sciences and Rush University Alzheimer’s Disease Center (JAS), Rush University Medical Center, Chicago, Illinois; Department of Pathology and Laboratory Medicine (JQT), Institute on Aging, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania; Departments of Neurology, Pathology, and Psychiatry and NYU Alzheimer’s Disease Center (TW), NYU Langone Medical Center, New York; Department of Pathology (RLW), Oregon Health and Science University, Portland, Oregon; and Civin Laboratory for Neuropathology (TGB), Banner Sun Health Research Institute, Sun City, Arizona – sequence: 2 givenname: Irina surname: Alafuzoff fullname: Alafuzoff, Irina – sequence: 3 givenname: Eileen surname: Bigio middlename: H. fullname: Bigio, Eileen H. – sequence: 4 givenname: Constantin surname: Bouras fullname: Bouras, Constantin – sequence: 5 givenname: Heiko surname: Braak fullname: Braak, Heiko – sequence: 6 givenname: Nigel surname: Cairns middlename: J. fullname: Cairns, Nigel J. – sequence: 7 givenname: Rudolph surname: Castellani middlename: J. fullname: Castellani, Rudolph J. – sequence: 8 givenname: Barbara surname: Crain middlename: J. fullname: Crain, Barbara J. – sequence: 9 givenname: Peter surname: Davies fullname: Davies, Peter – sequence: 10 givenname: Kelly surname: Tredici middlename: Del fullname: Tredici, Kelly Del – sequence: 11 givenname: Charles surname: Duyckaerts fullname: Duyckaerts, Charles – sequence: 12 givenname: Matthew surname: Frosch middlename: P. fullname: Frosch, Matthew P. – sequence: 13 givenname: Vahram surname: Haroutunian fullname: Haroutunian, Vahram – sequence: 14 givenname: Patrick surname: Hof middlename: R. fullname: Hof, Patrick R. – sequence: 15 givenname: Christine surname: Hulette middlename: M. fullname: Hulette, Christine M. – sequence: 16 givenname: Bradley surname: Hyman middlename: T. fullname: Hyman, Bradley T. – sequence: 17 givenname: Takeshi surname: Iwatsubo fullname: Iwatsubo, Takeshi – sequence: 18 givenname: Kurt surname: Jellinger middlename: A. fullname: Jellinger, Kurt A. – sequence: 19 givenname: Gregory surname: Jicha middlename: A. fullname: Jicha, Gregory A. – sequence: 20 givenname: Enikö surname: Kövari fullname: Kövari, Enikö – sequence: 21 givenname: Walter surname: Kukull middlename: A. fullname: Kukull, Walter A. – sequence: 22 givenname: James surname: Leverenz middlename: B. fullname: Leverenz, James B. – sequence: 23 givenname: Seth surname: Love fullname: Love, Seth – sequence: 24 givenname: Ian surname: Mackenzie middlename: R. fullname: Mackenzie, Ian R. – sequence: 25 givenname: David surname: Mann middlename: M. fullname: Mann, David M. – sequence: 26 givenname: Eliezer surname: Masliah fullname: Masliah, Eliezer – sequence: 27 givenname: Ann surname: McKee middlename: C. fullname: McKee, Ann C. – sequence: 28 givenname: Thomas surname: Montine middlename: J. fullname: Montine, Thomas J. – sequence: 29 givenname: John surname: Morris middlename: C. fullname: Morris, John C. – sequence: 30 givenname: Julie surname: Schneider middlename: A. fullname: Schneider, Julie A. – sequence: 31 givenname: Joshua surname: Sonnen middlename: A. fullname: Sonnen, Joshua A. – sequence: 32 givenname: Dietmar surname: Thal middlename: R. fullname: Thal, Dietmar R. – sequence: 33 givenname: John surname: Trojanowski middlename: Q. fullname: Trojanowski, John Q. – sequence: 34 givenname: Juan surname: Troncoso middlename: C. fullname: Troncoso, Juan C. – sequence: 35 givenname: Thomas surname: Wisniewski fullname: Wisniewski, Thomas – sequence: 36 givenname: Randall surname: Woltjer middlename: L. fullname: Woltjer, Randall L. – sequence: 37 givenname: Thomas surname: Beach middlename: G. fullname: Beach, Thomas G. |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25854769$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/22487856$$D View this record in MEDLINE/PubMed https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-174651$$DView record from Swedish Publication Index |
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| Issue | 5 |
| Keywords | Nervous system diseases Senescence Alzheimer disease Neuropathology Review Neurofibrillary tangle Epidemiology Cerebral disorder Neurofibrillary tangles Central nervous system disease Aging Degenerative disease Amyloid MAPT Dementia |
| Language | English |
| License | CC BY 4.0 |
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| PublicationDate | 2012-May |
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| PublicationTitle | Journal of neuropathology and experimental neurology |
| PublicationTitleAlternate | J Neuropathol Exp Neurol |
| PublicationYear | 2012 |
| Publisher | American Association of Neuropathologists, Inc Lippincott Williams & Wilkins Oxford University Press |
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12 2016030323380897000_71.5.362.24 2016030323380897000_71.5.362.23 Abner (2016030323380897000_71.5.362.151) 2011; 25 2016030323380897000_71.5.362.311 2016030323380897000_71.5.362.310 2016030323380897000_71.5.362.313 2016030323380897000_71.5.362.314 2016030323380897000_71.5.362.32 2016030323380897000_71.5.362.317 2016030323380897000_71.5.362.31 2016030323380897000_71.5.362.316 2016030323380897000_71.5.362.319 Hardy (2016030323380897000_71.5.362.55) 2006; 9 2016030323380897000_71.5.362.318 2016030323380897000_71.5.362.39 2016030323380897000_71.5.362.38 2016030323380897000_71.5.362.37 2016030323380897000_71.5.362.36 2016030323380897000_71.5.362.35 2016030323380897000_71.5.362.34 2016030323380897000_71.5.362.33 2016030323380897000_71.5.362.300 2016030323380897000_71.5.362.302 2016030323380897000_71.5.362.301 2016030323380897000_71.5.362.304 2016030323380897000_71.5.362.303 2016030323380897000_71.5.362.43 2016030323380897000_71.5.362.306 2016030323380897000_71.5.362.305 2016030323380897000_71.5.362.41 2016030323380897000_71.5.362.308 2016030323380897000_71.5.362.40 Selkoe (2016030323380897000_71.5.362.79) 2011; 17 2016030323380897000_71.5.362.307 2016030323380897000_71.5.362.309 Thal (2016030323380897000_71.5.362.52) 2000; 59 2016030323380897000_71.5.362.49 2016030323380897000_71.5.362.47 2016030323380897000_71.5.362.46 2016030323380897000_71.5.362.45 2016030323380897000_71.5.362.44 2016030323380897000_71.5.362.54 2016030323380897000_71.5.362.53 2016030323380897000_71.5.362.51 2016030323380897000_71.5.362.50 Wisniewski (2016030323380897000_71.5.362.315) 1968; 27 2016030323380897000_71.5.362.59 Gadad (2016030323380897000_71.5.362.92) 2011; 24 2016030323380897000_71.5.362.58 2016030323380897000_71.5.362.57 2016030323380897000_71.5.362.56 McKeel (2016030323380897000_71.5.362.246) 2004; 63 Sonnen (2016030323380897000_71.5.362.145) 2010; 19 Takashima (2016030323380897000_71.5.362.85) 2008; 14 2016030323380897000_71.5.362.63 2016030323380897000_71.5.362.62 Haroutunian (2016030323380897000_71.5.362.342) 2009; 11 2016030323380897000_71.5.362.61 2016030323380897000_71.5.362.60 2016030323380897000_71.5.362.69 2016030323380897000_71.5.362.68 2016030323380897000_71.5.362.67 2016030323380897000_71.5.362.66 2016030323380897000_71.5.362.191 2016030323380897000_71.5.362.190 2016030323380897000_71.5.362.193 2016030323380897000_71.5.362.192 2016030323380897000_71.5.362.195 2016030323380897000_71.5.362.194 2016030323380897000_71.5.362.197 2016030323380897000_71.5.362.196 2016030323380897000_71.5.362.199 2016030323380897000_71.5.362.198 Wong (2016030323380897000_71.5.362.124) 1996; 15 2016030323380897000_71.5.362.76 2016030323380897000_71.5.362.75 2016030323380897000_71.5.362.74 2016030323380897000_71.5.362.72 2016030323380897000_71.5.362.71 2016030323380897000_71.5.362.70 2016030323380897000_71.5.362.78 2016030323380897000_71.5.362.77 Yasha (2016030323380897000_71.5.362.241) 1997; 105 2016030323380897000_71.5.362.180 2016030323380897000_71.5.362.182 2016030323380897000_71.5.362.181 2016030323380897000_71.5.362.184 2016030323380897000_71.5.362.183 2016030323380897000_71.5.362.186 2016030323380897000_71.5.362.185 2016030323380897000_71.5.362.90 Jin (2016030323380897000_71.5.362.91) 2011; 108 2016030323380897000_71.5.362.188 2016030323380897000_71.5.362.187 2016030323380897000_71.5.362.189 Mann (2016030323380897000_71.5.362.312) 1985; 4 2016030323380897000_71.5.362.86 2016030323380897000_71.5.362.84 2016030323380897000_71.5.362.83 2016030323380897000_71.5.362.82 2016030323380897000_71.5.362.81 Duyckaerts (2016030323380897000_71.5.362.250) 1998; 98 2016030323380897000_71.5.362.80 2016030323380897000_71.5.362.89 2016030323380897000_71.5.362.88 2016030323380897000_71.5.362.290 2016030323380897000_71.5.362.9 2016030323380897000_71.5.362.171 2016030323380897000_71.5.362.8 2016030323380897000_71.5.362.170 2016030323380897000_71.5.362.291 2016030323380897000_71.5.362.173 2016030323380897000_71.5.362.294 2016030323380897000_71.5.362.172 2016030323380897000_71.5.362.293 2016030323380897000_71.5.362.175 2016030323380897000_71.5.362.296 2016030323380897000_71.5.362.174 2016030323380897000_71.5.362.295 2016030323380897000_71.5.362.177 2016030323380897000_71.5.362.298 2016030323380897000_71.5.362.176 2016030323380897000_71.5.362.297 2016030323380897000_71.5.362.179 2016030323380897000_71.5.362.178 2016030323380897000_71.5.362.299 Arai (2016030323380897000_71.5.362.30) 2001; 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24 Chen (2016030323380897000_71.5.362.65) 2011; 24 2016030323380897000_71.5.362.167 2016030323380897000_71.5.362.288 2016030323380897000_71.5.362.169 Hof (2016030323380897000_71.5.362.42) 1996; 11 Erkinjuntti (2016030323380897000_71.5.362.157) 1987; 76 Brayne (2016030323380897000_71.5.362.292) 2009; 18 Knopman (2016030323380897000_71.5.362.163) 2003; 62 2016030323380897000_71.5.362.270 2016030323380897000_71.5.362.272 2016030323380897000_71.5.362.150 2016030323380897000_71.5.362.271 2016030323380897000_71.5.362.153 2016030323380897000_71.5.362.274 2016030323380897000_71.5.362.152 2016030323380897000_71.5.362.273 Mattsson (2016030323380897000_71.5.362.333) 2011; 76 2016030323380897000_71.5.362.155 2016030323380897000_71.5.362.276 2016030323380897000_71.5.362.154 Thal (2016030323380897000_71.5.362.209) 2003; 62 2016030323380897000_71.5.362.275 2016030323380897000_71.5.362.278 2016030323380897000_71.5.362.156 2016030323380897000_71.5.362.277 2016030323380897000_71.5.362.159 2016030323380897000_71.5.362.158 2016030323380897000_71.5.362.279 Delacourte (2016030323380897000_71.5.362.87) 2008; 14 Jellinger (2016030323380897000_71.5.362.125 |
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doi: 10.1038/nm840 – ident: 2016030323380897000_71.5.362.296 doi: 10.1159/000017111 |
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| Snippet | ABSTRACTClinicopathologic correlation studies are critically important for the field of Alzheimer disease (AD) research. Studies on human subjects with autopsy... Clinicopathologic correlation studies are critically important for the field of Alzheimer disease (AD) research. Studies on human subjects with autopsy... |
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| SubjectTerms | Aged Aged, 80 and over Aging Alzheimer disease Alzheimer Disease - complications Alzheimer Disease - pathology Amyloid Amyloid beta-Peptides - metabolism Biological and medical sciences Brain Brain - metabolism Brain - pathology Cognition & reasoning Cognition Disorders - etiology Cognition Disorders - pathology Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Dementia Disease Epidemiology Humans MAPT Medical sciences Neurofibrillary tangles Neurofibrillary Tangles - pathology Neurology Neuropathology Plaque, Amyloid - pathology Statistics as Topic Studies |
| Title | Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/22487856 https://www.proquest.com/docview/1019841504 https://www.proquest.com/docview/1016675255 https://pubmed.ncbi.nlm.nih.gov/PMC3560290 https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-174651 |
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