Early Selective Vulnerability of the CA2 Hippocampal Subfield in Primary Age-Related Tauopathy
Abstract Primary age-related tauopathy (PART) is a neurodegenerative entity defined as Alzheimer-type neurofibrillary degeneration primarily affecting the medial temporal lobe with minimal to absent amyloid-β (Aβ) plaque deposition. The extent to which PART can be differentiated pathoanatomically fr...
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| Published in | Journal of neuropathology and experimental neurology Vol. 80; no. 2; pp. 102 - 111 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Oxford University Press
01.02.2021
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Abstract
Primary age-related tauopathy (PART) is a neurodegenerative entity defined as Alzheimer-type neurofibrillary degeneration primarily affecting the medial temporal lobe with minimal to absent amyloid-β (Aβ) plaque deposition. The extent to which PART can be differentiated pathoanatomically from Alzheimer disease (AD) is unclear. Here, we examined the regional distribution of tau pathology in a large cohort of postmortem brains (n = 914). We found an early vulnerability of the CA2 subregion of the hippocampus to neurofibrillary degeneration in PART, and semiquantitative assessment of neurofibrillary degeneration in CA2 was significantly greater than in CA1 in PART. In contrast, subjects harboring intermediate-to-high AD neuropathologic change (ADNC) displayed relative sparing of CA2 until later stages of their disease course. In addition, the CA2/CA1 ratio of neurofibrillary degeneration in PART was significantly higher than in subjects with intermediate-to-high ADNC burden. Furthermore, the distribution of tau pathology in PART diverges from the Braak NFT staging system and Braak stage does not correlate with cognitive function in PART as it does in individuals with intermediate-to-high ADNC. These findings highlight the need for a better understanding of the contribution of PART to cognitive impairment and how neurofibrillary degeneration interacts with Aβ pathology in AD and PART. |
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| AbstractList | Primary age-related tauopathy (PART) is a neurodegenerative entity defined as Alzheimer-type neurofibrillary degeneration primarily affecting the medial temporal lobe with minimal to absent amyloid-[beta] (A[beta]) plaque deposition. The extent to which PART can be differentiated pathoanatomically from Alzheimer disease (AD) is unclear. Here, we examined the regional distribution of tau pathology in a large cohort of postmortem brains (n = 914). We found an early vulnerability of the CA2 subregion of the hippocampus to neurofibrillary degeneration in PART, and semiquantitative assessment of neurofibrillary degeneration in CA2 was significantly greater than in CA1 in PART. In contrast, subjects harboring intermediate-to-high AD neuropathologic change (ADNC) displayed relative sparing of CA2 until later stages of their disease course. In addition, the CA2/CA1 ratio of neurofibrillary degeneration in PART was significantly higher than in subjects with intermediate-to-high ADNC burden. Furthermore, the distribution of tau pathology in PART diverges from the Braak NFT staging system and Braak stage does not correlate with cognitive function in PART as it does in individuals with intermediate-to-high ADNC. These findings highlight the need for a better understanding of the contribution of PART to cognitive impairment and how neurofibrillary degeneration interacts with A[beta] pathology in AD and PART. Primary age-related tauopathy (PART) is a neurodegenerative entity defined as Alzheimer-type neurofibrillary degeneration primarily affecting the medial temporal lobe with minimal to absent amyloid-β (Aβ) plaque deposition. The extent to which PART can be differentiated pathoanatomically from Alzheimer disease (AD) is unclear. Here, we examined the regional distribution of tau pathology in a large cohort of postmortem brains (n = 914). We found an early vulnerability of the CA2 subregion of the hippocampus to neurofibrillary degeneration in PART, and semiquantitative assessment of neurofibrillary degeneration in CA2 was significantly greater than in CA1 in PART. In contrast, subjects harboring intermediate-to-high AD neuropathologic change (ADNC) displayed relative sparing of CA2 until later stages of their disease course. In addition, the CA2/CA1 ratio of neurofibrillary degeneration in PART was significantly higher than in subjects with intermediate-to-high ADNC burden. Furthermore, the distribution of tau pathology in PART diverges from the Braak NFT staging system and Braak stage does not correlate with cognitive function in PART as it does in individuals with intermediate-to-high ADNC. These findings highlight the need for a better understanding of the contribution of PART to cognitive impairment and how neurofibrillary degeneration interacts with Aβ pathology in AD and PART. Primary age-related tauopathy (PART) is a neurodegenerative entity defined as Alzheimer-type neurofibrillary degeneration primarily affecting the medial temporal lobe with minimal to absent amyloid-β (Aβ) plaque deposition. The extent to which PART can be differentiated pathoanatomically from Alzheimer disease (AD) is unclear. Here, we examined the regional distribution of tau pathology in a large cohort of postmortem brains (n = 914). We found an early vulnerability of the CA2 subregion of the hippocampus to neurofibrillary degeneration in PART, and semiquantitative assessment of neurofibrillary degeneration in CA2 was significantly greater than in CA1 in PART. In contrast, subjects harboring intermediate-to-high AD neuropathologic change (ADNC) displayed relative sparing of CA2 until later stages of their disease course. In addition, the CA2/CA1 ratio of neurofibrillary degeneration in PART was significantly higher than in subjects with intermediate-to-high ADNC burden. Furthermore, the distribution of tau pathology in PART diverges from the Braak NFT staging system and Braak stage does not correlate with cognitive function in PART as it does in individuals with intermediate-to-high ADNC. These findings highlight the need for a better understanding of the contribution of PART to cognitive impairment and how neurofibrillary degeneration interacts with Aβ pathology in AD and PART.Primary age-related tauopathy (PART) is a neurodegenerative entity defined as Alzheimer-type neurofibrillary degeneration primarily affecting the medial temporal lobe with minimal to absent amyloid-β (Aβ) plaque deposition. The extent to which PART can be differentiated pathoanatomically from Alzheimer disease (AD) is unclear. Here, we examined the regional distribution of tau pathology in a large cohort of postmortem brains (n = 914). We found an early vulnerability of the CA2 subregion of the hippocampus to neurofibrillary degeneration in PART, and semiquantitative assessment of neurofibrillary degeneration in CA2 was significantly greater than in CA1 in PART. In contrast, subjects harboring intermediate-to-high AD neuropathologic change (ADNC) displayed relative sparing of CA2 until later stages of their disease course. In addition, the CA2/CA1 ratio of neurofibrillary degeneration in PART was significantly higher than in subjects with intermediate-to-high ADNC burden. Furthermore, the distribution of tau pathology in PART diverges from the Braak NFT staging system and Braak stage does not correlate with cognitive function in PART as it does in individuals with intermediate-to-high ADNC. These findings highlight the need for a better understanding of the contribution of PART to cognitive impairment and how neurofibrillary degeneration interacts with Aβ pathology in AD and PART. Primary age-related tauopathy (PART) is a neurodegenerative entity defined as Alzheimer-type neurofibrillary degeneration primarily affecting the medial temporal lobe with minimal to absent amyloid-β (Aβ) plaque deposition. The extent to which PART can be differentiated pathoanatomically from Alzheimer disease (AD) is unclear. Here, we examined the regional distribution of tau pathology in a large cohort of postmortem brains ( n = 914). We found an early vulnerability of the CA2 subregion of the hippocampus to neurofibrillary degeneration in PART, and semiquantitative assessment of neurofibrillary degeneration in CA2 was significantly greater than in CA1 in PART. In contrast, subjects harboring intermediate-to-high AD neuropathologic change (ADNC) displayed relative sparing of CA2 until later stages of their disease course. In addition, the CA2/CA1 ratio of neurofibrillary degeneration in PART was significantly higher than in subjects with intermediate-to-high ADNC burden. Furthermore, the distribution of tau pathology in PART diverges from the Braak NFT staging system and Braak stage does not correlate with cognitive function in PART as it does in individuals with intermediate-to-high ADNC. These findings highlight the need for a better understanding of the contribution of PART to cognitive impairment and how neurofibrillary degeneration interacts with Aβ pathology in AD and PART. Abstract Primary age-related tauopathy (PART) is a neurodegenerative entity defined as Alzheimer-type neurofibrillary degeneration primarily affecting the medial temporal lobe with minimal to absent amyloid-β (Aβ) plaque deposition. The extent to which PART can be differentiated pathoanatomically from Alzheimer disease (AD) is unclear. Here, we examined the regional distribution of tau pathology in a large cohort of postmortem brains (n = 914). We found an early vulnerability of the CA2 subregion of the hippocampus to neurofibrillary degeneration in PART, and semiquantitative assessment of neurofibrillary degeneration in CA2 was significantly greater than in CA1 in PART. In contrast, subjects harboring intermediate-to-high AD neuropathologic change (ADNC) displayed relative sparing of CA2 until later stages of their disease course. In addition, the CA2/CA1 ratio of neurofibrillary degeneration in PART was significantly higher than in subjects with intermediate-to-high ADNC burden. Furthermore, the distribution of tau pathology in PART diverges from the Braak NFT staging system and Braak stage does not correlate with cognitive function in PART as it does in individuals with intermediate-to-high ADNC. These findings highlight the need for a better understanding of the contribution of PART to cognitive impairment and how neurofibrillary degeneration interacts with Aβ pathology in AD and PART. Primary age-related tauopathy (PART) is a neurodegenerative entity defined as Alzheimer-type neurofibrillary degeneration primarily affecting the medial temporal lobe with minimal to absent amyloid-[beta] (A[beta]) plaque deposition. The extent to which PART can be differentiated pathoanatomically from Alzheimer disease (AD) is unclear. Here, we examined the regional distribution of tau pathology in a large cohort of postmortem brains (n = 914). We found an early vulnerability of the CA2 subregion of the hippocampus to neurofibrillary degeneration in PART, and semiquantitative assessment of neurofibrillary degeneration in CA2 was significantly greater than in CA1 in PART. In contrast, subjects harboring intermediate-to-high AD neuropathologic change (ADNC) displayed relative sparing of CA2 until later stages of their disease course. In addition, the CA2/CA1 ratio of neurofibrillary degeneration in PART was significantly higher than in subjects with intermediate-to-high ADNC burden. Furthermore, the distribution of tau pathology in PART diverges from the Braak NFT staging system and Braak stage does not correlate with cognitive function in PART as it does in individuals with intermediate-to-high ADNC. These findings highlight the need for a better understanding of the contribution of PART to cognitive impairment and how neurofibrillary degeneration interacts with A[beta] pathology in AD and PART. Key Words: Alzheimer disease, CA2, Cognitive status, Cornu ammonis, Hippocampal subfields, Neurodegenerative disease, Primary age-related tauopathy. |
| Audience | Academic |
| Author | Richardson, Timothy E Sakai, Kenji Stein, Thor D Corrada, María Keene, C Dirk Hansen, Lawrence A Kovacs, Gabor G Walker, Jamie M Attems, Johannes Schneider, Julie A Purohit, Dushyant P Sano, Mary Iida, Megan A Masliah, Eliezer Vonsattel, Jean-Paul Rissman, Robert A Flanagan, Margaret E Gearing, Marla White, Charles L Weintraub, Sandra Haroutunian, Vahram Cortes, Etty Franklin, Erin Nelson, Peter T Murray, Melissa Kofler, Julia Budson, Andrew Dickson, Dennis W Poon, Wayne Glass, Jonathan Teich, Andrew F Shang, Ping Beach, Thomas G Kawas, Claudia Yamada, Masahito Woltjer, Randall L Bigio, Eileen H Crary, John F Hof, Patrick R Troncoso, Juan C Lee, Edward B Trojanowski, John Q Ayalon, Gai Farrell, Kurt Mao, Qinwen Honig, Lawrence Pham, Thao Mesulam, M Marsel Wolk, David A McMillan, Corey T Foong, Chan Yu, Lei Perrin, Richard McKee, Ann C Cairns, Nigel J Fischer, Peter Lutz, Mirjam I |
| AuthorAffiliation | 23 Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania , Philadelphia, Pennsylvania, USA 21 Department of Pathology, University of Washington , Seattle, Washington, USA 3 Department of Pathology, State University of New York, Upstate Medical University , Syracuse, New York, USA 31 Division of Neuropathology, Department of Pathology, Johns Hopkins University School of Medicine , Baltimore, Maryland, USA 1 From the Department of Pathology, University of Texas Health Science Center , San Antonio, Texas, USA 25 Department of Neurology, Perelman School of Medicine, University of Pennsylvania , Philadelphia, Pennsylvania, USA 9 Department of Neuroscience, Genentech Inc. , South San Francisco, California, USA 11 Department of Pathology, Northwestern Cognitive Neurology and Alzheimer Disease Center, Northwestern University Feinberg School of Medicine , Chicago, Illinois, USA 27 Department of Pathology, |
| AuthorAffiliation_xml | – name: 5 Neuropathology Brain Bank & Research Core, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai , New York, New York, USA – name: 9 Department of Neuroscience, Genentech Inc. , South San Francisco, California, USA – name: 17 Department of Pathology and Laboratory Medicine, Emory University School of Medicine , Atlanta, Georgia, USA – name: 7 Department of Pathology, University of Texas Southwestern Medical Center , Dallas, Texas, USA – name: 20 Department of Neurology, Columbia University Irving Medical Center , New York, New York, USA – name: 29 Departments of Pathology and Neurological Sciences, Rush University Medical Center , Chicago, Illinois, USA – name: 23 Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania , Philadelphia, Pennsylvania, USA – name: 14 Institute for Memory Impairments and Neurological Disorders, UC Irvine , Irvine, California, USA – name: 11 Department of Pathology, Northwestern Cognitive Neurology and Alzheimer Disease Center, Northwestern University Feinberg School of Medicine , Chicago, Illinois, USA – name: 15 Department of Neuroscience, Mayo Clinic , Jacksonville, Florida, USA – name: 18 Departments of Neurosciences and Pathology, University of California , San Diego, La Jolla, California, USA – name: 2 Glenn Biggs Institute for Alzheimer’s & Neurodegenerative Diseases, University of Texas Health Science Center , San Antonio, Texas, USA – name: 27 Department of Pathology, Oregon Health Sciences University , Portland, Oregon, USA – name: 1 From the Department of Pathology, University of Texas Health Science Center , San Antonio, Texas, USA – name: 26 Department of Pathology and Sanders-Brown Center on Aging, University of Kentucky , Lexington, Kentucky, USA – name: 3 Department of Pathology, State University of New York, Upstate Medical University , Syracuse, New York, USA – name: 8 Institute for Ageing and Health, Newcastle University , Newcastle upon Tyne, United Kingdom – name: 10 Neuropathology, Banner Sun Health Research Institute , Sun City, Arizona, USA – name: 6 Ronald M. Loeb Center for Alzheimer’s Disease, Icahn School of Medicine at Mount Sinai , New York, New York, USA – name: 16 Department of Laboratory Medicine and Pathobiology, University of Toronto, Laboratory Medicine Program, University Health Network, and Tanz Centre for Research in Neurodegenerative Disease, Krembil Brain Institute , Toronto, Ontario, Canada – name: 22 Department of Pathology, University of Pittsburgh Medical Center , Pittsburgh, Pennsylvania, USA – name: 30 Department of Pathology & Cell Biology and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Medical Center , New York, New York, USA – name: 24 Institute of Neurology, Medical University of Vienna , Vienna, Austria – name: 31 Division of Neuropathology, Department of Pathology, Johns Hopkins University School of Medicine , Baltimore, Maryland, USA – name: 19 Department of Psychiatry and Alzheimer’s Disease Research Center, Icahn School of Medicine at Mount Sinai , New York, New York, USA – name: 28 Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Sciences , Kanazawa, Japan – name: 13 Department of Pathology and Immunology, Washington University School of Medicine , St. Louis, Missouri, USA – name: 21 Department of Pathology, University of Washington , Seattle, Washington, USA – name: 12 Department of Pathology, VA Medical Center & Boston University School of Medicine , Boston, Massachusetts, USA – name: 25 Department of Neurology, Perelman School of Medicine, University of Pennsylvania , Philadelphia, Pennsylvania, USA – name: 4 Department of Pathology and Nash Family Neuroscience, Icahn School of Medicine at Mount Sinai , New York, New York, USA |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33367843$$D View this record in MEDLINE/PubMed |
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| Keywords | Hippocampal subfields Cornu ammonis Alzheimer disease CA2 Cognitive status Neurodegenerative disease Primary age-related tauopathy |
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Primary age-related tauopathy (PART) is a neurodegenerative entity defined as Alzheimer-type neurofibrillary degeneration primarily affecting the... Primary age-related tauopathy (PART) is a neurodegenerative entity defined as Alzheimer-type neurofibrillary degeneration primarily affecting the medial... |
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| SubjectTerms | Age factors in disease Aged Aged, 80 and over Aging - metabolism Aging - pathology Amyloid beta-Peptides - metabolism Brain diseases CA2 Region, Hippocampal - metabolism CA2 Region, Hippocampal - pathology Degeneration Development and progression Female Health aspects Hippocampus (Brain) Humans Male Middle Aged Nervous system Neurofibrillary Tangles - metabolism Neurofibrillary Tangles - pathology Neurons - metabolism Neurons - pathology Original Pathology Plaque, Amyloid - metabolism Plaque, Amyloid - pathology Risk factors Tau proteins tau Proteins - metabolism Tauopathies - metabolism Tauopathies - pathology |
| Title | Early Selective Vulnerability of the CA2 Hippocampal Subfield in Primary Age-Related Tauopathy |
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