Tau and Aβ imaging, CSF measures, and cognition in Alzheimer's disease
Alzheimer's disease (AD) is characterized by two molecular pathologies: cerebral β-amyloidosis in the form of β-amyloid (Aβ) plaques and tauopathy in the form of neurofibrillary tangles, neuritic plaques, and neuropil threads. Until recently, only Aβ could be studied in humans using positron em...
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| Published in | Science translational medicine Vol. 8; no. 338; p. 338ra66 |
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| Main Authors | , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
11.05.2016
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| Subjects | |
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| Abstract | Alzheimer's disease (AD) is characterized by two molecular pathologies: cerebral β-amyloidosis in the form of β-amyloid (Aβ) plaques and tauopathy in the form of neurofibrillary tangles, neuritic plaques, and neuropil threads. Until recently, only Aβ could be studied in humans using positron emission tomography (PET) imaging owing to a lack of tau PET imaging agents. Clinical pathological studies have linked tau pathology closely to the onset and progression of cognitive symptoms in patients with AD. We report PET imaging of tau and Aβ in a cohort of cognitively normal older adults and those with mild AD. Multivariate analyses identified unique disease-related stereotypical spatial patterns (topographies) for deposition of tau and Aβ. These PET imaging tau and Aβ topographies were spatially distinct but correlated with disease progression. Cerebrospinal fluid measures of tau, often used to stage preclinical AD, correlated with tau deposition in the temporal lobe. Tau deposition in the temporal lobe more closely tracked dementia status and was a better predictor of cognitive performance than Aβ deposition in any region of the brain. These data support models of AD where tau pathology closely tracks changes in brain function that are responsible for the onset of early symptoms in AD. |
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| AbstractList | Alzheimer's disease (AD) is characterized by two molecular pathologies: cerebral β-amyloidosis in the form of β-amyloid (Aβ) plaques and tauopathy in the form of neurofibrillary tangles, neuritic plaques, and neuropil threads. Until recently, only Aβ could be studied in humans using positron emission tomography (PET) imaging owing to a lack of tau PET imaging agents. Clinical pathological studies have linked tau pathology closely to the onset and progression of cognitive symptoms in patients with AD. We report PET imaging of tau and Aβ in a cohort of cognitively normal older adults and those with mild AD. Multivariate analyses identified unique disease-related stereotypical spatial patterns (topographies) for deposition of tau and Aβ. These PET imaging tau and Aβ topographies were spatially distinct but correlated with disease progression. Cerebrospinal fluid measures of tau, often used to stage preclinical AD, correlated with tau deposition in the temporal lobe. Tau deposition in the temporal lobe more closely tracked dementia status and was a better predictor of cognitive performance than Aβ deposition in any region of the brain. These data support models of AD where tau pathology closely tracks changes in brain function that are responsible for the onset of early symptoms in AD. |
| Author | Su, Yi Friedrichsen, Karl McCarthy, John Benzinger, Tammie L S Ances, Beau M Morris, John C Gordon, Brian Aldea, Patricia Christensen, Jon Owen, Christopher Hassenstab, Jason Fagan, Anne M Cairns, Nigel J Brier, Matthew R Holtzman, David M Stern, Ari |
| Author_xml | – sequence: 1 givenname: Matthew R surname: Brier fullname: Brier, Matthew R organization: Department of Neurology, Washington University in St. Louis, St. Louis, MO 63110, USA – sequence: 2 givenname: Brian surname: Gordon fullname: Gordon, Brian organization: Department of Radiology, Washington University in St. Louis, St. Louis, MO 63110, USA. Knight Alzheimer's Disease Research Center, Washington University in St. Louis, St. Louis, MO 63110, USA – sequence: 3 givenname: Karl surname: Friedrichsen fullname: Friedrichsen, Karl organization: Department of Radiology, Washington University in St. Louis, St. Louis, MO 63110, USA – sequence: 4 givenname: John surname: McCarthy fullname: McCarthy, John organization: Department of Mathematics, Washington University in St. Louis, St. Louis, MO 63110, USA – sequence: 5 givenname: Ari surname: Stern fullname: Stern, Ari organization: Department of Mathematics, Washington University in St. Louis, St. Louis, MO 63110, USA – sequence: 6 givenname: Jon surname: Christensen fullname: Christensen, Jon organization: Department of Radiology, Washington University in St. Louis, St. Louis, MO 63110, USA – sequence: 7 givenname: Christopher surname: Owen fullname: Owen, Christopher organization: Department of Radiology, Washington University in St. Louis, St. Louis, MO 63110, USA – sequence: 8 givenname: Patricia surname: Aldea fullname: Aldea, Patricia organization: Department of Radiology, Washington University in St. Louis, St. Louis, MO 63110, USA – sequence: 9 givenname: Yi surname: Su fullname: Su, Yi organization: Department of Radiology, Washington University in St. Louis, St. Louis, MO 63110, USA – sequence: 10 givenname: Jason surname: Hassenstab fullname: Hassenstab, Jason organization: Department of Neurology, Washington University in St. Louis, St. Louis, MO 63110, USA. Knight Alzheimer's Disease Research Center, Washington University in St. Louis, St. Louis, MO 63110, USA – sequence: 11 givenname: Nigel J surname: Cairns fullname: Cairns, Nigel J organization: Department of Neurology, Washington University in St. Louis, St. Louis, MO 63110, USA. Knight Alzheimer's Disease Research Center, Washington University in St. Louis, St. Louis, MO 63110, USA. Department of Pathology, Washington University in St. Louis, St. Louis, MO 63110, USA – sequence: 12 givenname: David M surname: Holtzman fullname: Holtzman, David M organization: Department of Neurology, Washington University in St. Louis, St. Louis, MO 63110, USA. Knight Alzheimer's Disease Research Center, Washington University in St. Louis, St. Louis, MO 63110, USA. Hope Center for Neurological Disorders, Washington University in St. Louis, St. Louis, MO 63110, USA – sequence: 13 givenname: Anne M surname: Fagan fullname: Fagan, Anne M organization: Department of Neurology, Washington University in St. Louis, St. Louis, MO 63110, USA. Knight Alzheimer's Disease Research Center, Washington University in St. Louis, St. Louis, MO 63110, USA. Hope Center for Neurological Disorders, Washington University in St. Louis, St. Louis, MO 63110, USA – sequence: 14 givenname: John C surname: Morris fullname: Morris, John C organization: Department of Neurology, Washington University in St. Louis, St. Louis, MO 63110, USA. Knight Alzheimer's Disease Research Center, Washington University in St. Louis, St. Louis, MO 63110, USA. Department of Pathology, Washington University in St. Louis, St. Louis, MO 63110, USA. Hope Center for Neurological Disorders, Washington University in St. Louis, St. Louis, MO 63110, USA – sequence: 15 givenname: Tammie L S surname: Benzinger fullname: Benzinger, Tammie L S organization: Department of Radiology, Washington University in St. Louis, St. Louis, MO 63110, USA. Knight Alzheimer's Disease Research Center, Washington University in St. Louis, St. Louis, MO 63110, USA. Department of Neurosurgery, Washington University in St. Louis, St. Louis, MO 63110, USA – sequence: 16 givenname: Beau M surname: Ances fullname: Ances, Beau M email: bances@wustl.edu organization: Department of Neurology, Washington University in St. Louis, St. Louis, MO 63110, USA. Department of Radiology, Washington University in St. Louis, St. Louis, MO 63110, USA. Knight Alzheimer's Disease Research Center, Washington University in St. Louis, St. Louis, MO 63110, USA. Hope Center for Neurological Disorders, Washington University in St. Louis, St. Louis, MO 63110, USA. bances@wustl.edu |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27169802$$D View this record in MEDLINE/PubMed |
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| Snippet | Alzheimer's disease (AD) is characterized by two molecular pathologies: cerebral β-amyloidosis in the form of β-amyloid (Aβ) plaques and tauopathy in the form... |
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| SubjectTerms | Aged Aged, 80 and over Alzheimer Disease - cerebrospinal fluid Alzheimer Disease - diagnostic imaging Alzheimer Disease - physiopathology Amyloid beta-Peptides - cerebrospinal fluid Amyloid beta-Peptides - metabolism Brain - diagnostic imaging Brain - metabolism Cognition - physiology Female Humans Male Peptide Fragments - cerebrospinal fluid Peptide Fragments - metabolism Positron-Emission Tomography tau Proteins - cerebrospinal fluid tau Proteins - metabolism |
| Title | Tau and Aβ imaging, CSF measures, and cognition in Alzheimer's disease |
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