Correction to: Different aspects of Alzheimer's disease-related amyloid β-peptide pathology and their relationship to amyloid positron emission tomography imaging and dementia
Autor: | Jochen Walter, Aruna Chakrabarty, Christine A. F. von Arnim, Adrian Smith, Kerstin Heurling, Thomas G. Beach, Azzam Ismail, Mathieu Vandenbulcke, Ajeet Rijal Upadhaya, Johan Lilja, Karthikeyan Balakrishnan, Gill Farrar, Rik Vandenberghe, Sathish Kumar, Alicja Ronisz, Thomas Tousseyn, Christopher Buckley, Markus Otto, Dietmar Rudolf Thal |
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Rok vydání: | 2020 |
Předmět: |
Pathology
medicine.medical_specialty Staging Amyloid lcsh:RC346-429 Pathology and Forensic Medicine Angiopathy Cellular and Molecular Neuroscience mental disorders Insoluble amyloid medicine Dementia Senile plaques lcsh:Neurology. Diseases of the nervous system Amyloid maturation medicine.diagnostic_test Soluble amyloid business.industry Research Neurofibrillary tangle Human brain Amyloid load medicine.disease [18F]flutemetamol medicine.anatomical_structure Positron emission tomography Amyloid PET Neurology (clinical) Cerebral amyloid angiopathy Amyloid β peptide business Alzheimer’s disease |
Zdroj: | Acta Neuropathologica Communications Acta Neuropathologica Communications, Vol 8, Iss 1, Pp 1-3 (2020) |
ISSN: | 2051-5960 |
Popis: | Alzheimer’s disease (AD)-related amyloid β-peptide (Aβ) pathology in the form of amyloid plaques and cerebral amyloid angiopathy (CAA) spreads in its topographical distribution, increases in quantity, and undergoes qualitative changes in its composition of modified Aβ species throughout the pathogenesis of AD. It is not clear which of these aspects of Aβ pathology contribute to AD progression and to what extent amyloid positron emission tomography (PET) reflects each of these aspects. To address these questions three cohorts of human autopsy cases (in total n = 271) were neuropathologically and biochemically examined for the topographical distribution of Aβ pathology (plaques and CAA), its quantity and its composition. These parameters were compared with neurofibrillary tangle (NFT) and neuritic plaque pathology, the degree of dementia and the results from [18F]flutemetamol amyloid PET imaging in cohort 3. All three aspects of Aβ pathology correlated with one another, the estimation of Aβ pathology by [18F]flutemetamol PET, AD-related NFT pathology, neuritic plaques, and with the degree of dementia. These results show that one aspect of Aβ pathology can be used to predict the other two, and correlates well with the development of dementia, advancing NFT and neuritic plaque pathology. Moreover, amyloid PET estimates all three aspects of Aβ pathology in-vivo. Accordingly, amyloid PET-based estimates for staging of amyloid pathology indicate the progression status of amyloid pathology in general and, in doing so, also of AD pathology. Only 7.75% of our cases deviated from this general association. |
Databáze: | OpenAIRE |
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