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Different aspects of Alzheimer's disease-related amyloid beta-peptide pathology and their relationship to amyloid positron emission tomography imaging and dementia

Artikel i vetenskaplig tidskrift
Författare D. R. Thal
A. Ronisz
T. Tousseyn
A. R. Upadhaya
K. Balakrishnan
R. Vandenberghe
M. Vandenbulcke
C. A. F. von Arnim
M. Otto
T. G. Beach
J. Lilja
Kerstin Heurling
A. Chakrabarty
A. Ismail
C. Buckley
A. P. L. Smith
S. Kumar
G. Farrar
J. Walter
Publicerad i Acta Neuropathologica Communications
Volym 7
Nummer/häfte 1
Sidor 16
ISSN 2051-5960
Publiceringsår 2019
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Wallenberg Centre for Molecular and Translational Medicine
Sidor 16
Språk en
Länkar dx.doi.org/10.1186/s40478-019-0837-...
Ämnesord Alzheimer's disease, Amyloid beta peptide, Staging, Amyloid load, Soluble amyloid, Insoluble amyloid, Amyloid maturation, Amyloid PET, [F-18]flutemetamol, a-beta, neuropathologic assessment, neurofibrillary tangles, cognitive, impairment, national institute, senile plaques, human brain, pet, deposition, angiopathy, Neurosciences & Neurology
Ämneskategorier Neurologi

Sammanfattning

Alzheimer's disease (AD)-related amyloid beta-peptide (A beta) 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 A beta species throughout the pathogenesis of AD. It is not clear which of these aspects of A beta 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 A beta 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 [F-18]flutemetamol amyloid PET imaging in cohort 3. All three aspects of A beta pathology correlated with one another, the estimation of A beta pathology by [F-18]flutemetamol PET, AD-related NFT pathology, neuritic plaques, and with the degree of dementia. These results show that one aspect of A beta 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 A beta 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.

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Utskriftsdatum: 2020-04-10