Cerebral perfusion in the predementia stages of Alzheimer’s disease

Objectives To investigate arterial spin-labelling (ASL) cerebral blood flow (CBF) changes in predementia stages of Alzheimer’s disease (AD). Methods Data were obtained from 177 patients with subjective complaints, mild cognitive impairment and AD from the Amsterdam Dementia Cohort. AD stages were ba...

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Veröffentlicht in:European radiology 2016-02, Vol.26 (2), p.506-514
Hauptverfasser: Binnewijzend, Maja A. A., Benedictus, Marije R., Kuijer, Joost P. A., van der Flier, Wiesje M., Teunissen, Charlotte E., Prins, Niels D., Wattjes, Mike P., van Berckel, Bart N.M., Scheltens, Philip, Barkhof, Frederik
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Sprache:eng
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Zusammenfassung:Objectives To investigate arterial spin-labelling (ASL) cerebral blood flow (CBF) changes in predementia stages of Alzheimer’s disease (AD). Methods Data were obtained from 177 patients with subjective complaints, mild cognitive impairment and AD from the Amsterdam Dementia Cohort. AD stages were based on diagnosis and cerebrospinal fluid biomarkers amyloid-β (Aβ) and total-tau (tau). General-linear-models were used to assess relationships between AD stages and total and regional CBF, correcting for age and sex. Results Decreasing CBF was related to more advanced AD stages in all supratentorial regions (p for trend < 0.05). Post-hoc testing revealed that CBF was lower in AD compared to controls and stage-1 predementia patients (i.e. abnormal Aβ and normal tau) in temporal and parietal regions, and compared to stage-2 predementia patients (i.e. abnormal Aβ and tau) in temporal regions. CBF values of stage-2 predementia patients were numerically in between those of stage-1 predementia patients and AD. Conclusion The continuing decrease of CBF along the continuum of AD indicates the potential of ASL-CBF as a measure for disease progression. Key Points • Decreasing CBF relates to more advanced AD stages in all supratentorial regions . • The reduction of CBF does not reach a bottom level . • ASL-CBF has potential as a measure for disease progression in AD .
ISSN:0938-7994
1432-1084
DOI:10.1007/s00330-015-3834-9