Affiliations: [a] Department of Radiology, Keck School of Medicine of USC, University of Southern California, USA
| [b] Department of Radiology, University of Cambridge School of Clinical Medicine, Cambridge, UK
| [c] Department of Neurology, University of California Irvine, CA, USA
| [d] Department of Radiology, Cambridge University Hospitals, Cambridge, UK
| [e] Department of Psychiatry, University of Cambridge School of Clinical Medicine, Cambridge, UK
Correspondence:
[*]
Correspondence to: Nasim Sheikh-Bahaei, Department of Radiology, Keck School of Medicine of USC, 1520 San Pablo St., LA, CA, 90033. Tel.: +1 949 7714040; E-mail: nasim_sh@me.com.
Abstract: Background:Despite the well-documented relationship between lobar cerebral microbleeds (lCMB) and Alzheimer’s disease (AD), there is limited knowledge about the role of lCMB in AD pathology. Objective:To understand the nature of this relationship, we investigated the association between lCMB, amyloid load, perfusion, and metabolism. Methods:Participants with AD, mild cognitive impairment (MCI), and healthy controls were recruited and scanned with 11C-Pittsburg-Compound B (PiB), Fluorodeoxyglucose (FDG) PET, and susceptibility-weighted MRI. Early PiB-PET frames were used to estimate perfusion. The association between lCMB and PET uptake in each anatomical lobe was measured using multiple regression models. Results:The presence of lCMB predicted increased total (p < 0.001) and regional (p = 0.0002) PiB uptake, as well as decreased cerebral perfusion (p = 0.03). Cases with lCMB had hypometabolism in their temporal lobe (p = 0.04). Conclusion:There are significant relationships between lCMBs and various markers of AD pathology. lCMB has a spatial association with Aβ load and a complex effect on perfusion and metabolism.
