Cerebral small vessel disease in aging and Alzheimer's disease: a comparative study using MRI and SPECT

Authors

  • I. Makedonov,

    Corresponding author
    1. Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, ON, Canada
    • Heart and Stroke Foundation Centre for Stroke Recovery, Toronto, ON, Canada
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  • S. E. Black,

    1. Heart and Stroke Foundation Centre for Stroke Recovery, Toronto, ON, Canada
    2. Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, ON, Canada
    3. LC Campbell Cognitive Neurology Research Unit, Brain Science Research Program, Sunnybrook Research Institute, Toronto, ON, Canada
    4. Rotman Research Institute,, Baycrest, Toronto, ON, Canada
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  • B. J. MacIntosh

    1. Heart and Stroke Foundation Centre for Stroke Recovery, Toronto, ON, Canada
    2. Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada
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  • See editorial by Gurol on page 214.

Correspondence: I. Makedonov, Sunnybrook Health Sciences Centre, A406, 2075 Bayview Avenue, Toronto, ON, M4N 3M5, Canada

(tel: 416 480 6100, ext. 7348; fax: 416 480 5775; e-mail: makedon1@sri.utoronto.ca).

Abstract

Background

White matter hyperintensities (WMH) are associated with aging and are prevalent in various brain pathologies. The purpose of the current study was to characterize WMH perfusion in age-matched elderly controls (ECs) and patients with Alzheimer's disease (ADs).

Methods

Fifty ECs (23 men) and 61 ADs (33 men) underwent magnetic resonance imaging (MRI), 99mTc-ECD single-photon emission computed tomography (SPECT) and cognitive testing. Brain tissue type was classified on T1 weighted images, and WMH were identified on interleaved proton density/T2 weighted images. Co-registered MR images were used to characterize SPECT perfusion patterns.

Results

WMH perfusion was lower than normal appearing white matter (NAWM) perfusion (< 0.001) in both EC and AD groups. There was no WMH perfusion difference between groups when considering the mean perfusion from all WMH voxels (P > 0.43). However, locations that were likely to be considered WMH tended to have lower perfusion in ADs compared with ECs. Perfusion gradients along watershed white matter regions were significantly different between EC and AD groups (P < 0.05). A relationship was found between the volume of a WMH lesion and its mean perfusion (P < 0.001) in both ECs and ADs.

Conclusion

Global WMH were hypoperfused compared with NAWM to the same degree in EC and AD participants, which suggests a common WMH etiology between groups. However, white matter locations that were likely to contain WMH tended to be hypoperfused in ADs compared with healthy aging. This finding is suggestive of AD-specific pathology that reduces the perfusion at anatomic locations susceptible to the formation of WMH through either the neurodegenerative process or AD-related vasculopathy or both.

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