Affiliations: [a] Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, Japan | [b] Clinical Research Department, the Medical and Pharmacological Research Center Foundation, Hakui, Ishikawa, Japan | [c] Division of Nuclear Medicine, Department of Radiology, Saitama Medical University Hospital, Iruma, Saitama, Japan | [d] Dementia Medical Center, Department of Neurology, and Institute for Clinical Research, National Hospital Organization Hokuriku Hospital, Nanto, Toyama, Japan
Correspondence:
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Correspondence to: Masahito Yamada, Department of Neuro-logy and Neurobiology of Aging, Kanazawa University Graduate School of Medical Sciences, 13-1, Takara-machi, Kanazawa, Ishikawa 920-8640, Japan. Tel.: +81 76 265 2290; Fax: +81 76 234 4253; m-yamada@med.kanazawa-u.ac.jp
Abstract:
Background: Microbleeds (MBs) are frequently observed in Alzheimer’s disease (AD); however, the relevance to AD pathophysiology has not been elucidated.
Objectives: We investigated correlation of MBs, especially cerebral amyloid angiopathy (CAA)-related MBs with cognitive function, gray matter volume, and glucose metabolism in AD.
Methods: We performed magnetic resonance imaging including T2*-weighted imaging sequence for 206 patients with AD. Among them, 158 AD patients with no focal brain lesions except for MBs were investigated with cognitive tests, voxel-based morphometry, and 18F-fluorodeoxyglucose positron emission tomography in a cross-sectional observational study.
Results: Of the 158 patients with no hemorrhagic and/or ischemic stroke lesions except for MBs, 27 patients had MBs, in which 17 patients showed CAA-related MBs that located only in cortex/subcortex (CAA-related MBs), and 10 patients showed CAA-unrelated MBs that located in deep regions regardless of the presence of MBs in cortical/subcortical regions. There were slightly but significant differences in cognitive functions between the patients without MBs, those with CAA-related MBs, and those with CAA-unrelated MBs. MBs were recognized frequently in the occipital lobe in the patients with CAA-related MBs. The patients with CAA-related MBs showed gray matter atrophy in the temporal lobe and cerebellum, and glucose hypometabolism in the temporal lobe compared with those without MBs.
Conclusions: Our results indicate that MBs, particularly CAA-related MBs would cause gray matter atrophy and glucose hypometabolism in AD.
