Affiliations: [a] Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan
| [b] Department of Clinical Research, the Medical and Pharmacological Research Center Foundation, Hakui, Japan, Division of Nuclear Medicine, Department of Radiology, Saitama Medical University Hospital, Saitama, Japan
| [c] Department of Neurology, Showa University School of Medicine
| [d] Department of Environmental and Preventive Medicine, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan
Correspondence:
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Correspondence to: Professor Masahito Yamada, MD, PhD, Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Science, 13-1 Takara-machi, Kanazawa 920-8640, Japan. Tel.: +81 76 265 2290; Fax: +81 76 265 4253; E-mail: m-yamada@med.kanazawa-u.ac.jp.
Abstract: Background: Alzheimer’s disease (AD) commonly accompanies cerebral amyloid angiopathy (CAA). Objective: We aimed to reveal associations between CAA-related brain microbleeds and cerebrospinal fluid (CSF) markers in AD patients. Methods: Patients with probable AD (n = 88) from consecutive patients in our memory clinic were evaluated for patient demographics, vascular risk factors, neuropsychological tests, apolipoprotein E phenotype, MRI including T2*-weighted image and fluid attenuated inversion recovery sequence, and CSF amyloid and tau markers. Results: The 88 patients with AD included 15 with microbleeds only in cortical/subcortical regions (cortical microbleeds) that could be CAA-related, 16 with microbleeds only in deep locations (deep microbleeds), 3 with microbleeds in both cortical and deep locations (mixed microbleeds), and 54 without microbleeds. The CSF levels of amyloid β-protein 1–40 (Aβ40) and amyloid β-protein 1–42 (Aβ42) were significantly lower in patients with cortical microbleeds than in those without microbleeds (p = 0.001 and p = 0.027, respectively). The result remained unchanged after adjustment for age, sex, apolipoprotein E E4 presence, and leukoaraiosis. Conclusions: CAA-related cortical microbleeds would be associated with lower CSF levels of Aβ40 and Aβ42 in AD, reflecting the deposition of both Aβ40 and Aβ42 in the cerebrovasculature.
