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Relationship between cerebral amyloid angiopathy and plasma homocysteine levels in Alzheimer’s disease
Author(s) -
Kanemaru Kazutomi,
Kanemaru Akiko,
Murayama Shigeo
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.042109
Subject(s) - cerebral amyloid angiopathy , homocysteine , medicine , alzheimer's disease , gastroenterology , pathology , lumbar puncture , angiopathy , disease , cerebrospinal fluid , endocrinology , dementia , diabetes mellitus
Background Cerebral amyloid angiopathy (CAA) is the characteristic vascular pathology in Alzheimer’s disease (AD). The vascular changes including CAA contribute to mental decline in AD. Elevated plasma total homocysteine (tHcy) is reported to be an independent risk factor for Alzheimer’s disease (AD). Elevated tHcy is also reported to result in CAA in mice. Here we investigated the relationship between CAA and plasma tHcy levels in AD. Method The subjects of this study consisted of clinically diagnosed 136 patients with AD (83 females, 53 males, age 75.2±8.8 years). The cortical microbleeds shown by T2*‐weighted MRI images could be CAA‐related. We divided the AD patients into two groups; CAA(+) (AD with CAA, n=46) and CAA(‐) (AD without CAA, n=90). We compared the levels of plasma tHcy between the two groups: CAA(+) and CAA(‐). We also compared CSF biomarkers (tau, ptau‐181 and Abeta42) and MMSE scores between the two groups. The CSF samples were obtained by lumbar puncture after informed consent was obtained. The CSF levels of tau, ptau‐181 and Abeta42 were measured by ELISA (Fujirebio, Belgium) according to the manufacturer’s protocol. Result The tHcy levels were 14.3±10.5 nmol/ml in the CAA(+) group and 11.6±4.0 in the CAA(‐) group. The tHct levels showed no significant difference between the two groups. The CSF Abeta42 levels were significantly lower in the CAA(+) group (274.2±108.7 pg/ml) than those in the CAA(‐) group (316.8±112.1 pg/ml, p<0.05, t‐test), whereas the CSF tau and ptau levels showed no difference between the two groups. MMSE scores were lower in the CAA(+) group (16.5±7.0) than those in the CAA(‐) group (20.3±6.3) (p<0.005, t‐test). The tHcy levels were not related to any of CSF biomarkers (tau, ptau‐181 or Abeta42) . Conclusion Plasma tHct levels showed no significant difference between the two groups: CAA(+) and CAA(‐).CSF levels of Abeta42 and MMSE scores were lower in the CAA(+) group than those in the CAA(‐) group.