Serum cystatin C and the risk of Alzheimer disease in elderly men  

Oleh:

Sundelof, J. ; Arnlov, J. ; Ingelsson, E.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Neurology (Official Journal of The American Academy of Neurology) vol. 71 no. 14 (Sep. 2008), page 1072-1079.
Topik: SERUM CYSTATIN C; BODY MASS INDEX

Ketersediaan

Perpustakaan FK Nomor Panggil: N11.K.2008.03 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Background: Multiple lines of research suggest that increased cystatin C activity in the brain protects against the development of Alzheimer disease (AD). Methods: Serum cystatin C levels were analyzed at two examinations of the Uppsala Longitudinal Study of Adult Men, a longitudinal, community-based study of elderly men (age 70 years, n = 1,153 and age 77 years, n = 761, a subset of the age 70 examination). Cox regressions were used to examine associations between serum cystatin C and incident AD. AD cases were identified by cognitive screening and comprehensive medical chart review in all subjects. Results: On follow-up (median 11.3 years), 82 subjects developed AD. At age 70 years, lower cystatin C was associated with higher risk of AD independently of age, APOE4 genotype, glomerular filtration rate, diabetes, hypertension, stroke, cholesterol, body mass index, smoking, education level, and plasma amyloid-ß protein 40 and 42 levels (hazard ratio [HR] for lowest [<1.12 µmol/L] vs highest [>1.30 µmol/L] tertile = 2.67, 95% CI 1.22–5.83, p < 0.02). The results were similar at age 77 years (43 participants developed AD during follow-up). Furthermore, a 0.1-µmol/L decrease of cystatin C between ages 70 and 77 years was associated with a 29% higher risk of incident AD (HR 1.29, 95% CI 1.03–1.63, p < 0.03). Conclusions: Low levels of serum cystatin C precede clinically manifest Alzheimer disease (AD) in elderly men free of dementia at baseline and may be a marker of future risk of AD. These findings strengthen the evidence for a role for cystatin C in the development of clinical AD.

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