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N‐3 fatty acid treatment and plasma transthyretin in patients with Alzheimer's disease
Author(s) -
Faxen Irving Gerd,
FreundLevi Yvonne,
EriksdotterJönhagen Maria,
Basun Hans,
Palmblad Jan,
Vedin Inger,
Wahlund LarsOlof,
Cederholm Tommy
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.543.10
Subject(s) - transthyretin , medicine , endocrinology , cognitive decline , disease , dementia
Background Transthyretin (TTR) binds Abeta and may reduce brain Abeta, a key pathogenetic feature in Alzheimer's disease (AD). N‐3 fatty acids (FA), i.e. DHA and EPA, increase TTR transcription in rat brain. We studied the effects of n‐3 FAs on plasma TTR levels in patients with AD. Methods: 204 outpatients with AD were randomised to DHA/EPA (80/20%), 4 g/d during 6 mo (EPAX, Pronova AS) or placebo (n‐6 FA). After 6 mo all patients received EPAX for another 6 mo. Cognitive function was assessed by MMSE and ADASCog. Results Baseline plasma TTR was 260[plusmn]80 in the EPAX‐group (89 pat, 75 y, 57% w) and 264[plusmn]55 mg/l in the controls (85 pat, 75 y, 46% w) (ns). After 6 mo TTR levels was 250[plusmn]59 and 229[plusmn]51 in the EPAX and control groups, respectively (p<0.015). Repeated measures ANOVA indicated an increase in TTR by EPAX treatment (P=0.04), most evident in the men. From 6 to 12 mo TTR increased significantly in both groups. MMSE correlated to TTR at 12 mo (r=0.16, P=0.03) and inversely to ADAS‐Cog (r=‐0.2, P=0.01). In multiple regression analyses increased TTR at 6 mo was independently related to n‐3 treatment (OR 2.1, 95% CI 1.01‐4.2) Conclusion N3 FA treatment in patients with AD appeared to increase TTR. Since n3 FA may prevent cognitive decline, and TTR may decrease Abeta deposition, the results warrant further exploration. & [beta] & [plusmn]