ω-3 Supplementation increases amyloid-β phagocytosis and resolvin D1 in patients with minor cognitive impairment.
Level 4 - case-series / case-control
Uncontrolled before-and-after interventional case series.
PubMed 25805829 · doi:10.1096/fj.14-264218
What was done
A single-arm interventional study evaluated the effects of 4 to 17 months of supplementation with omega-3 fatty acids and antioxidants (Smartfish drink) in 21 participants: 12 with minor cognitive impairment (MCI; MMSE ≥ 19), 2 with pre-MCI (normal MMSE), and 7 with Alzheimer disease (AD; MMSE < 19). Assessed outcomes included amyloid-β 1-42 (Aβ) phagocytosis by monocytes via flow cytometry and microscopy, transcription of inflammatory genes via RT-PCR, production of resolvin D1 (RvD1) via enzyme immunoassay, and cognitive status via Mini-Mental State Examination (MMSE).
What was found
In patients with MCI and pre-MCI (n = 14), monocyte phagocytosis of Aβ increased significantly from 530 to 1306 mean fluorescence intensity units (P = 0.016); the increase in patients with AD was not significant. Macrophage RvD1 production increased in 80% of patients with MCI and pre-MCI (mean increase 9.95 pg/ml; not statistically significant). Inflammatory gene mRNA transcription increased only in a subgroup with low transcription at baseline and showed no significant change in those with high baseline levels. Mean MMSE score in MCI and pre-MCI patients was 25.9 at baseline and 25.7 after follow-up (not statistically significant).
Why it matters
This study provides preliminary human evidence that omega-3 and antioxidant supplementation may enhance peripheral monocyte clearance of amyloid-β in early-stage cognitive impairment.
Limits
The study is an uncontrolled, open-label case series with a very small sample size (n = 21 across three subgroups). The intervention duration varied widely from 4 to 17 months, there was no placebo control arm to account for natural variability or confounding, and no meaningful cognitive improvement was observed.
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- partial Patients with Alzheimer's disease show a reduced capacity of peripheral blood mononuclear cells/macrophages to phagocytose beta-amyloid, which returns to normal following the Bredesen protocol.