A study published in the recent issue of JAMA has shown the relation between the use of Docosahexaenoic acid DHA and cognitive functions in Alzheimers disease.
DHA is an omega-3 fatty acid identified as a potential treatment for Alzheimer disease. Epidemiological studies have shown that omega-3 fatty acid consumption reduces Alzheimer disease risk and DHA modifies the expression of Alzheimer-like brain pathology in mouse models.
A randomized, double-blind, placebo-controlled trial was conducted by the Alzheimer’s Disease Cooperative Study (ADCS) a consortium of academic medical centers and private Alzheimer disease clinics funded by the National Institute on Aging to conduct clinical trials on Alzheimer disease. Participants were recruited between February and November 2007 and the Clinical activity was completed in May 2009.
Inclusion criteria: Individuals with probable Alzheimer disease, if they had the following: (1) their Mini-Mental State Examination (MMSE) score was between 14 and 26, (2) they were medically stable, (3) they consumed on average no more than 200 mg/d of DHA (as assessed by a brief 7-item food frequency questionnaire), and (4) they were not taking DHA or omega-3 fatty acid supplements.
Exclusion criteria: if they were taking drugs with central anticholinergic effects or sedatives or were receiving any investigational treatment for Alzheimer disease. Stable use (
Study drug: Aalgal-derived DHA (Martek Biosciences, Columbia , Maryland
Two Primary outcome measures: The rate of change over 18 months on the cognitive subscale of the Alzheimer’s Disease Assessment Scale (ADAS-cog) and on the Clinical Dementia Rating (CDR) sum of boxes.
The primary analysis was an intent-to-treat analysis including all randomized participants. That is, participants were analyzed in the group to which they were randomized, regardless of medication adherence. All available assessments for ADAS-cog and CDR sum of boxes were used in the analysis for individuals who discontinued medication.
Results: Plasma phospholipid DHA increased in the DHA treatment group from 3.18 weight percentage at baseline to 9.80 weight percentage at 6 months, 10.20 weight percentage at 12 months, and 9.82 weight percentage at 18 months (207% increase, P < .001) with no significant change in plasma phospholipid DHA in the placebo group.
Subgroup of 44 participants volunteering for cerebrospinal fluid collection at baseline and 18 months (DHA group: 29; placebo group: 15), a significant 38% increase in cerebrospinal fluid DHA was observed in the DHA group (2.53 weight percentage at baseline and 3.46 weight percentage at 18 months; P < .001) but not in the placebo group.
The rate of mean change in ADAS-cog score over 18 months was 8.27 points for the placebo group compared with 7.98 points for the DHA group (linear mixed-effects model: P = .41). The rate of points change on CDR sum of boxes over 18 months was 2.93 (95% CI, 2.44-3.42) for the placebo group compared with 2.87 (95% CI, 2.44-3.30) for the DHA group. The linear mixed-effects analysis revealed a rate of decline on the ADCS-ADL of 11.51 (95% CI, 9.57 to 13.45) points change over 18 months for the DHA group compared with the points change of 10.43 (95% CI, 8.41 to 12.45) for the placebo group.
The hypothesis that DHA slows the progression of mild to moderate Alzheimer disease was not supported, so there is no basis for recommending DHA supplementation for patients with Alzheimer disease. A large proportion of randomized participants (28% of the DHA group and 24% of the placebo group) did not complete the study.
The authors concluded that the supplementation with DHA compared with placebo did not slow the rate of cognitive and functional decline in patients with mild to moderate Alzheimer disease.
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