Docosahexaenoic acid supplementation and cognitive decline in Alzheimer disease: a randomized trial
Quinn JF, Raman R, Thomas RG, Yurko-Mauro K, Nelson EB, Van Dyck C, Galvin JE, Emond J, Jack CR, Weiner M, Shinto L, Aisen PS
JAMA · 527 citas
Cómo se estudió
- Diseño
- Ensayo controlado aleatorizado (indexado por PubMed)
- Estudiado en
- Personas
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiación independiente
- Gobierno
- National Institute on Aging
- Gobierno
- NIA NIH HHS
- Subvenciones
- National Institute on Aging (U19 AG010483); National Institute on Aging (U01‐AG10483); National Institute on Aging (P30AG008051); National Institute on Aging (U01AG010483)
Según 2 financiadores declarados.
Publicación
- Publicado
- 2010-11-02 · JAMA · vol. 304 · número 17 · pág. 1903
- Editorial
- American Medical Association
- Citado
- 764 citas · más que el 100% de estudios similares · 45.7× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 44 trabajos
- Acceso
- Acceso abierto (copia en repositorio)
- Áreas de investigación
- Fatty Acid Research and Health · Dementia and Cognitive Impairment Research · Alzheimer's disease research and treatments
- Palabras clave
- docosahexaenoic acid, omega-3 fatty acids, Alzheimer's disease, cognitive decline, functional decline, algal oil, dietary supplementation, brain atrophy, long-chain polyunsaturated fatty acids, ADAS-Cog, Clinical Dementia Rating, Alzheimer's disease prevention, Alzheimer's disease treatment, Alzheimer's disease risk factors, Alzheimer's disease biomarkers
- MeSH
- brain, humans, alzheimer disease, atrophy, disease progression, docosahexaenoic acids, magnetic resonance imaging, treatment outcome, double-blind method, cognition disorders, dietary supplements, aged, aged, 80 and over, female, male, apolipoprotein e4
12 autores
- Joseph F. Quinn🇺🇸 · autor de correspondenciaOregon Health & Science University
- Rema Raman🇺🇸University of California San Diego
- Ronald G. Thomas🇺🇸University of California San Diego
- Karin Yurko‐Mauro
- EDWARD B. NELSON
- Christopher H. van Dyck🇺🇸Yale University
- James E. Galvin🇺🇸New York University
- Jennifer A. Emond🇺🇸University of California San Diego
- Clifford R. Jack🇺🇸Mayo Clinic
- Michael Walter Weiner🇺🇸University of California, San Francisco
- Lynne H. Shinto🇺🇸Oregon Health & Science University
- Paul S. S Aisen🇺🇸University of California San Diego
Resumen
El texto original del estudio, en el idioma en que se publicó.
Context
Docosahexaenoic acid (DHA) is the most abundant long-chain polyunsaturated fatty acid in the brain. Epidemiological studies suggest that consumption of DHA is associated with a reduced incidence of Alzheimer disease. Animal studies demonstrate that oral intake of DHA reduces Alzheimer-like brain pathology.
Objective
To determine if supplementation with DHA slows cognitive and functional decline in individuals with Alzheimer disease.
Design, setting, and patients
A randomized, double-blind, placebo-controlled trial of DHA supplementation in individuals with mild to moderate Alzheimer disease (Mini-Mental State Examination scores, 14-26) was conducted between November 2007 and May 2009 at 51 US clinical research sites of the Alzheimer's Disease Cooperative Study.
Intervention
Participants were randomly assigned to algal DHA at a dose of 2 g/d or to identical placebo (60% were assigned to DHA and 40% were assigned to placebo). Duration of treatment was 18 months.
Main outcome measures
Change in the cognitive subscale of the Alzheimer's Disease Assessment Scale (ADAS-cog) and change in the Clinical Dementia Rating (CDR) sum of boxes. Rate of brain atrophy was also determined by volumetric magnetic resonance imaging in a subsample of participants (n = 102).
Results
A total of 402 individuals were randomized and a total of 295 participants completed the trial while taking study medication (DHA: 171; placebo: 124). Supplementation with DHA had no beneficial effect on rate of change on ADAS-cog score, which increased by a mean of 7.98 points (95% confidence interval [CI], 6.51-9.45 points) for the DHA group during 18 months vs 8.27 points (95% CI, 6.72-9.82 points) for the placebo group (linear mixed-effects model: P = .41). The CDR sum of boxes score increased by 2.87 points (95% CI, 2.44-3.30 points) for the DHA group during 18 months compared with 2.93 points (95% CI, 2.44-3.42 points) for the placebo group (linear mixed-effects model: P = .68). In the subpopulation of participants (DHA: 53; placebo: 49), the rate of brain atrophy was not affected by treatment with DHA. Individuals in the DHA group had a mean decline in total brain volume of 24.7 cm(3) (95% CI, 21.4-28.0 cm(3)) during 18 months and a 1.32% (95% CI, 1.14%-1.50%) volume decline per year compared with 24.0 cm(3) (95% CI, 20-28 cm(3)) for the placebo group during 18 months and a 1.29% (95% CI, 1.07%-1.51%) volume decline per year (P = .79).
Conclusion
Supplementation with DHA compared with placebo did not slow the rate of cognitive and functional decline in patients with mild to moderate Alzheimer disease.
Trial registration
clinicaltrials.gov Identifier: NCT00440050.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial.
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