08.05.24
Supplementation with fish oil may help to protect brain function in carriers of the APOE4 gene, which is considered a predisposition to Alzheimer’s disease, according to a new study published in JAMA Network Open.
In the study, researchers recruited 102 adults over the age of 75 who had relatively low blood levels of omega-3 fatty acids, to examine the potential cognitive benefits of fish oil supplementation versus placebo over a three-year window. Participants enrolled in the study had relatively high levels of white lesions in the brain but were otherwise healthy and didn’t have dementia.
At baseline, and annually across a three-year treatment with either 1.65 grams of omega-3s (975 mg of EPA and 650 mg of DHA) or a placebo, participants underwent MRI scans of their brains to assess white matter lesions. These lesions are associated with the risk of developing dementia later in life.
After the treatment period, the general population had a slight reduction in the progression of these lesions, but not enough to be statistically significant between treatment and placebo groups.
However, among APOE4 carriers, the authors of the study noted a in the breakdown of brain cell integrity which was observed by year one of the study.
The authors of the study noted that the trial was not powered to detect differences between the APOE4 carriers and noncarriers. However, differential effects in APOE4 carriers has not yet been reported, and the findings will require further confirmation. “These results will enable improved study design and sample size calculations for future efforts of a relatively cheap, safe, and well-tolerated therapy for primary and secondary dementia prevention,” the authors of the study concluded.
In the study, researchers recruited 102 adults over the age of 75 who had relatively low blood levels of omega-3 fatty acids, to examine the potential cognitive benefits of fish oil supplementation versus placebo over a three-year window. Participants enrolled in the study had relatively high levels of white lesions in the brain but were otherwise healthy and didn’t have dementia.
At baseline, and annually across a three-year treatment with either 1.65 grams of omega-3s (975 mg of EPA and 650 mg of DHA) or a placebo, participants underwent MRI scans of their brains to assess white matter lesions. These lesions are associated with the risk of developing dementia later in life.
After the treatment period, the general population had a slight reduction in the progression of these lesions, but not enough to be statistically significant between treatment and placebo groups.
However, among APOE4 carriers, the authors of the study noted a in the breakdown of brain cell integrity which was observed by year one of the study.
The authors of the study noted that the trial was not powered to detect differences between the APOE4 carriers and noncarriers. However, differential effects in APOE4 carriers has not yet been reported, and the findings will require further confirmation. “These results will enable improved study design and sample size calculations for future efforts of a relatively cheap, safe, and well-tolerated therapy for primary and secondary dementia prevention,” the authors of the study concluded.