Anti-aging

Alzheimer's: Omega-3s May Slow Neurodegenerative Processes

Alzheimer’s Disease: Can Fish Oil Slow Neurodegenerative Processes?


Omega-3 EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) taken as supplements can cross the blood-brain barrier in Alzheimer’s patients, positively affecting neurodegenerative processes. A high DHA level corresponds to changes in disease and inflammation markers.

This was discovered by researchers at the Karolinska Institutet in Sweden, during a study investigating the effect of Omega-3 supplementation on fatty acid concentrations in cerebrospinal fluid. The discovery was published in the Journal of Internal Medicine.



Omega-3 and Alzheimer’s


Omega-3s, especially DHA, are components of neuron membranes, providing stability and ensuring their proper growth and function. Thanks to their anti-inflammatory action, DHA and EPA protect the nervous system from cognitive decline and other diseases. Several studies have shown that Omega-3s may protect against Alzheimer’s by reducing the risk of developing the disease. Other research has demonstrated that many neuropathies can influence the fatty acid profile of the central nervous system (CNS). In Alzheimer’s, a lower-than-normal DHA concentration has been observed. Omega-3 and other polyunsaturated fatty acids accumulate in the CNS during gestation and are continuously replaced throughout life. However, it is not yet clear how this mechanism works or whether dietary changes can influence Omega-3 passage through the blood-brain barrier. This barrier is a structure between the blood and CNS that selectively regulates the passage of chemicals to and from the brain, protecting the nervous system. It also blocks drug passage. In light of this knowledge, the researchers aimed to understand the effect of Omega-3 supplementation in patients already diagnosed with Alzheimer’s disease.



The action of DHA on disease markers


The study, part of a larger project, involved 33 Alzheimer’s patients. For six months, 18 of them received daily, without knowing its content, a supplement containing 2.3 grams of Omega-3 (rich in DHA), while the other 15 received a placebo. After treatment, concentrations of DHA and EPA were measured in plasma and cerebrospinal fluid surrounding the CNS. These analyses revealed that in subjects who received the supplement, plasma and cerebrospinal fluid Omega-3 levels increased, while no such changes were evident in the placebo group. Furthermore, DHA levels were related to Alzheimer’s progression and disease markers. In the cerebrospinal fluid, DHA levels were inversely correlated with phosphorylated Tau protein concentration, a marker of Alzheimer’s, and directly correlated with levels of the soluble interleukin-1 receptor, a molecule involved in inflammatory processes.



Omega-3 reach the central nervous system


Based on these findings, researchers hypothesize that Omega-3 can cross the blood-brain barrier to reach the nervous system and influence its fatty acid composition, as previously observed in animal studies where DHA supplementation corresponded to higher molecule concentration in the CNS. Moreover, increased DHA in the CNS strongly correlates with typical disease biomarkers and inflammatory status. The study thus confirms the link between Alzheimer’s disease and inflammation. However, traditional anti-inflammatory treatments used so far have proven ineffective in improving symptoms. Further studies will be needed to understand how Omega-3s can be used to treat the disease and halt the memory loss affecting Alzheimer’s patients.


Source: Y. Freund Levi, I. Vedin, T. Cederholm4, H. Basun5, G. Faxén Irving, M. Eriksdotter, E. Hjorth, M. Schultzberg, B. Vessby, L.-O. Wahlund, N. Salem Jr, J. Palmblad. “Transfer of omega-3 fatty acids across the blood–brain barrier after dietary supplementation with a docosahexaenoic acid-rich omega-3 fatty acid preparation in patients with Alzheimer's disease: the OmegAD study” Journal of Internal Medicine. Article first published online: 11 JAN 2014 DOI: 10.1111/joim.12166.