Alzheimer’s Disease Prevention: The Role of Omega-3 and Its Derivatives

Certain molecules derived from Omega-3 may reverse the progression of Alzheimer’s disease by promoting healing from inflammation. They also appear to aid in the reabsorption of beta-amyloid protein, responsible for cellular damage and the formation of brain plaques characteristic of the disease.This is revealed by a study conducted at the Karolinska Institutet (Sweden), which investigated the role of inflammation in Alzheimer’s disease. The work was published in the journal Alzheimer & Dementia.

Omega-3 Against Inflammation

Resolution is the final phase of the inflammatory process during which tissue healing occurs. When this mechanism fails, chronic inflammation arises, as seen in the brains of patients with Alzheimer’s disease. This is the most common form of dementia and is characterized by neuronal death associated with progressive memory deterioration. A hallmark of Alzheimer-affected brain tissue is the accumulation of a protein called beta-amyloid, which aggregates outside nerve cells forming so-called amyloid plaques. These trigger inflammatory reactions that disrupt nerve transmission and cause cell death. Due to their well-known anti-inflammatory action, Omega-3 fatty acids have long been studied for their benefits in various diseases. A recent discovery by the same researchers at the Karolinska Institutet demonstrated that Omega-3s can cross the blood-brain barrier—the structure separating blood from nervous tissue—and alter the lipid profile and levels of harmful substances in the brains of Alzheimer’s patients.

Resolution Molecules Are Deficient in Alzheimer’s Patients

In the study, researchers analyzed cerebrospinal fluid—the fluid surrounding the central nervous system—of 15 Alzheimer’s patients, 20 with cognitive decline, and 21 healthy subjects. They also examined brain tissue from 10 Alzheimer’s patients and 10 healthy controls. The aim was to identify the presence and levels of molecules involved in resolution, including receptors, enzymes, and specialized pro-resolving mediators (SPMs). Analyses showed these molecules were present in both brain and cerebrospinal fluid, but their concentrations were lower in Alzheimer’s patients compared to healthy individuals. Researchers noted that levels of one SPM called LXA4 were low in Alzheimer’s patients, both in cerebrospinal fluid and the hippocampus. An enzyme involved in LXA4 synthesis and two SPM receptors were found in high amounts in diseased brain tissue. The analyses also revealed that deficiencies in LXA4 and RvD1—a pro-resolution mediator derived from Omega-3—in cerebrospinal fluid were associated with poorer cognitive ability, assessed by the Mini-Mental State Examination test. Omega-3–derived molecules also appeared to promote the reabsorption of amyloid plaques.

Further Studies to Develop New Treatments

According to Marianne Schultzberg, who led the study, the inflammation resolution mechanism exists in the brain but is severely impaired in Alzheimer’s patients. Stimulating resolution in these individuals could reduce neuronal death and slow disease progression. This novel approach offers opportunities for future treatment development. Considering prior research and the fact that specialized resolution molecules derive from polyunsaturated fatty acids, scientists are now conducting studies in cell cultures and animal models to examine Omega-3 effects on neuronal loss and memory.

Source: Xiuzhe Wang, Mingqin Zhu, Erik Hjorth, Veronica Cortés Toro, Helga Eyjolfsdottir, Caroline Graff, Inger Nennesmo, Jan Palmblad, Maria Eriksdotter, Kumar Sambamurti, Jonathan M. Fitzgerald, Charles N. Serhan, Ann-harlotte Granholm, Marianne Schultzberg. “Resolution of inflammation is altered in Alzheimer's disease.” Alzheimers Dement. 2014 Feb 12. pii: S1552-5260(14)00030-2. doi: 10.1016/j.jalz.2013.12.024