Alzheimer's disease prevention: the role of omega-3 and its derivatives

Certain molecules originating from omega-3s could reverse the progression of Alzheimer's disease by stimulating healing from inflammation. They also appear to promote reabsorption of the beta amyloid protein, which is responsible for the cellular damage and formation of brain plaques typical of the disease.This was revealed in a study, carried out at Karolinska Institutet (Sweden), which investigated the role of inflammation in Alzheimer's disease. The work was published in the journal Alzheimer's & Dementia.

Omega-3 against inflammation

Resolution is the final stage of the inflammatory process in which tissue healing occurs. When this mechanism fails, chronic inflammation arises, as occurs, for example, 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 increasing memory impairment. A characteristic feature of Alzheimer's-affected brain tissue is the accumulation of a protein, called beta amyloid, ch and siaggregates on the outside of nerve cells forming so-called amyloid plaques. These result in inflammatory reactions that alter nerve transmission causing cell death. Precisely because of their known anti-inflammatory action, Omega-3s have been studied for years for their benefits in various diseases. A recent discovery by the same researchers at Karolinska Institutet showed that Omega-3s can cross the blood-brain barrier, the structure between blood and nerve tissue, and change the lipid profile and amount of harmful substances in the brains of patients with Alzheimer's disease.

Resolution molecules are scarce in patients with the disease

During the study, researchers analyzed cerebrospinal fluid, the fluid surrounding the central nervous system, from 15 Alzheimer's patients, 20 patients with cognitive decline and 21 healthy subjects. They also observed the brain tissue of 10 Alzheimer's patients and 10 healthy subjects. The aim was to identify the presence, and levels, of molecules involved in resolution, including receptors, enzymes, and so-called specialized mediators in the resolution process (SPMs). The results of the analysis showed the presence of these molecules in the brain and cerebrospinal fluid. In Alzheimer's patients, however, their concentrations were lower than in healthy subjects. The researchers noted that levels of an SPM, called LXA4 were low in patients with the disease, both in cerebrospinal fluid and in the 'hippocampus. An enzyme involved in the synthesis of LXA4, and two receptors for SPMs were present in high amounts in diseased brain tissue. Among other things, the analyses revealed that deficiency of LXA4 and RvD1 a pro-resolution mediator derived from Omega-3s, in cerebrospinal fluid was associated with lower cognitive ability, examined by a specific test (Mini-Mental State Examination). Omega-3-derived molecules also appeared to promote the reabsorption of amyloid plaques.

Further studies to implement new treatments

According to Marianne Schultzberg, who directed the study, the mechanism that leads to the resolution of inflammation is present in the brain, but is severely impaired in Alzheimer's patients. By stimulating resolution in these subjects, neuronal death and disease progression could be reduced. An approach, which is completely new and offers an opportunity to study future treatments. Considering previous research and the fact that molecules specialized in resolution are derived from polyunsaturated fatty acids, scientists are now conducting studies, in cell cultures and animal models, on the effect of Omega-3 in neuronal and memory loss. 

Source Xiuzhe Wang,Mingqin Zhu,Erik Hjorth,Veronica CortésToro,Helga Eyjolfsdottir,Caroline Graff,,Inger Nennesmo,Jan Palmblad,Maria Eriksdotter,Kumar SambamurtiJonathan,M. Fitzgerald,CharlesN. 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