Omega-3 backed for Alzheimer’s disease potential
The new study, published in the journal Alzheimer’s & Dementia, demonstrates a new approach to dementia and Alzheimer’s disease – suggesting that omega-3 fatty acid derivatives stimulate the uptake of amyloid-beta proteins that are suggested to kill brain cells and form Alzheimer's disease plaques.
Led by Professor Marianne Schultzberg from the Karolinska Institutet, Sweden, the team behind the research revealed that the normal inflammatory processes should ultimately lead to tissue repair in a process known as restoration. However, with Alzheimer's disease this normal process is interrupted – meaning that rather than repair and restore tissue, debris from dead cells and other microorganisms fails to clear.
"Our hypothesis is that stimulation of resolution of inflammation in Alzheimer's disease may result in reduced neuronal death in the brain, and in turn have a beneficial effect in disease progression and cognition,” explained Schultzberg.
“This is an entirely new approach and provides the opportunity to develop new treatment principles for Alzheimer's disease," she said.
The Swedish team found omega-3 fatty acid derivatives help to induce the resolution process and stimulate the uptake of amyloid-beta proteins that have been linked to the progression of Alzheimer's disease via the development of plaques.
They are continuing their studies in animal models to see if omega-3 fatty acids can prevent memory loss and further loss of brain cells.
Study details
The team analysed cerebrospinal fluid from 15 patients with Alzheimer's disease, 20 patients with mild cognitive impairment and 21 control subjects. They also analysed brain tissue from 10 Alzheimer's patients and 10 control subjects.
Schultzberg and her team looked for the presence, and relative levels of several inflammatory molecules and receptors involved in the resolution pathway – including specialised pro-resolving mediators (SPMs), receptors, biosynthetic enzyme, and downstream effectors - in postmortem hippocampal tissue from AD patients and non-AD subjects.
SPMs were also measured in cerebrospinal fluid (CSF).
The team found that SPMs and SPM receptors were detected in the human brain – indicating the resolution pathway does exist in the brain. They also found that levels of the SPM lipoxin A4 (LXA4) were reduced in AD patients, both in the CSF and hippocampus.
In addition, an enzyme involved in LXA4 synthesis and two SPM receptors were elevated in AD brains, said the team, while LXA4 and RvD1 levels in CSF correlated with Mini-Mental State Examination (MMSE) scores.
As a result, the team concluded that the resolution pathway exists in the brain, adding that the alterations identified in the study “strongly suggest” a dysfunction of this pathway in Alzheimer’s disease.
They added that treatment with SPMs, or in other ways stimulating the resolution pathway – such as omega-3 fatty acid supplementation – “is suggested as a new and promising therapy in neurodegenerative disorders such as Alzheimer’s disease.”
Source: Alzheimer's & Dementia
Published online ahead of print, doi: 10.1016/j.jalz.2013.12.024
“Resolution of inflammation is altered in Alzheimer's disease”
Authors: Xiuzhe Wang, Mingqin Zhu, et al
