Supplementation with omega-3 fatty
acids could help to prevent and even reverse the progression of Alzheimer’s
disease.
The connection is resolving inflammation. The beneficial fats may come to the affected person’s rescue by
stimulating newly identified ‘resolution pathways’ in the brain, according to
research outlining an ‘entirely new’ approach to the condition.
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. The proteins are
the alleged culprits in the deteriorating health of brains affected by this
dreadful disease. They apparently kill brain cells and form Alzheimer's disease
hallmark plaques.
Led by Professor Marianne
Schultzberg from the Karolinska Institute, Sweden, the team behind the research
revealed that 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 be cleared away, and instead accumulates in the brain, wreaking havoc.
"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 protective compounds formed in the brain from omega-3 fatty acids help to
induce the resolution process and stimulate the uptake or clearing away of amyloid-beta proteins
that have been linked to the progression of Alzheimer's disease through the
development of plaques.
The team will now try to prove
the hypothesis by using animal models to see if omega-3 fatty acids can prevent
memory loss and further loss of brain cells.
In the
study, Dr Schultberg and her group examined cerebrospinal fluid from 15 patients with Alzheimer's disease, 20 patients with
mild cognitive impairment and 21 control subjects. They also analyzed brain
tissue from 10 Alzheimer's patients and 10 control subjects.
Schultzberg and her team looked for
the presence, and comparative 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 alternatively, by stimulating the resolution pathway – such as might occur with omega-3
fatty acid supplementation – “is suggested as a new and promising therapy in
neurodegenerative disorders such as Alzheimer’s disease.”
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