1. A documented 33% dementia chance post-stroke from an Australian study? May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research. July 2013.
4. A 2-fold increase in dementia risk in this study Jan. 2017
http://www.sciencedirect.com/science/article/pii/S0197018616303345
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Highlights
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- Coconut oil and MCFAs protect against Aβ-induced neurotoxicity in primary rat cortical neurons.
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- Coconut oil inhibits Aβ-induced elevation of markers of cellular stress (Cl Caspase3, ROS).
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- Coconut oil and MCFAs promote a modest increased in ketone bodies.
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- Coconut oil promotes neuroprotection by activating Akt and ERK signalling pathways.
Abstract
Alzheimer's
disease is a progressive neurodegenerative disease that has links with
other conditions that can often be modified by dietary and life-style
interventions. In particular, coconut oil has received attention as
having potentially having benefits in lessening the cognitive deficits
associated with Alzheimer's disease. In a recent report, we showed that
neuron survival in cultures co-treated with coconut oil and Aβ was
rescued compared to cultures exposed only to Aβ. Here we investigated
treatment with Aβ for 1, 6 or 24 h followed by addition of coconut oil
for a further 24 h, or treatment with coconut oil for 24 h followed by
Aβ exposure for various periods. Neuronal survival and several cellular
parameters (cleaved caspase 3, synaptophysin labeling and ROS) were
assessed. In addition, the influence of these treatments on relevant
signaling pathways was investigated with Western blotting. In terms of
the treatment timing, our data indicated that coconut oil rescues cells
pre-exposed to Aβ for 1 or 6 h, but is less effective when the
pre-exposure has been 24 h. However, pretreatment with coconut oil prior
to Aβ exposure showed the best outcomes. Treatment with octanoic or
lauric acid also provided protection against Aβ, but was not as
effective as the complete oil. The coconut oil treatment reduced the
number of cells with cleaved caspase and ROS labeling, as well as
rescuing the loss of synaptophysin labeling observed with Aβ treatment.
Treatment with coconut oil, as well as octanoic, decanoic and lauric
acids, resulted in a modest increase in ketone bodies compared to
controls. The biochemical data suggest that Akt and ERK activation may
contribute to the survival promoting influence of coconut oil. This was
supported by observations that a PI3-Kinase inhibitor blocked the rescue
effect of CoOil on Aβ amyloid toxicity. Further studies into the
mechanisms of action of coconut oil and its constituent medium chain
fatty acids are warranted.
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