Omega 3 fatty acids and Alzheimer’s

We have all heared about omega-3 fatty acids and that they are good for your health. Over the last couple of months I have collected some literature and knowledge around this magic stuff made out of fish oil to understand better what is going on.

Studying Wikipedia, we learn that omega 3 seems not to help against cancer and cardiovascular diseases, two of the major causes of death.

The body human body is not able cannot synthesize omega-3 and other fatty acids, they can only be supplied by a diet (rich in oily fish, etc.). It seems however, that Omega 3 helps to fight inflammation, maintain mental health as well as reduce the risk of dementia. Given that there is quite a lot of literature on Alzheimer’s related to inflammation (“inflammation hypothesis”), there might be also a chance that Omega 3 helps to prevent the outbreak of AD or at least delay its onset.

Sciencedaily wrote about a study be Pinot et al who explain how neural singaling may be facilitated by polyunsaturated lipids of which Omega 3 is a member:

Pinot et al (2014) show that cell- or artificial membranes rich in polyunsaturated lipids are much more sensitive to the action of two proteins, dynamin and endophilin (see below), which facilitate membrane deformation and fission (“cracking”). Other measurements in the study and in simulations suggest that these lipids also make the membranes more malleable (deformable). By facilitating the deformation and scission necessary for endocytosis (the cell absorbing external molecules, see below), the presence of polyunsaturated lipids could explain rapid synaptic vesicle recycling. Synaptic vesicle recycling means that the transport of a signal between two nerve cells can happen faster (or more specifically, “recycling” of the signalling materials is accelerated and therefore the nerve cells communication can be more “efficient”). The abundance of these lipids in the brain could then represent a major advantage for cognitive function.

When cells incorporated polyunsaturated fatty acids into phospholipids (PLs), the plasma membrane became more amenable to deformation by a pulling force and the rate of endocytosis was accelerated, in particular, under conditions in which cholesterol was limiting. Molecular dynamics simulations and biochemical measurements indicated that polyunsaturated PLs adapted their conformation to membrane curvature. Thus, by reducing the energetic cost of membrane bending and fission, polyunsaturated PLs may help to support rapid endocytosis.

If all this is true, Omega 3 should help the neural apparatus become sort of more effiicent. It is also interesting that it may work to reduce inflammation. When fighting Alzheimer’s there a couple of methods to do this, one is to use so-called NSAIDs (nonsteroidal anti-inflammatory drugs).  Rubio-Perez & Morillas-Ruiz 2011 cite epidemiological  studies that reduce the risk of developing AD when people were treated with NSAIDs. However, NSAIDs seem not to work if AD is already diagnosed.

Another method to treat patients is medication using Acetylcholinesterase inhibitors. This revolves around the idea that the neurotransmitter Acetylcholine is reduced in AD brains and preventing (thus “inhibitors”) the mechanisms that decompose these molecules (“-esterase”) should help keep levels higher. It’s been shown that this treatment can help reduce the symptoms to some degree. From this perspective Pinot et al’s findings could support the hypothesis that patients treated with Acetylcholinesterase inhibitors may actually benefit from an addition of Omega 3 to their treatment. I’m not aware of studies contrasting patients with and without Omega 3, but to me, it seems worth a try.

(It’s noteworthy to state that obviously not only ACh levels are disturbed in AD but also other neurotransmitters, so that ACh-esterase inhibitors only work on some of the deficits. See here for more information.)

What is…


“One well-supported function of acetylcholine (ACh) in cortex is increased responsiveness to sensory stimuli, a form of attention. Phasic increases of ACh during visual, auditory and somatosensory stimulus presentations have been found to increase the firing rate of neurons in the corresponding primary sensory cortices.” In the context of Alzeheimer’s this would mean that reduced ACh prevents relevant information to enter higher cognition.


“Endocytosis is an energy-using process by which cells absorb molecules (such as proteins) by engulfing them. It is used by all cells of the body because most substances important to them are large polar molecules that cannot pass through the hydrophobic plasma or cell membrane.”


Dynamins are principally involved in the scission of newly formed vesicles from the membrane of one cellular compartment and their targeting to, and fusion with, another compartment, both at the cell surface (particularly caveolae internalization) as well as at the Golgi apparatus.


Kjaerulff et al (2011): Endophilins are members of the BAR domain protein superfamily. They are essential elements of cellular traffic. Endophilins are among the best studied BAR domain proteins. They have a prominent function in synaptic vesicle endocytosis (SVE), receptor trafficking and apoptosis (programmed cell death), and in other processes that require remodeling of the membrane structure.

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