More Proof To Move!

Disclaimer: my following blog is going to be highly persuasive, with a confirming bias.

Now that I have gotten the aforementioned out of the way: it’s time to discuss with you about a protein named Irisin— and it’s newly found role in the brain as an exercise-induced messenger (1). Irisin, or: Fibronectin type III domain-containing protein 5, which is an absolute mouthful! and will not be used for the entirety of this blog! is a myokine—  a type of cytokine (protein) that was first discovered and involved in fat -metabolism (1). Recently, Irisin has been found to be involved in neuroprotection, especially in Alzheimer’s rodent models (2).

So how does Irisin work with exercise?

Irisin is released in the muscle during exercise (muscle contractions). Which initiates a cell-signalling pathway, that is able to facilitate the human cortex by the means of plasticity (in lame terms). Studies in vivo Alzheimer’s rodent models have shown that: exercise was able to prevent the aggregation of the well known protein: Amyloid-beta in Alzheimer phenotypical rodents which is a neurotoxic protein (1). Amyloid-Beta, are plaques that interfere with neuronal signaling— just like plaques in an artery that can cause atherosclerosis. Although big pharma companies have been unable to discover a drug that removes amyloid-beta from the human cortex. There are other well established adjuncts, such as aerobic exercise— that is a well known panacea for the cognitively aging (and young!), whilst also being incredibly important for an array of other health benefits which will not be discussed. Irisin, via exercise-induced signalling: targets the neurotoxic proteins by increasing the strength of the dendritic spine of the neuron/s (neuronal communication) which thus can promote long term potentiation (1) which is the consolidation of short term memory, to long term memory. I think of Irisin like the well-studied nuerotrophin: Brain-Derived-Neurotrophic-Factor (BDNF). BDNF is known in lame terms as fertilizer for the brain. And just as a plant requires a process to grow and develop; so too do nerve cells. Exercise is an acute stress. Acute stressors are excellent from: bone and tissue stress during strength training, a cognitively demanding task, to aerobic exercise. For neurons to survive. They require stress (as one means among many). And stress via aerobic exercise is an excellent means to activate powerful cellular pathways such as Irisin and BDNF. I get super excited knowing that each time I hop (metaphorically speaking) on the cross-trainer; I am activating such a powerful pathway, whilst increasing my longevity— and significantly decreasing the risk of dementia later in life.

From an aerobic exercise prescription. Physical activity guidelines recommend: One-hundred and fifty minutes of moderate intensity aerobic activity over ones week. Or, seventy-minutes of intense physical activity once per week. With consultation with one’s GP and exercise physiologist. One can be guided safely through exercise; that is in concordance with ones current level of cardiovascular fitness. This will ensure appropriate prescription and safety. Now, any exercise at any age is beneficial. However, exercising at a earlier age, and maintaining through ones life has the best evidence for robustness against dementia. And going a little beyond the physical activity guidelines, by introducing- strength training, or some short high-intensity-intervals will contribute as a drug on it’s own accord!

So think of exercise (especially aerobic) like your superannuation: each time you exercise, you are investing in your long-term health. So move! seek expert advice! and give your brain the best health that it deserves.

James

References

1. Chen, X. and Gan, L. (2019). An exercise-induced messenger boosts memory in Alzheimer’s disease. Nature Medicine, 25(1), pp.20-21.

2. Lourenco, M., Frozza, R., de Freitas, G., Zhang, H., Kincheski, G., Ribeiro, F., Gonçalves, R., Clarke, J., Beckman, D., Staniszewski, A., Berman, H., Guerra, L., Forny-Germano, L., Meier, S., Wilcock, D., de Souza, J., Alves-Leon, S., Prado, V., Prado, M., Abisambra, J., Tovar-Moll, F., Mattos, P., Arancio, O., Ferreira, S. and De Felice, F. (2019). Exercise-linked FNDC5/irisin rescues synaptic plasticity and memory defects in Alzheimer’s models. Nature Medicine, 25(1), pp.165-175.

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