Neural Regeneration Research ›› 2019, Vol. 14 ›› Issue (4): 735-735.doi: 10.4103/1673-5374.247482

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Human survival and immune mediated mitophagy in neuroplasticity disorders

Ian James Martins 1, 2, 3   

  1. 1 Centre of Excellence in Alzheimer’s Disease Research and Care, Sarich Neuroscience Research Institute, Edith Cowan University, Nedlands, Western Australia, Australia;
    2 School of Psychiatry and Clinical Neurosciences, The University of Western Australia, Nedlands, Western  Australia, Australia;
    3 McCusker Alzheimer’s Research Foundation, Hollywood Medical Centre, Nedlands, Western Australia, Australia
  • Online:2019-04-15 Published:2019-04-15
  • Contact: Ian James Martins, PhD, i.martins@ecu.edu.au.
  • Supported by:

    This work was supported by grants from Edith Cowan University, the McCusker Alzheimer’s Research Foundation and the National Health and Medical Research Council.

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Abstract:

Neurodegenerative diseases are now associated with the global obesity and diabetes epidemic in the developing and developed world. Neurodegenerative diseases are a heterogeneous group of disorders with complex factors such as neurohumoral, endocrine and environmental factors involved in induction of these neurodegenerative diseases. The future of science and medicine in neurodegenerative diseases is now dependent on nutritional genomics with insulin resistance a major factor in the induction of neurodegenerative diseases. Nutritional genomics now involves the anti-aging gene Sirtuin 1 (Sirt 1) that is important to the prevention of insulin resistance with its critical involvement in the immune system. Sirt 1 inactivation leads to toxic immune reactions connected to the acceleration of neuron death in various communities. Appetite control with relevance to immunometabolism has become of critical importance to the treatment of neurodegeneration. Nutritional diets activate the heat shock gene Sirt 1 to prevent the increase in heat shock proteins connected to autoimmune disease, mitophagy and irreversible programmed cell death in global populations.