Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Sirtuins, Mitochondria and the Melatonergic Pathway in Alzheimer’s Disease

Version 1 : Received: 27 February 2020 / Approved: 27 February 2020 / Online: 27 February 2020 (10:52:33 CET)

How to cite: Anderson, G.; Maes, M. Sirtuins, Mitochondria and the Melatonergic Pathway in Alzheimer’s Disease . Preprints 2020, 2020020396 (doi: 10.20944/preprints202002.0396.v1). Anderson, G.; Maes, M. Sirtuins, Mitochondria and the Melatonergic Pathway in Alzheimer’s Disease . Preprints 2020, 2020020396 (doi: 10.20944/preprints202002.0396.v1).

Abstract

Alzheimer's disease (AD) has been the subject of extensive investigation as to its biological underpinnings. However, this has produced little of therapeutic benefit or indeed provided any accepted biomarkers that could tailor treatment. This chapter reviews data on the main pathophysiologic processes that have been widely shown to be altered in AD, including circadian dysregulation, mitochondrial dysfunction, gut dysbiosis, and immune-glia-platelet activation. It is proposed that alterations in the gut microbiome, including gut dysbiosis and increased gut permeability drive changes in mitochondrial function that are intimately associated with significant variations in sirtuin expression. Both mitochondria-located and nucleus/cytoplasm located sirtuins can act on mitochondrial function in different cells and body systems to co-ordinate the ageing-associated changes that underpin AD. The sirtuins are therefore key aspect to a developmental model of AD that is more 'holistic' in perspective, thereby providing a framework for the detection of earlier biomarkers and more successful treatment for the heterogenous nature of AD pathoetiology.

Subject Areas

Alzheimer's disease; sirtuins; mitochondria; leaky gut; inflammation; neuroimmune

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