Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Bacteria, Lipopolysaccharides, Amyloid and the Role of Iron Dysregulation in Parkinson’s Disease

Version 1 : Received: 12 November 2020 / Approved: 13 November 2020 / Online: 13 November 2020 (13:22:10 CET)

How to cite: Vuuren, M.J.V.; Nell, T.A.; Carr, J.A.; Kell, D.B.; Pretorius, E. Bacteria, Lipopolysaccharides, Amyloid and the Role of Iron Dysregulation in Parkinson’s Disease. Preprints 2020, 2020110380 (doi: 10.20944/preprints202011.0380.v1). Vuuren, M.J.V.; Nell, T.A.; Carr, J.A.; Kell, D.B.; Pretorius, E. Bacteria, Lipopolysaccharides, Amyloid and the Role of Iron Dysregulation in Parkinson’s Disease. Preprints 2020, 2020110380 (doi: 10.20944/preprints202011.0380.v1).

Abstract

Neuronal lesions in Parkinson’s disease (PD) are commonly associated with α-synuclein (α-Syn)-induced cell damage that are present both in the central and peripheral nervous systems of patients, with the enteric nervous system also being especially vulnerable. Here we bring together evidence that the development and presence of PD depends on specific sets of interlinking factors that include neuro-inflammation, systemic inflammation, α-Syn-induced cell damage, vascular dysfunction, iron dysregulation, gut and periodontal dysbiosis. We argue that there is significant evidence that bacterial inflammagens fuel this systemic inflammation, and might be central to the development of PD. We also discuss the processes whereby lipopolysaccharides may be involved in causing nucleation of proteins, including of α-Syn. Lastly, we review evidence that pre-and probiotics, as well as antibiotics and faecal transplant treatment might be valuable treatments in PD. A most important consideration, however, is that these therapeutic options need to be validated and tested in randomized controlled clinical trials. However, targeting underlying mechanisms of PD, including gut dysbiosis and iron toxicity, have potentially opened up possibilities of a wide variety of novel treatments which may relieve the characteristic non-motor deficits of PD, and may even slow the progression and/or accompanying gut-related conditions of the disease.

Subject Areas

Bacteria; Lipopolysaccharides; Gingipains; Amyloid and Parkinson’s disease; α-Synuclein

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