Journal
FREE RADICAL BIOLOGY AND MEDICINE
Volume 115, Issue -, Pages 80-91Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2017.10.379
Keywords
Aging; Inflammation; Inflammaging; Neuroinflammation; Hormesis; Parkinson's Disease
Funding
- Italian Ministry of Health [GR-2013-02358026]
- University of Florence
- European Union (EU) [634821]
- EU JPND 'Adage'
- EU NU-AGE [266486]
- EU Project HUMAN [602757]
- Italian Ministry of University and Research [CTN01 00230 413096]
- US Air Force [FA9550-13-1-0047]
- ExxonMobil Foundation [S18200000000256]
- European Union's Horizon Research and Innovation Programme [720270: HBP SGA1]
- AEHS Foundation
- National Center for Advancing Translational Sciences [UL1TR001409]
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In order to better understand the pathogenesis of Parkinson's Disease (PD) it is important to consider possible contributory factors inherent to the aging process, as age-related changes in a number of physiological systems (perhaps incurred within particular environments) appear to influence the onset and progression of neurode-generative disorders. Accordingly, we posit that a principal mechanism underlying PD is inflammaging, i.e. the chronic inflammatory process characterized by an imbalance of pro-and anti-inflammatory mechanisms which has been recognized as operative in several age-related, and notably neurodegenerative diseases. Recent conceptualization suggests that inflammaging is part of the complex adaptive mechanisms (re-modeling) that are ongoing through the lifespan, and which function to prevent or mitigate endogenous processes of tissue disruption and degenerative change(s). The absence of an adequate anti-inflammatory response can fuel inflammaging, which propagates on both local (i.e.- from cell to cell) and systemic levels (e.g.- via exosomes and other molecules present in the blood). In general, this scenario is compatible with the hypothesis that inflammaging represents a hormetic or hormetic-like effect, in which low levels of inflammatory stress may prompt induction of anti-inflammatory mediators and mechanisms, while sustained pro-inflammatory stress incurs higher and more durable levels of inflammatory substances, which, in turn prompt a local-to-systemic effect and more diverse inflammatory response(s). Given this perspective, new treatments of PD may be envisioned that strategically are aimed at exerting hormetic effects to sustain anti-inflammatory responses, inclusive perhaps, of modulating the inflammatory influence of the gut microbiota.
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