Journal
JOURNAL OF NEUROSCIENCE RESEARCH
Volume 96, Issue 10, Pages 1641-1662Publisher
WILEY
DOI: 10.1002/jnr.24244
Keywords
adaptation; aging; hormesis; neuroprotection; preconditioning; Parkinson's disease
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Funding
- U.S. Air Force [FA9550-13-1-0047]
- ExxonMobil Foundation [S18200000000256]
- National Center for Advancing Translational Sciences (NCATS), National Institutes of Health, through the Clinical and Translational Science Awards Program (CTSA), a trademark of the Department of Health and Human Services, part of the Roadmap Initiative, [UL1TR001409]
- AEHS Foundation
- Austin and Ann O'Malley Visiting Chair in Bioethics of Loyola Marymount University, CA, USA
- European Union (EU) [634821]
- Ministry of Education and Science of the Russian Federation [074-02-2018-330]
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Age-related changes in the brain reflect a dynamic interaction of genetic, epigenetic, phenotypic, and environmental factors that can be temporally restricted or more longitudinally present throughout the lifespan. Fundamental to these mechanisms is the capacity for physiological adaptation through modulation of diverse molecular and biochemical signaling occurring from the intracellular to the network-systemic level throughout the brain. A number of agents that affect the onset and progression of Parkinson's disease (PD)-like effects in experimental models exhibit temporal features, and mechanisms of hormetic dose responses. These findings have particular significance since the hormetic dose response describes the amplitude and range of potential therapeutic effects, thereby affecting the design and conduct of studies of interventions against PD (and other neurodegenerative diseases), and may also be important to a broader consideration of hormetic processes in resilient adaptive responses that might afford protection against the onset and/or progression of PD and related disorders.
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