Research Papers:

Astaxanthin is neuroprotective in an aged mouse model of Parkinson’s disease

Beth Grimmig, Lauren Daly, Meena Subbarayan, Ched Hudson, Robert Williamson, Kevin Nash and Paula C. Bickford _

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Oncotarget. 2018; 9:10388-10401. https://doi.org/10.18632/oncotarget.23737

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Beth Grimmig1,2, Lauren Daly1, Meena Subbarayan1,2, Ched Hudson3, Robert Williamson4, Kevin Nash2,5 and Paula C. Bickford1,2,3

1Center of Excellence for Aging and Brain Repair, Department of Neurosurgery and Brain Repair, USF Morsani College of Medicine, Tampa, 33612 FL

2Department of Molecular Pharmacology and Physiology, USF Morsani College of Medicine, Tampa, 33612 FL

3Research Service, James A Haley Veterans Hospital, Tampa, 33620 FL

4Sanford Burnham Prebys Medical Discovery Institute at Lake Nona, Orlando, 32827 FL

5USF Health Byrd Alzheimer’s Institute, Morsani College of Medicine, University of South Florida, Tampa, 33613 FL

Correspondence to:

Paula C. Bickford, email: [email protected]

Keywords: astaxanthin; neuroprotection; neurodegeneration; neuroinflammation; aging

Received: October 05, 2017     Accepted: December 21, 2017     Published: December 28, 2017


Parkinson’s disease (PD) is the second most common neurodegenerative disorder and prevalence increases with age. Normal physiological changes that occur during the aging process reflect the pathological characteristics of Parkinson’s disease. It is also recognized that age related changes significantly interact with the pathological mechanisms that underlie the neurodegeneration in PD and perpetuate the disease process. Despite the fact that aging is considered to be a primary risk factor for developing PD, the use of aged animal models are still under-utilized in pre-clinical research, thus reducing the translatability of experimental findings. Here, we use a natural compound astaxanthin (AXT) with multiple biological activities to attenuate neurotoxicity in a mouse model of Parkinson’s disease in both young and aged mice. We observed that AXT preserved neurons in the substantia nigra of both young and aged mice that were exposed to the MPTP neurotoxin. However, AXT was less efficacious in the aged animals, as AXT was not able to protect against the MPTP induced loss of tyrosine hydroxylase (TH) throughout the aged nigro-striatal circuit. This disparity in the neuroprotective effect of AXT suggests that aging is a critical factor to consider during the development of novel therapeutics for neurodegenerative diseases and should be more rigorously evaluated in preclinical models.

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