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Cell Rep. 2019 Feb 12;26(7):1727-1733.e6. doi: 10.1016/j.celrep.2019.01.015.

Age- and α-Synuclein-Dependent Degeneration of Dopamine and Noradrenaline Neurons in the Annual Killifish Nothobranchius furzeri.

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Department of Neuroscience of Disease, Center for Transdisciplinary Research, Niigata University, Niigata 951-8585, Japan; Brain Research Institute, Niigata University, Niigata 951-8585, Japan; Department of Neuroscience, University of Miyazaki, Faculty of Medicine, Miyazaki 889-1692, Japan. Electronic address:
Frontier Science Research Center, University of Miyazaki, Miyazaki 889-1692, Japan.
Cellular and Molecular Neurobiology, Zoological Institute, Technical University Braunschweig, 38106 Braunschweig, Germany.


Parkinson's disease (PD) is a neurodegenerative disease characterized by α-synuclein-positive inclusion bodies and loss of neurons, including dopaminergic neurons. Difficulty in replicating PD phenotypes using animal models partly limits the understanding of PD and the therapy required. Although PD is strongly associated with aging, most experimental animals may not exhibit age-related symptoms. Herein, we demonstrate that Nothobranchius furzeri, a rapidly aging teleost with a short life span, exhibits age-dependent degeneration of dopaminergic and noradrenergic neurons and progression of α-synuclein pathologies. These pathological phenotypes are similar to those observed in human patients with PD. Amelioration of the cell loss by genetic depletion of α-synuclein suggests that α-synuclein is not a bystander but a causative protein of neurodegeneration. N. furzeri can reveal mechanisms underlying PD, especially of the idiopathic form that affects a majority of patients with PD, including α-synuclein-dependent neurodegeneration, age-dependent phenotypes, and progression of α-synuclein pathology.


Nothobranchius furzeri; Parkinson’s disease; aging; α-synuclein

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