Human cu/zn superoxide dismutase (SOD1) overexpression in mice causes mitochondrial vacuolization, axonal degeneration, and premature motoneuron death and accelerates motoneuron disease in mice expressing a familial amyotrophic lateral sclerosis mutant SO

Dick Jaarsma; Elize Haasdijk; JAC (Janine) Grashorn; Henrieke Aalsburg; W van Duijn; HW Verspaget; J London; Joan Holstege

doi:10.1006/nbdi.2000.0299

Human cu/zn superoxide dismutase (SOD1) overexpression in mice causes mitochondrial vacuolization, axonal degeneration, and premature motoneuron death and accelerates motoneuron disease in mice expressing a familial amyotrophic lateral sclerosis mutant SO

Dick Jaarsma
, Elize Haasdijk
, JAC (Janine) Grashorn
, Henrieke Aalsburg
, W van Duijn
, HW Verspaget
, J London
, Joan Holstege

Neurosciences

Research output: Contribution to journal › Article › Academic › peer-review

306 Citations (Scopus)

Original language	Undefined/Unknown
Pages (from-to)	623-643
Number of pages	21
Journal	Neurobiology of Disease
Volume	7
DOIs	https://doi.org/10.1006/nbdi.2000.0299
Publication status	Published - 2000

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Research programs

EMC ONWAR-01-94-01

Access to Document

10.1006/nbdi.2000.0299

http://hdl.handle.net/1765/65407

Cite this

Jaarsma, D., Haasdijk, E., Grashorn, JAC., Aalsburg, H., van Duijn, W., Verspaget, HW., London, J., & Holstege, J. (2000). Human cu/zn superoxide dismutase (SOD1) overexpression in mice causes mitochondrial vacuolization, axonal degeneration, and premature motoneuron death and accelerates motoneuron disease in mice expressing a familial amyotrophic lateral sclerosis mutant SO. Neurobiology of Disease, 7, 623-643. https://doi.org/10.1006/nbdi.2000.0299

Jaarsma, Dick ; Haasdijk, Elize ; Grashorn, JAC (Janine) et al. / Human cu/zn superoxide dismutase (SOD1) overexpression in mice causes mitochondrial vacuolization, axonal degeneration, and premature motoneuron death and accelerates motoneuron disease in mice expressing a familial amyotrophic lateral sclerosis mutant SO. In: Neurobiology of Disease. 2000 ; Vol. 7. pp. 623-643.

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title = "Human cu/zn superoxide dismutase (SOD1) overexpression in mice causes mitochondrial vacuolization, axonal degeneration, and premature motoneuron death and accelerates motoneuron disease in mice expressing a familial amyotrophic lateral sclerosis mutant SO",

author = "Dick Jaarsma and Elize Haasdijk and Grashorn, \{JAC (Janine)\} and Henrieke Aalsburg and \{van Duijn\}, W and HW Verspaget and J London and Joan Holstege",

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Jaarsma, D, Haasdijk, E, Grashorn, JAC, Aalsburg, H, van Duijn, W, Verspaget, HW, London, J & Holstege, J 2000, 'Human cu/zn superoxide dismutase (SOD1) overexpression in mice causes mitochondrial vacuolization, axonal degeneration, and premature motoneuron death and accelerates motoneuron disease in mice expressing a familial amyotrophic lateral sclerosis mutant SO', Neurobiology of Disease, vol. 7, pp. 623-643. https://doi.org/10.1006/nbdi.2000.0299

Human cu/zn superoxide dismutase (SOD1) overexpression in mice causes mitochondrial vacuolization, axonal degeneration, and premature motoneuron death and accelerates motoneuron disease in mice expressing a familial amyotrophic lateral sclerosis mutant SO. / Jaarsma, Dick; Haasdijk, Elize; Grashorn, JAC (Janine) et al.
In: Neurobiology of Disease, Vol. 7, 2000, p. 623-643.

Research output: Contribution to journal › Article › Academic › peer-review

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AU - Jaarsma, Dick

AU - Haasdijk, Elize

AU - Grashorn, JAC (Janine)

AU - Aalsburg, Henrieke

AU - van Duijn, W

AU - Verspaget, HW

AU - London, J

AU - Holstege, Joan

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Jaarsma D, Haasdijk E, Grashorn JAC, Aalsburg H, van Duijn W, Verspaget HW et al. Human cu/zn superoxide dismutase (SOD1) overexpression in mice causes mitochondrial vacuolization, axonal degeneration, and premature motoneuron death and accelerates motoneuron disease in mice expressing a familial amyotrophic lateral sclerosis mutant SO. Neurobiology of Disease. 2000;7:623-643. doi: 10.1006/nbdi.2000.0299