Publication

PET Imaging of Disease Progression and Treatment Effects in the Experimental Autoimmune Encephalomyelitis Rat Model

Faria, D. D. P., Vlaming, M. L. H., Copray, S. C. V. M., Tielen, F., Anthonijsz, H. J. A., Sijbesma, J. W. A., Buchpiguel, C. A., Dierckx, R. A. J. O., van der Hoorn, J. W. A. & de Vries, E. F. J., Aug-2014, In : Journal of Nuclear Medicine. 55, 8, p. 1330-1335 6 p.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Faria, D. D. P., Vlaming, M. L. H., Copray, S. C. V. M., Tielen, F., Anthonijsz, H. J. A., Sijbesma, J. W. A., Buchpiguel, C. A., Dierckx, R. A. J. O., van der Hoorn, J. W. A., & de Vries, E. F. J. (2014). PET Imaging of Disease Progression and Treatment Effects in the Experimental Autoimmune Encephalomyelitis Rat Model. Journal of Nuclear Medicine, 55(8), 1330-1335. https://doi.org/10.2967/jnumed.114.137216

Author

Faria, Daniele de Paula ; Vlaming, Maria L. H. ; Copray, Sjef C. V. M. ; Tielen, Frans ; Anthonijsz, Herma J. A. ; Sijbesma, Jurgen W. A. ; Buchpiguel, Carlos A. ; Dierckx, Rudi A. J. O. ; van der Hoorn, Jose W. A. ; de Vries, Erik F. J. / PET Imaging of Disease Progression and Treatment Effects in the Experimental Autoimmune Encephalomyelitis Rat Model. In: Journal of Nuclear Medicine. 2014 ; Vol. 55, No. 8. pp. 1330-1335.

Harvard

Faria, DDP, Vlaming, MLH, Copray, SCVM, Tielen, F, Anthonijsz, HJA, Sijbesma, JWA, Buchpiguel, CA, Dierckx, RAJO, van der Hoorn, JWA & de Vries, EFJ 2014, 'PET Imaging of Disease Progression and Treatment Effects in the Experimental Autoimmune Encephalomyelitis Rat Model', Journal of Nuclear Medicine, vol. 55, no. 8, pp. 1330-1335. https://doi.org/10.2967/jnumed.114.137216

Standard

PET Imaging of Disease Progression and Treatment Effects in the Experimental Autoimmune Encephalomyelitis Rat Model. / Faria, Daniele de Paula; Vlaming, Maria L. H.; Copray, Sjef C. V. M.; Tielen, Frans; Anthonijsz, Herma J. A.; Sijbesma, Jurgen W. A.; Buchpiguel, Carlos A.; Dierckx, Rudi A. J. O.; van der Hoorn, Jose W. A.; de Vries, Erik F. J.

In: Journal of Nuclear Medicine, Vol. 55, No. 8, 08.2014, p. 1330-1335.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Faria DDP, Vlaming MLH, Copray SCVM, Tielen F, Anthonijsz HJA, Sijbesma JWA et al. PET Imaging of Disease Progression and Treatment Effects in the Experimental Autoimmune Encephalomyelitis Rat Model. Journal of Nuclear Medicine. 2014 Aug;55(8):1330-1335. https://doi.org/10.2967/jnumed.114.137216


BibTeX

@article{de7519f9f93c4b23b26500bbbf2dcdbc,
title = "PET Imaging of Disease Progression and Treatment Effects in the Experimental Autoimmune Encephalomyelitis Rat Model",
abstract = "The experimental autoimmune encephalomyelitis model is a model of multiple sclerosis that closely mimics the disease characteristics in humans. The main hallmarks of multiple sclerosis are neuroinflammation (microglia activation, monocyte invasion, and T-cell infiltration) and demyelination. PET imaging may be a useful non-invasive technique for monitoring disease progression and drug treatment efficacy in vivo. Methods: Experimental autoimmune encephalomyelitis was induced by myelin-oligodendrocyte glycoprotein immunization in female Dark Agouti rats. Experimental autoimmune encephalomyelitis rats were imaged at baseline and at days 6, 11, 15, and 19 after immunization to monitor monocyte and microglia activation (C-11-PK11195) and demyelination (C-11-MeDAS) during normal disease progression and during treatment with dexamethasone. Results: C-11-PK11195 PET detected activation of microglia and monocytes in the brain stem and spinal cord during disease progression. The uptake of C-11-PK11195 was elevated in dexamethasone-treated animals that had shown mild clinical symptoms that had resolved at the time of imaging. Demyelination was not detected by C-11-MeDAS PET, probably because of the small size of the lesions (average, 0.13 mm). Conclusion: PET imaging of neuroinflammation can be used to monitor disease progression and the consequences of treatment in the experimental autoimmune encephalomyelitis rat model. PET imaging was more sensitive than clinical symptoms for detecting inflammatory changes in the central nervous system.",
keywords = "multiple sclerosis, PET imaging, neuroinflammation, demyelination, POSITRON-EMISSION-TOMOGRAPHY, PERIPHERAL BENZODIAZEPINE-RECEPTOR, IN-VIVO QUANTIFICATION, MULTIPLE-SCLEROSIS, SPINAL-CORD, TRANSLOCATOR PROTEIN, NERVOUS-SYSTEM, MYELIN, ACTIVATION, EXPRESSION",
author = "Faria, {Daniele de Paula} and Vlaming, {Maria L. H.} and Copray, {Sjef C. V. M.} and Frans Tielen and Anthonijsz, {Herma J. A.} and Sijbesma, {Jurgen W. A.} and Buchpiguel, {Carlos A.} and Dierckx, {Rudi A. J. O.} and {van der Hoorn}, {Jose W. A.} and {de Vries}, {Erik F. J.}",
note = "{\textcopyright} 2014 by the Society of Nuclear Medicine and Molecular Imaging, Inc.",
year = "2014",
month = aug,
doi = "10.2967/jnumed.114.137216",
language = "English",
volume = "55",
pages = "1330--1335",
journal = "Journal of Nuclear Medicine",
issn = "0161-5505",
publisher = "SOC NUCLEAR MEDICINE INC",
number = "8",

}

RIS

TY - JOUR

T1 - PET Imaging of Disease Progression and Treatment Effects in the Experimental Autoimmune Encephalomyelitis Rat Model

AU - Faria, Daniele de Paula

AU - Vlaming, Maria L. H.

AU - Copray, Sjef C. V. M.

AU - Tielen, Frans

AU - Anthonijsz, Herma J. A.

AU - Sijbesma, Jurgen W. A.

AU - Buchpiguel, Carlos A.

AU - Dierckx, Rudi A. J. O.

AU - van der Hoorn, Jose W. A.

AU - de Vries, Erik F. J.

N1 - © 2014 by the Society of Nuclear Medicine and Molecular Imaging, Inc.

PY - 2014/8

Y1 - 2014/8

N2 - The experimental autoimmune encephalomyelitis model is a model of multiple sclerosis that closely mimics the disease characteristics in humans. The main hallmarks of multiple sclerosis are neuroinflammation (microglia activation, monocyte invasion, and T-cell infiltration) and demyelination. PET imaging may be a useful non-invasive technique for monitoring disease progression and drug treatment efficacy in vivo. Methods: Experimental autoimmune encephalomyelitis was induced by myelin-oligodendrocyte glycoprotein immunization in female Dark Agouti rats. Experimental autoimmune encephalomyelitis rats were imaged at baseline and at days 6, 11, 15, and 19 after immunization to monitor monocyte and microglia activation (C-11-PK11195) and demyelination (C-11-MeDAS) during normal disease progression and during treatment with dexamethasone. Results: C-11-PK11195 PET detected activation of microglia and monocytes in the brain stem and spinal cord during disease progression. The uptake of C-11-PK11195 was elevated in dexamethasone-treated animals that had shown mild clinical symptoms that had resolved at the time of imaging. Demyelination was not detected by C-11-MeDAS PET, probably because of the small size of the lesions (average, 0.13 mm). Conclusion: PET imaging of neuroinflammation can be used to monitor disease progression and the consequences of treatment in the experimental autoimmune encephalomyelitis rat model. PET imaging was more sensitive than clinical symptoms for detecting inflammatory changes in the central nervous system.

AB - The experimental autoimmune encephalomyelitis model is a model of multiple sclerosis that closely mimics the disease characteristics in humans. The main hallmarks of multiple sclerosis are neuroinflammation (microglia activation, monocyte invasion, and T-cell infiltration) and demyelination. PET imaging may be a useful non-invasive technique for monitoring disease progression and drug treatment efficacy in vivo. Methods: Experimental autoimmune encephalomyelitis was induced by myelin-oligodendrocyte glycoprotein immunization in female Dark Agouti rats. Experimental autoimmune encephalomyelitis rats were imaged at baseline and at days 6, 11, 15, and 19 after immunization to monitor monocyte and microglia activation (C-11-PK11195) and demyelination (C-11-MeDAS) during normal disease progression and during treatment with dexamethasone. Results: C-11-PK11195 PET detected activation of microglia and monocytes in the brain stem and spinal cord during disease progression. The uptake of C-11-PK11195 was elevated in dexamethasone-treated animals that had shown mild clinical symptoms that had resolved at the time of imaging. Demyelination was not detected by C-11-MeDAS PET, probably because of the small size of the lesions (average, 0.13 mm). Conclusion: PET imaging of neuroinflammation can be used to monitor disease progression and the consequences of treatment in the experimental autoimmune encephalomyelitis rat model. PET imaging was more sensitive than clinical symptoms for detecting inflammatory changes in the central nervous system.

KW - multiple sclerosis

KW - PET imaging

KW - neuroinflammation

KW - demyelination

KW - POSITRON-EMISSION-TOMOGRAPHY

KW - PERIPHERAL BENZODIAZEPINE-RECEPTOR

KW - IN-VIVO QUANTIFICATION

KW - MULTIPLE-SCLEROSIS

KW - SPINAL-CORD

KW - TRANSLOCATOR PROTEIN

KW - NERVOUS-SYSTEM

KW - MYELIN

KW - ACTIVATION

KW - EXPRESSION

U2 - 10.2967/jnumed.114.137216

DO - 10.2967/jnumed.114.137216

M3 - Article

C2 - 24914056

VL - 55

SP - 1330

EP - 1335

JO - Journal of Nuclear Medicine

JF - Journal of Nuclear Medicine

SN - 0161-5505

IS - 8

ER -

ID: 14255987