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Microcebus murinus retina: a new model to assess prion-related neurotoxicity in primates
Joan Torrent1, Chadi Soukkarieh, Guy Lenaers
1Univ Montpellier 2, Montpellier, F-34095 France. joan.torrent@inserm.fr <joan.torrent@inserm.fr>
Abstract:
No effective treatment currently exists for prion diseases and therefore the development of experimental non-human primate models of prion neurotoxicity, to better understand the underlying mechanism and to test new treatments relevant to humans, represents an urgent medical need. However, the establishment of such models is challenging due to animal welfare and cost considerations. We describe here the use of Microcebus murinus retina, in primary cultures and in vivo, as a new experimental primate model to rapidly examine the effects in the central nervous system of PrP(106-126), a neurotoxic fragment of the human prion protein. We demonstrate that PrP(106-126) triggered rod photoreceptor cell loss by apoptosis and a change in morphology of microglial cells in mixed neuronal-glial cultures of retinal cells. In addition, 2days after intravitreal injection of PrP(106-126), retinas showed a significant increase in the number of apoptotic nuclei, mainly in the ganglion cell layer.
Insights
Developing new primate models for prion diseases is crucial. Researchers used the Microcebus murinus retina to study prion protein neurotoxicity, showing it causes photoreceptor cell death and retinal damage.
Area of Science:
- Neuroscience
- Prion Disease Research
- Ophthalmology
Background:
- Prion diseases lack effective treatments, necessitating new research models.
- Developing non-human primate models for prion neurotoxicity is vital for understanding disease mechanisms and testing therapies.
- Animal welfare and cost are significant challenges in establishing such models.
Purpose of the Study:
- To establish a new experimental primate model using Microcebus murinus retina for studying prion neurotoxicity.
- To investigate the effects of the neurotoxic prion protein fragment PrP(106-126) in the central nervous system.
- To rapidly examine prion-related effects in a relevant primate model.
Main Methods:
- Utilized Microcebus murinus retinal cells in primary cultures and in vivo.
- Examined the impact of the neurotoxic prion protein fragment PrP(106-126).
- Assessed effects on rod photoreceptor cells, microglial cells, and retinal cell layers.
Main Results:
- PrP(106-126) induced apoptosis and cell loss in rod photoreceptor cells.
- Observed morphological changes in microglial cells in retinal cultures.
- Intravitreal injection of PrP(106-126) led to increased apoptotic nuclei in the ganglion cell layer within two days.
Conclusions:
- The Microcebus murinus retina serves as a viable and rapid experimental primate model for prion neurotoxicity.
- PrP(106-126) directly causes retinal cell damage, including photoreceptor apoptosis and ganglion cell layer disruption.
- This model holds promise for future research into prion disease mechanisms and therapeutic interventions.
