From neuroinflammation control to neuroprotection - identification of targets and mechanisms behind retinal neurodegeneration
Portugal (PorMSIC) - University of Coimbra, Coimbra
Institute for Biomedical Imaging and Life Sciences, Faculty of Medicine, University of Coimbra, Azinhaga de Santa Comba, 3000-548 Coimbra, Portugal
Ana Raquel Sarabando Santiago
Ana Raquel Sarabando Santiago
4 weeks
Cities/Months Jan Feb Mar Apr May Jun Jul Augt Sep Oct Nov Dec
No No No No No No Yes No No No No No
Type of Research Project
- Basic science
What is the background of the project?
Glaucoma is a progressive retinal degenerative disease and the second cause of vision loss in the world. It is characterized by damage of the optic nerve and retinal ganglion cell (RGC) loss. The degeneration of RGCs in glaucoma is accompanied by a neuroinflammatory response involving retinal microglial cells. The etiology of glaucoma is unknown, but elevated intraocular pressure (IOP) has been identified as the main risk factor. Currently, IOP is the only modifiable risk factor and the main target for therapeutic interventions. However, vision loss progresses in up to 45% of glaucoma patients undergoing an IOP-lowering regimen. Therefore, new and more effective treatments are necessary, and neuroprotection of RGCs is considered to offer potential as an alternative therapy. Adenosine is a neuromodulator in central nervous system (CNS) acting on metabotropic adenosine receptors (A1, A2A, A2B and A3). The blockade of A2A receptors has been demonstrated to confer robust neuroprotection against noxious brain conditions, probably through the control of microglia-mediated neuroinflammation.
What is the aim of the project?
The aim of the project is to identify potential therapeutic strategies to prevent the loss of retinal ganglion cells in glaucoma.
What techniques and methods are used?
Techniques Used: Preparation of neural cultures from the retina, preparation of lysates for analysis of protein expression, immunocytochemistry.
What is the role of the student?
- The student will observe the practical experiments but will be highly involved in the analysis of the results
- The tasks will be done under supervision
What are the tasks expected to be accomplished by the student?
The student will mainly follow the experiments that are being performed in the lab.
Will there be any theoretical teaching provided (preliminary readings, lectures, courses, seminars etc)
The student can attend the seminars that regularly take place at the institute and will be given papers related with the project.
What is expected from the student at the end of the research exchange? What will be the general outcome of the student?
- No specific outcome is expected
What skills are required of the student? Is there any special knowledge or a certain level of studies needed?
Are there any legal limitations in the student’s involvement
Type of students accepted
This project accepts:
- Medical students
- Caffeine administration prevents retinal neuroinflammation and loss of retinal ganglion cells in an animal model of glaucoma. Madeira MH; Ortin-Martinez A; Nadal-Nicolas F; Ambrosio AF; Vidal-Sanz M; Agudo-Barriuso M; Santiago AR. Sci Rep. 2016 Jun 8;6:27532. doi: 10.1038/srep27532.
- Selective A2A receptor antagonist prevents microglia-mediated neuroinflammation and protects retinal ganglion cells from high intraocular pressure-induced transient ischemic injury. Madeira MH; Boia R; Elvas F; Martins T; Cunha RA; Ambrosio AF; Santiago AR. Transl Res. 2016 Mar;169:112-28. doi: 10.1016/j.trsl.2015.11.005.
- Adenosine A3 receptor activation is neuroprotective against retinal neurodegeneration. Galvao J; Elvas F; Martins T; Cordeiro MF; Ambrosio AF; Santiago AR. Exp Eye Res. 2015 Nov;140:65-74. doi: 10.1016/j.exer.2015.08.009.
- Adenosine A2AR blockade prevents neuroinflammation-induced death of retinal ganglion cells caused by elevated pressure. Madeira MH; Elvas F; Boia R; Goncalves FQ; Cunha RA; Ambrosio AF; Santiago AR. J Neuroinflammation. 2015 Jun 10;12:115. doi: 10.1186/s12974-015-0333-5.