CV Science

Florian Sennlaub MD PhD

Course and current status

Current situation

Directeur de Recherche 2^ièmeClasse INSERM (Institut national de la santé et recherche médicale):  

Team Director Equipe14: Inflammation, degeneration and vascular remodeling in retinal pathologies

Director of the Department of Thearpeutics

Institut de la Vision

17, rue Moreau, 75012 Paris

Tel.: +33 1 53 46 26 93

Degrees and diplomas:

2008 : « Directeur de Recherche classe 2 » Inserm promotion

2007 : Habilitation à Diriger des Recherches Université Paris 5

2005 : « Chargé de Recherche classe 1 » Inserm (staff researcher) recruitment

2002-2005 : Post doctorat: Pharmacology, Hôpital Ste Justine, Montréal, Sylvain Chemtob.

2002: Ph.D. in molecular and cellular biology Université Paris 5.

2001: Doctor Medizinae. Magna cum laude. Charité, Université d‘Humboldt, Berlin.

1999: DEA in “Biologie et Pharmacologie de l`Hémostase et des Vaisseaux“.

1996: 3^rd Staatsexamen (Final Medical State Exam) Munich, Germany.

Additional training:

1996-97: Department of Ophthalmology Charité, Humboldt University, Berlin (Resident / Interne).

Scientific summary

Age-related Macular Degeneration (AMD) is the leading cause of legal blindness in industrialized countries. The pathology is characterized by lesions of photoreceptors, retinal pigment epithelium (RPE), Bruch’s membrane (BM) and choriocapillaris. There are two clinical forms of late AMD: the fast progressive “wet” form defined by choroidal neovascularisation, responsible for the most part of legal blindness in AMD and the more slowly progressf “atrophic” form characterized by RPE atrophy, photoreceptor degeneration and choroidal involution and obliteration.

It has been recognized that macrophages and microglial cells are activated in AMD lesions. Others and our group has shown that they and accumulate in the photoreceptor cell layer that is physiologically devoid of Macrophages and microglial cells.Macrophages are together with the retinal pigment epithelium main VEGF producers and their inhibition significantly inhibits choroidal neovascularization in animal models. Moreover, the prolonged presence of macrophages in the subretinal space is associated with photoreceptor degeneration. The goal of my group is to decipher mechanisms involved in angiogenesis, neovascularization and retinal degeneration with an emphasis on macrophages and microglial cells with the goal to identify new drug targets to treat neovascular and more importantly atrophic AMD.