CV Science

Jean-Philippe LOEFFLER PhD

Course and current status

EDUCATION

BSc of Biochemistry and Physiology , Université Louis Pasteur Strasbourg(1980)
DEA of physiology (with honnor), Université Louis Pasteur Strasbourg (1981)
Doctorat d'Université (PhD), Université Louis Pasteur Strasbourg (1984)
RESEARCH PRACTICAL

1980-1984: PhD student in Dr P. Feltz, ULP Strasbourg.
1984-1987: Post-Doctorant fellow at Dept. of Neuropharmacology, Max Plank Institute of Psychatry, Munich, Gerany, Dir: A. Hertz.
Since 1987 : Tenure position at INSERM from 1987 to 1996 as researcher (CR). From 1996 to present as Research Director.
1994-2000: Visiting Associate professor of Molecular Neurobiology (faculty member) at the  Mount Sinaï Hospital, New York, USA
2001- : Director of the laboratory of « Molecular Signalling and Neurodegeneration » U692 INSERM
Research fields: understanding of pathological mechanisms of ALS underlying MN degeneration.

Scientific summary

    Originally dedicated to studies on molecular mechanisms of neuronal death, my laboratory progressively focussed on basic research and clinical studies on amyotrophic lateral sclerosis (ALS). Since more than ten years, we have pursued our investigations by studying the disease not only in the mutant SOD1 mouse, which is the best known model of familial ALS, but also in patients presenting with the commoner, sporadic form (which represents about 90% of cases).
    Our work has generated about 40 publications in the field, many of these being published in international high ranking journals, such as Journal of Neuroscience, Annals of Neurology, Human Molecular Genetics, PNAS or Lancet Neurology.
    During this period, we have accomplished two major achievements:
    1- the discovery and validation of a clinically meaningful biomarker of disease progression (NogoA), and
    2- the demonstration that abnormal energy homeostasis is critical in ALS pathogenesis.
It is important to mention that our discovery of the implication of Nogo-A in local NMJ injury has supported the notion of treating ALS patients by neutralising anti-Nogo-A strategies, which is currently under investigation in the pharmaceutical domain.
Collectively, these results indicated that ALS can be the result of the interplay of central and peripheral pathogenic mechanisms, whose ultimate consequence is the selective degeneration of motor neurons. In addition, they bring about important clinical implications for the management of the nutritional status of ALS patients. In this respect, our findings are currently being used as a basis for developing nutritional strategies of therapeutic potential.