Dr Hélène Marie Institute of Molecular & Cellular Pharmacology (IPMC) Valbonne – The European Brain Research Institute in Rome

  • Alumni

Molecular mechanisms of neuronal plasticity in health and disease

  • Institute of Molecular & Cellular Pharmacology (IPMC) Valbonne
  • [email protected]>
  • +33 4 93 95 34 40
  • +33 4 93 95 34 08
  • France

About Dr Hélène Marie

Our team is interested in understanding how physiological and pathological conditions shape neuronal plasticity. We have an integrated approach to delineate how molecular changes translate into behavioural outcomes. We have strong expertise in in vitro electrophysiology on brain slices (field and patch clamp recordings) and in behaviour. We use viral approaches for in vivo protein expression as well as transgenic lines to alter brain molecular mechanisms. We are also currently developing biochemical and cell imaging tools to address our questions.

Our research focuses on 3 main axes.

Alzheimer disease. AD is the most frequent neurodegenerative disorder. Chronic stress is known to be a key risk factor in the development of the pathology. We therefore seek to understand how stress and dysregulation of the corticotrope axis contributes to the onset of AD-related synaptic alterations and how these modifications translate into impaired mnemonic functions. Also, neuropathologically, AD is characterized by progressive appearance of oligomers of b-amyloid peptide (Ab) and plaques. Since increased Ab load per se cannot fully account for the deficits observed in AD, we explore the functional role of other peptides produced by APP processing.

Epilepsy. Epilepsy is a devastating neurological disorder, which can impair brain function. In collaboration with the team of Dr. Mantegazza (IPMC), we seek to understand how synaptic function and memory are perturbed in mouse models of this disorder.

Social stress. When overwhelming, stress increases the morbidity for psychiatric disorders such as major depression and inability to socially perform. These aberrant behaviours are reproduced in mice repetitively exposed to social defeat stress. This results in a persistent boost of dopamine (DA) transmission. This project aims at identifying the inputs that shape DA responsiveness in response to social stress. This may form the pathophysiological basis for major psychiatric disorders.

In collaboration with computational neuroscientists, we are also interested in modelling disease-related synaptic alterations to understand how these impact the function of hippocampal neurons at the single cell level and at the network level.

For more information, please see here.

A full publication record can be found here.