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Professor Adelaide Fernandes

Adelaide Fernandes

Professor Adelaide Fernandes

Adelaide Fernandes received her degree in pharmaceutical sciences in 2002. From that time, she initiated her PhD in the neuroscience field, focusing on glia reactivity during the neonatal development, at the Faculty of Pharmacy, Universidade de Lisboa (FFULisboa), which she completed in 2006. From 2006 to 2010, she undertook post-doctoral studies dissecting how different early postnatal conditions can affect neuronal development and myelination at the Research Institute for Medicines, FFULisboa (iMed.Ulisboa) and the Department of Neuroscience, University of Minneapolis, Minnesota, USA. Since 2010, Adelaide has been an assistant professor at FFUlisboa, developing research at iMed.ULisboa on neuron–glial interplay during neurodevelopment and neurodegenerative disorders. Her research focuses on the role of neuroinflammation and immune cell recruitment in multiple sclerosis-related central nervous system pathogenesis and psychological/psychiatric comorbidities.

Targeting multiple sclerosis immune- and psycho-pathophysiology by modulation of neuroinflammation

Project summary

Besides the typical central nervous system pathogenesis of multiple sclerosis (MS) (e.g. demyelination, axonal degeneration, inflammation and immune cell activation), greater clinical attention is now drawn to concomitant psychopathology of patients with MS, which hinders the ability to cope with the associated disability.

Importantly, inflammation has also been linked with the psychopathology of MS, suggesting that targeting inflammation may effectively reduce both pathogenesis and psychopathology. Recently, the pro-inflammatory protein S100B has been suggested as a biomarker of central nervous system damage. Interestingly, we showed that S100B is increased in the cerebrospinal fluid/serum of patients with MS at diagnosis and highly expressed in active post-mortem MS lesions. We further demonstrated that neutralization of S100B in an ex vivo demyelinating model prevented not only the induced demyelination but also the axonal injury and inflammatory response. Most interestingly, increased S100B has been also associated with several psychiatric and mood disorders.

In our study, we aim to use a holistic approach, looking at data from both patients with MS and animal models to clarify how neuroinflammation, using S100B as a biomarker, may be involved in the emergence of the psychopathological symptoms of MS and whether we may prevent them by targeting S100B.

Ultimately, we aim to translate the results of the present project to benefit patients, using personalized medicine to reduce both MS-related central nervous system damage and psychiatric comorbidity.

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