Matteo Bergami

Faculty of Medicine

Brain Plasticity and Repair

While mostly lacking a full regenerative capacity, the adult mammalian brain maintains a significant degree of tissue plasticity. Dissecting how such plasticity mechanisms are regulated at the cellular and tissue level holds potential for brain repair.

Research Focus

Our group investigates the mechanisms by which specific experiences or injurious conditions promote brain tissue plasticity. Specifically, we aim at revealing the principles governing the generation and circuit incorporation of new neurons in the adult brain, and how these processes are linked to experience. Our findings extend to models of brain injury and disease, in which we study how the activity of neuronal and glial networks can be manipulated to improve tissue repair.

We study mechanisms of neuronal and glial cell plasticity induced by experience and brain injury.

Our Goals

For the most part, the adult brain lacks the capacity to regenerate functional brain cells. Many neurological and degenerative diseases are characterized by a progressive and largely irreversible disruption of nerve cell integrity that ultimately affects the functioning of brain circuits. Within this context, cell replacement-based strategies require any newly-generated neuron to establish the proper connectivity with pre-existing nerve cells.

  • Our working group focuses on the molecular processes that allow the proper formation and connectivity establishment of neural stem cell-derived new neurons in the adult brain. We specifically address how these processes are sculpted by experience, for instance significant changes in environmental and social inputs, which are sites of intervention in treating forms of dementia.
  • Second, we investigate mechanisms underlying the re-modelling of pre-existing circuits during brain injury, and particularly the role played by glial cells in these settings. Ultimately, we aim at laying the groundwork for potential therapeutic approaches that promote brain plasticity and repair.

Key Publications


  1. Wani, G.A., Sprenger, H.G., Ndoci, K., Chandragiri, S., Acton, R.J., Schatton, D., Kochan, S.M.V., Sakthivelu, V., Jevtic, M., Seeger, J.M., et al. (2022). Metabolic control of adult neural stem cell self-renewal by the mitochondrial protease YME1L. Cell reports 38, 110370,  10.1016/j.celrep.2022.110370
  2. Göbel, J., Engelhardt, E., Pelzer, P., Sakthivelu, V., Jahn, H.M., Jevtic, M., Folz-Donahue, K., Kukat, C., Schauss, A., Frese, C.K., et al. (2020). Mitochondria-Endoplasmic Reticulum Contacts in Reactive Astrocytes Promote Vascular Remodeling. Cell Metab 31, 791-808 e798,  10.1016/j.cmet.2020.03.005
  3. Bergami, M., Masserdotti, G., Temprana, S.G., Motori, E., Eriksson, T.M., Gobel, J., Yang, S.M., Conzelmann, K.K., Schinder, A.F., Gotz, M., et al. (2015). A critical period for experience-dependent remodeling of adult-born neuron connectivity. Neuron 85, 710-717,  10.1016/j.neuron.2015.01.001
  4. Zuccaro, E., Bergami, M., Vignoli, B., Bony, G., Pierchala, B.A., Santi, S., Cancedda, L., and Canossa, M. (2014). Polarized expression of p75(NTR) specifies axons during development and adult neurogenesis. Cell reports 7, 138-152, 10.1016/j.celrep.2014.02.039
  5. Deshpande, A., Bergami, M., Ghanem, A., Conzelmann, K.K., Lepier, A., Gotz, M., and Berninger, B. (2013). Retrograde monosynaptic tracing reveals the temporal evolution of inputs onto new neurons in the adult dentate gyrus and olfactory bulb. Proc Natl Acad Sci U S A,  1218991110 [pii] 10.1073/pnas.1218991110