Ceccatelli Laboratory

Our research focuses on the mechanisms of neurodevelopmental damage that trigger alterations in cell differentiation and behavioral impairment later in life.

Research focus

Epidemiological and experimental data link alterations in the programming during critical periods of nervous system development to adverse consequences that increase the propensity for pathological conditions in adults. Neurotoxicology studies have shown that chemical contaminants are among the factors that have detrimental effects on neurodevelopment.

Our research focuses on the mechanisms of neurodevelopmental damage that trigger alterations in cell differentiation and behavioral impairment later in life.

Currently our studies focus on the developmental alterations caused by excess glucocorticoids (GC) or by oxidative stress-inducers, including chemical contaminants at levels relevant for human exposure. By using in vivo (rodents and zebrafish) as well as in vitro (rodent and human neural progenitor cells) models, and methods ranging from behavioral to single-cell analysis, we aim to:

  • Clarify the mechanisms behind the long-term alterations in affective behavior, i.e. depression, induced by developmental exposure to high levels of GC;
  • Investigate specific circadian rhythms alterations that precede the onset of depression;
  • Identify the molecular cascade that lead to alterations in neural progenitor cell survival and differentiation potential;
  • Identify potential preventive and therapeutic strategies.

Group members

Group picture of the Ceccatelli group

Former group members

  • Mirko Conti PhD 2017
  • Raj Bose PhD 2014
  • Wan Ibrahim PhD 2012
  • Sandra Luecke PhD 2010
  • Roshan Tofighi PhD 2007
  • Christoffer Tamm PhD 2007
  • Nesar Akanda PhD 2006)
  • Ming Chen PhD 2005
  • Ping Huang PhD 2003
  • Elisabetta Daré PhD 2002
  • Eva Ahlbom PhD 2000

Selected publications

Desipramine restores the alterations in circadian entrainment induced by prenatal exposure to glucocorticoids.
Spulber S, Conti M, Elberling F, Raciti M, Borroto-Escuela DO, Fuxe K, Ceccatelli S
Transl Psychiatry 2019 10;9(1):263

NRXN1 Deletion and Exposure to Methylmercury Increase Astrocyte Differentiation by Different Notch-Dependent Transcriptional Mechanisms.
Raciti M, Salma J, Spulber S, Gaudenzi G, Khalajzeyqami Z, Conti M, Anderlid BM, Falk A, Hermanson O, Ceccatelli S
Front Genet 2019 ;10():593

Methylmercury interferes with glucocorticoid receptor: Potential role in the mediation of developmental neurotoxicity.
Spulber S, Raciti M, Dulko-Smith B, Lupu D, Rüegg J, Nam K, Ceccatelli S
Toxicol Appl Pharmacol 2018 09;354():94-100

Glucocorticoids alter neuronal differentiation of human neuroepithelial-like cells by inducing long-lasting changes in the reactive oxygen species balance.
Raciti M, Ong J, Weis L, Edoff K, Battagli C, Falk A, et al
Neuropharmacology 2016 08;107():422-431

Alterations in circadian entrainment precede the onset of depression-like behavior that does not respond to fluoxetine.
Spulber S, Conti M, DuPont C, Raciti M, Bose R, Onishchenko N, et al
Transl Psychiatry 2015 Jul;5():e603

Tet3 mediates stable glucocorticoid-induced alterations in DNA methylation and Dnmt3a/Dkk1 expression in neural progenitors.
Bose R, Spulber S, Kilian P, Heldring N, Lönnerberg P, Johnsson A, et al
Cell Death Dis 2015 Jun;6():e1793


Publications 2012-2007


Publications 2006-2000


Sandra Ceccatelli

C4 Neurovetenskap