Increased BDNF levels after a trauma A pilot study on clinical and non-clinical samples, exposed or non-exposed to an earthquake

Paolo Stratta 1, Roberto L. Bonanni 1, Francesca Pacitti 2, Adriano Angelucci 2, Nicola Origlia 3, Luciano Domenici 3 4 †, Claudia Carmassi 5, Liliana Dell’Osso 5, Alessandro Rossi 4

1Department of Mental Health, ASL 1, L’Aquila, Italy; 2 Cellular Pathology Laboratory, Department of Applied Clinical Sciences and Biotechnology, University of L’Aquila, Italy; 3 Neuroscience Institute, CNR, Pisa, Italy; 4 Department of Applied Clinical Sciences and Biotechnology, University of L’Aquila, Italy; 5 Department of Clinical and Experimental Medicine, University of Pisa, Italy

DOI 10.36148/2284-0249-363


Brain-Derived Neurotrophic Factor (BDNF) modulates synaptic modifications that can constitute part of brain adaptive processes in the aftermath of trauma exposure. Thus, BDNF increase could be determined either in psychiatric patients or healthy subjects who, despite exposed to stressful events, did not develop stress-related symptoms. 


BDNF plasma levels were evaluated in a clinical and a non-clinical populations exposed to the 2009 L’Aquila earthquake and in a comparable population not exposed to such event or other trauma.


Statistically significant differences emerged according to diagnosis (clinical samples vs. controls), while a trend toward significance was found according to exposure (exposed vs. not-exposed subjects). The exposed clinical sample showed statistically significant higher BDNF levels than the not-exposed one.


Lack of statistical difference between exposed and not exposed subjects suggests that no BDNF modification intervened after the stressful event. Exposed samples however showed the highest BDNF levels with a trend toward significance. A ceiling effect that impede the possibility of exceeding a possible maximum level in the control sample can be hypothesized. Clinical sample shows instead room for stress related BDNF increase. If so, such a BDNF increase could have a neuroprotective adaptive role after stress.

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