Prof. Mario Valentino

Prof. Mario Valentino

Prof. Mario Valentino



Biomedical Sciences Building
University of Malta
  +356 2340 2775
Professor in Translational Neuroscience. Dr Valentino obtained his Ph.D in 2001 through a scholarship by the Max Planck Society following collaborative work as a research guest fellow at the Max Planck Institute for Neurological Research in Cologne during 1998. His Ph.D study involved the investigation of the haemodynamic and cellular mechanisms of ischemic brain damage caused by strokes. Subsequently, he was awarded a 3-year post-doctoral fellowship in the Dept. of Neurology, Washington University, St.Louis, MO and the Hope Centre For Neurological Disorders, USA, to study the neuropathology of white matter damage in the context of ischemia and hypoglycemia using advanced imaging techniques. In Malta he established the Laboratory for the Study of Neurological Disorders that is centred around the study of mechanisms of injury and recovery after Stroke with special emphasis towards combined optical in vivo imaging techniques and electrophysiology. He is an active member of The Society of Neuroscience, International Brain Research Organization, Federation of Neuroscience Society and the New York Academy of Science. Prof. Valentino serves as ad hoc reviewer for the editorial boards of several high impact journals in the neurosciences. He has supervised several post-doctoral, doctoral and masters projects in his field, and has published extensively in high impact journals and book chapters. He serves as an abstract reviewer for the World Stroke Conference series since 2015. He also holds a role as Review and Guest Editor for Frontiers in Cellular Neuroscience and Frontiers in Cellular Neuropathology and topical advisor for Applied Biosciences and Engineering and Guest editor and reviewer for Applied Sciences. He previously served as a scientific advisor to the Foundation to fight H-ABC, a rare progressive leukodystrophy that affects children.
  • Stroke and neurovascular coupling
  • White matter injury
  • Brain injury and repair
  • Rodent models of stroke
  • Two-photon imaging of live brain
  • Neuroprotection
  • Spinal cord and traumatic brain injury
  • MDS1037 - Organisation of the Body
  • MDS2029 - Integrated Biomedical Sciences
  • MDS2033 - Nervous System 2
  • PHB2015 - Neurophysiology
  • PHB3503 - From Molecular to Translational Neuroscience
Cenciarini M, Valentino M, Belia S, Sforna L, Rosa P, Ronchetti S, D’Adamo M.C, Pessia M.
Dexamethasone in glioblastoma Multiforme therapy: Mechanisms and controversies. Frontiers
Mol. Neurosci. (2019); doi:10.3389/fnmol.2019.00065

Vesicular glutamate release from central axons contributes to myelin damage. Nature
Communications, 2018; 9 (1) DOI: 10.1038/s41467-018-03427-1

Early Loss of Blood-Brain Barrier Integrity Precedes NOX2 Elevation in the Prefrontal Cortex
of an Animal Model of Psychosis (2016). Mol.Neurobiology; DOI 10.1007/s12035-016-9791-8.

Hsp60 response in experimental and human temporal lobe epilepsy (2015). Scientific Reports
5: 9434, DOI: 10.1038/srep09434.

The central role of Aquaporins in the Pathophysiology of Ischemic Stroke (2015). Frontiers
in Cellular Neuroscience.

Cerebral White Matter Injury following a Hypoxic/Ischemic Insult during the Perinatal
Period: Pathophysiology, Prognostic Factors, and Treatment Approach (2015). Current
Pharmaceutical Design. DOI:10.2174/1381612821666150105122008.

Oligodendrocyte pathophysiology and treatment strategies in cerebral ischemia (2014).
CNSNeuroscience and Therapeutics. 20(7):603-12.

B-adrenergic receptors protect axons during energetic stress but do not influence basal
glio-axonal lactate shuttling in mouse white matter (2014). Neuroscience, 26;277:367-74.

High dose of 8-OH-DPAT decreases maximal dentate gyrus activation and facilitates granular
cell plasticity (2013). Exp Brain Res.230(4):441-51.

Dysfunction of voltage-gated K+ Channels Kv1.1 in sciatic nerve causes spontaneous and
stress- induced neuromuscular hyperexcitability (2012). Neurobiology of Disease, 47, 310-

Central axons preparing for myelination are highly sensitivity to ischemic injury due to the
transient expression of Ca2+ channels (2012). Ann. Neurology 72:936-951.