Abstract
This study aimed to assess the neuro-regenerative properties of co-ultramicronized PEALut (Glialia®), composed of palmitoylethanolamide (PEA) and the flavonoid luteolin (Lut), in an in vivo model of traumatic brain injury (TBI) and patients affected by moderate TBI. An increase in neurogenesis was seen in the mice at 72 h and 7 d after TBI. The co-ultra PEALut treatment helped the neuronal reconstitution process to restore the basal level of both novel and mature neurons; moreover, it induced a significant upregulation of the neurotrophic factors, which ultimately led to progress in terms of memory recall during behavioral testing. Moreover, our preliminary findings in a clinical trial suggested that Glialia® treatment facilitated neural recovery on working memory. Thus, co-ultra PEALut (Glialia®) could represent a valuable therapeutic agent for intensifying the endogenous repair response in order to better treat TBI.
Highlights
Traumatic Brain Injury (TBI) is a leading cause of disability and death in young adults of industrialized countries [1,2]
The same situation was found in the CA3 area at 7 d where, following co-ultra PEALut treatment, cell differentiation significantly declined compared to the TBI group (Figure 1F, see particle Figure 1f)
Treatment with co-ultra PEALut significantly reduced the number of Beclin 1/Caspase-3 positive hippocampal neurons at 72 h after injury (Figure 4C,G), with a particular decrease observed 7 d after TBI (Figure 4F,G). These results suggest that cells overexpressing Beclin 1 may exhibit damaged DNA but not yet be directed towards neuronal death; the reduction of Beclin 1/Caspase-3 positive staining in co-ultra PEALut group may represent a reduction in autophagy and apoptosis, as a mechanism to discard neurons only partially injured to whole damaged cells, recycling cellular component and reducing brain damage
Summary
Traumatic Brain Injury (TBI) is a leading cause of disability and death in young adults of industrialized countries [1,2]. During the weeks following a trauma, the central nervous system (CNS) maintains its original capacity for regeneration, carrying out secondary compensatory mechanisms designed to help with the lesion [4]. In this context, one possible mechanism is characterized by the neurogenesis process [5,6,7,8,9], which acts in a central role in the formation of new nerve cells from neural stem cells or progenitor cells [10]. The correlation between TBI and neurogenesis processes has been extensively investigated in the last decade [11,12] This link could constitute a new key for a more complete understanding of the molecular mechanisms underlying brain damage, leading to the development of new pharmacological strategies
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