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Traumatic brain injury (TBI) is a serious cause of disability and death among young and adult individuals, displaying complex pathophysiology including cellular and molecular mechanisms that are not fully elucidated. Many experimental and clinical studies investigated the potential relationship between TBI and the process by which neurons are formed in the brain, known as neurogenesis. Currently, there are no available treatments for TBI's long-term consequences being the search for novel therapeutic targets, a goal of highest scientific and clinical priority. Some studies evaluated the benefits of treatments aimed at improving neurogenesis in TBI. In this scenario, herein, we reviewed current pre-clinical studies that evaluated different approaches to improving neurogenesis after TBI while achieving better cognitive outcomes, which may consist in interesting approaches for future treatments., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Traumatic Brain Injury (TBI) is a major public health problem. It is the leading cause of death and disability, especially among children and young adults. The neurobiology basis underlying TBI pathophysiology remains to be fully revealed. Over the past years, emerging evidence has supported the hypothesis that TBI is an inflammatory based condition, paving the way for the development of potential therapeutic targets. There is no treatment capable to prevent or minimize TBIassociated outcomes. Therefore, the search for effective therapies is a priority goal. In this context, animal models have become valuable tools to study molecular and cellular mechanisms involved in TBI pathogenesis as well as novel treatments. Herein, we discuss therapeutic strategies to treat TBI focused on immunomodulatory and/or anti-inflammatory approaches in the pre-clinical setting., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: The Renin-Angiotensin System (RAS) is a key regulator of cardiovascular and renal homeostasis, but also plays important roles in mediating physiological functions in the central nervous system (CNS). The effects of the RAS were classically described as mediated by angiotensin (Ang) II via angiotensin type 1 (AT1) receptors. However, another arm of the RAS formed by the angiotensin converting enzyme 2 (ACE2), Ang-(1-7) and the Mas receptor has been a matter of investigation due to its important physiological roles, usually counterbalancing the classical effects exerted by Ang II., Objective: We aim to provide an overview of effects elicited by the RAS, especially Ang-(1-7), in the brain. We also aim to discuss the therapeutic potential for neuropsychiatric disorders for the modulation of RAS., Method: We carried out an extensive literature search in PubMed central., Results: Within the brain, Ang-(1-7) contributes to the regulation of blood pressure by acting at regions that control cardiovascular functions. In contrast with Ang II, Ang-(1-7) improves baroreflex sensitivity and plays an inhibitory role in hypothalamic noradrenergic neurotransmission. Ang-(1-7) not only exerts effects related to blood pressure regulation, but also acts as a neuroprotective component of the RAS, for instance, by reducing cerebral infarct size, inflammation, oxidative stress and neuronal apoptosis., Conclusion: Pre-clinical evidence supports a relevant role for ACE2/Ang-(1-7)/Mas receptor axis in several neuropsychiatric conditions, including stress-related and mood disorders, cerebrovascular ischemic and hemorrhagic lesions and neurodegenerative diseases. However, very few data are available regarding the ACE2/Ang-(1-7)/Mas receptor axis in human CNS., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.)