![]() Resident microglia are central players in this process because of their active role in immune surveillance. The PRRs comprise a family of membrane-bound toll-like receptors (TLRs), C-type lectin receptors (CLRs), cytoplasmic receptors, RIG-like receptors (RLRs), and NOD-like receptors expressed mainly on resident microglia ( Dokalis and Prinz, 2019). DAMPs bind on pattern recognition receptors (PRRs), leading to cellular activation, that triggers inflammatory response. The inflammatory processes may be initiated by the endogenous host-derived cell debris originated from acute cell death or that accumulate with age due to increased production or impaired elimination ( Sochocka et al., 2017). Here, we provide a general overview of the process. There are several possible mechanisms of inflaming. Inflammation can be transient and self-limited, facilitating tissue repair or persistent and dysregulated, leading to a chronic inflammatory state, resulting in tissue degeneration ( Tansey et al., 2007). Neuroinflammation will vary in type and range depending on the context, duration, and course of the primary insult. Neuroinflammation is a common feature in many neurological diseases such as brain trauma, stroke, multiple sclerosis (MS), Alzheimer’s disease (AD), and Parkinson’s disease (PD) ( Stephenson et al., 2018). The definition of neuroinflammation is an inflammatory process within the brain or spinal cord ( DiSabato et al., 2016 Wang Y. Inflammation is a complex biological process in the body in response to cell and tissue damage ( Chen et al., 2017). Cellular and Molecular Responses to Brain Injuries Inflammatory Response Brain injuries reduce the quality of life of the injured person and their families, besides its high cost to healthcare systems ( Humphreys et al., 2013). The outcome of brain injuries is cell death, with high chances of functional and cognitive limitations, such as movement deficits, mood disorders, headaches, disturbances of memory, emotion, and behavior, and increased risk of development of neurodegenerative diseases ( Riggio, 2011 Sulhan et al., 2020). In 2016, neurological disorders were the world’s leading cause of disability-adjusted life-years, defined as the sum of years of life lost and years lived with disability, afflicting 276 million people and the second leading death cause, killing 90 million people ( GBD 2016 Neurology Collaborators, 2019). Injuries are divided into two types: (i) traumatic brain injury (TBI), caused by an external force to the head, such as a bump, blow, or penetrating object, and (ii) injury associated with a neurologic illness or condition, such as stroke, brain cancer, and other neurogenerative diseases ( Stephenson et al., 2018 Cabrera, 2021). Moreover, this review also draws attention to emerging possibilities and prospects in this field.īrain injuries are a significant cause of mortality and morbidity across the world. The purpose of this review is to highlight the existing research in the growing field of bioscaffolds’ development and neural tissue engineering. The challenge in neural tissue engineering remains in the fabrication of scaffolds with precisely controlled topography and biochemical cues capable of directing and controlling neuronal cell fate. More recently, researchers were able to engineer brain organoids, neural networks, and even 3D printed neural tissue. The use of these external bioscaffolds and the creation of cell platforms provide the basis for tissue engineering. ![]() Bioscaffolds can assume different shapes and may or may not carry a diversity of content, such as stem cells, growth factors, exosomes, and si/miRNA that promote specific therapeutic effects and stimulate brain repair. A variety of natural and synthetic materials is available and have been used to replace damaged tissue. ![]() In the past decade, we witnessed the rise of studies regarding bioscaffolds’ use as support for neuro repair. After brain injury, the hostile microenvironment and the lack of structural support for neural cell repopulation, anchoring, and synapse formation reduce successful repair chances. Repairing the human brain remains a challenge, despite the advances in the knowledge of inflammatory response to injuries and the discovery of adult neurogenesis.
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