Traumatic Brain Injury

…The project asks how repetitive mild traumatic brain injury leads to long-term memory decline, focusing on lasting inflammatory and neurogenic changes in the human hippocampus involving microglia, astrocytes and immature neurons. The candidate runs single-nucleus RNA sequencing pipelines on postmorte

This Medical Research Future Fund call supports research on traumatic brain injury outcomes and economic burden. Stream 1 funds a prospective longitudinal study and national registry covering injuries of all severities, including repeated concussion and injuries associated with violence or military service. Stream 2 addresses the economic impact of moderate to severe traumatic brain injury in Australia. The intended outputs inform continuing care and quantify national costs. Stream 1 projects run for up to five years and Stream 2 projects for up to two years. Mandatory minimum data are due at

Brain metabolism supplies the energy underlying brain injury, recovery and aging. This webinar brings together three complementary approaches to understanding how repetitive mild traumatic brain injury affects these processes. Sakthivel Ravi examines repetitive mild TBI and aging through multimodal imaging and molecular profiling. Adam Khalifa presents wireless brain glucose sensing for TBI research, and Joe Abisambra discusses disruption of bioenergetic pathways following repetitive mild TBI. The talks are followed by a moderated question-and-answer discussion.

Neuroscience is experiencing unprecedented growth in dataset size both within individual brains and across populations. Large-scale, multimodal datasets are transforming our understanding of brain structure and function, creating opportunities to address previously unexplored questions. However, managing this increasing data volume requires new training and technology approaches. Modern data technologies are reshaping neuroscience by enabling researchers to tackle complex questions within a Ph.D. or postdoctoral timeframe. I will discuss cloud-based platforms such as brainlife.io, that provide

Traumatic brain injury causes axon tearing and synapse degeneration resulting in multiple neurological dysfunctions and early neurodegenerations; the repair of axonal and synapse structures is critical in maintaining neuronal function. C-C Motif Chemokine Ligand 5 (CCL5) shows neuroprotective function by promoting neurite outgrowth and synaptogenesis. This study used a weight-drop model to induce mild brain trauma in both C57BL/6 (wildtype, WT) and CCL5 knockout (CCL5-KO) mice. The recovery of motor and sensory neurological functions, and synapse structure and proteins were impaired in CCL5-KO

Tauopathy is a hallmark of a broad category of neurodegenerative conditions and Traumatic Brain Injury (TBI). Progression of tau pathology may lead to impaired cognitive conditions leading to dementia. However, previous studies have reported cognitively healthy patients with cortical tau pathologies. The mechanism for this cognitive protection in a tauopathy environment is being investigated by various groups. Astrocytes are essential for physiological homeostasis of brain and reactive astrogliosis is an associated pathology in neuroinflammation associated with TBI. The correlation between lev

A traumatic brain injury (TBI) is a severe form of neurotrauma resulting from the disruption of normal brain function due to external forces such as direct impact, rapid acceleration/deceleration or a penetrating object. TBIs have been attributed to long-term deficits including physical and cognitive changes, sensory effects, and social-emotional alterations. Current therapeutic options are limited to handling the acute trauma; however, drugs preventing nerve damage and promoting healing are not available. In recent years, the therapeutic use of bioactive peptides (small chains of amino acids,

Traumatic brain injury (TBI) can cause life-changing neurological deficits. There are currently no neuroprotective treatments in TBI. The high content of oxidation-sensitive polyunsaturated fatty acids (PUFAs) in the brain generates an environment vulnerable to TBI-related oxidative damage. We hypothesised that partial replacement of tissue PUFAs with deuterium - enriched PUFAs (D-PUFAs), could act as a brake against oxidation and improve outcome.A moderately severe TBI was induced using a controlled cortical impact (CCI) in adult male and female CD1 mice. Animals received a control or a D-PUF

Traumatic brain injury (TBI) is one of the leading causes for death or disability involving an initial mechanical damage that leads to the destruction of the brain matter and adjacent vasculature, producing a lesion cavity. The treatment options are limited to stabilizing the patients and treating secondary symptoms. Those secondary injuries appear in a time-shifted manner and include axonal injury leading to neuronal death, a process not fully understood yet. For several central nervous system (CNS) injury models including spinal cord injury, it was already shown that the growth factor-activa

Traumatic brain injury (TBI) remains the leading cause of death and disability worldwide with no existing effective treatment. The early phase after TBI induction triggers numerous molecular cascades to regulate adaptive processes and cortical network activity. Kinases play a particularly prominent role in modifying peptide substrates, which include ion channels, receptors, transcription factors and inflammatory mediators. This project aimed to better understand the post-injury serine/threonine kinome; 1) Which kinases conduct phosphorylation-induced alterations of target peptides following un

Numerous studies have shown the involvement of Traumatic Brain Injury (TBI) in increasing the risk of developing dementia and Alzheimer’s Disease (AD) with age, yet the intricate details of how TBI could increase the risk of such afflictions remain obscure. The scarcity of research in this area can be attributed partially to the lack of suitable animal models that can carry humanized versions of the genes known to pose a risk for developing AD. We used two cohorts of 6 months old mice, each consisting of 10 animals (5 males), carrying humanized versions of Amyloid Precursor Protein (APP), Tau

Traumatic Brain Injury (TBI) is known to impair motor coordination and affect cognitive functions. Parvalbumin-positive interneurons (PV-INs) are one subpopulation of GABAergic cells, which can balance their inhibitory output on connected pyramidal neurons, thereby influencing cortical network excitability. Here we investigated TBI-induced, morphological and functional changes of PV-Basket Cells (PV-BCs) in the ipsilateral hemisphere of somatosensory cortex and the underlying mechanisms. We used our established TBI model and performed immunohistochemistry, fluorescence in situ hybridization an

Due to the complexity of the events in the tissue after the traumatic brain injury, adequate therapeutic protocols still need to be improved. A growing number of data suggests that hyperbaric oxygenation (HBO) can influence the activity of adult neural stem cells (NSCs). The aim of this study was to investigate the effects of sensorimotor cortex ablation (SCA) and HBO on processes of neurogenesis in the subventricular zone (SVZ), rostral migratory stream (RMS) and around the lesion site. The experiments were performed on adult male Wistar rats, ten weeks old. Animals were randomized into two g

Traumatic brain injury (TBI) is a major cause of mortality and morbidity, including long-lasting cognitive impairment – linked to disrupted brain connectivity. Phospholipids (PL) are key components of cellular membranes, also essential for synaptic structural integrity. It has been shown that the multi-nutrient combination Souvenaid® which contains PL precursors, improves neurological outcomes in experimental TBI. We hypothesised that this intervention could support brain recovery, and we tested the feasibility of providing this multi-nutrient to TBI patients.In a randomised, placebo-controlle

…reporters, offer a precious window on brain functions and on its mechanisms of development, ageing or disease progression. Nonetheless, the existing methods are still shortsighted with respect to the complex biomolecular alterations that accompany these physiological and pathological dynamics. As a result, our grasp of the multifaceted components of brain activity is still partial. To mitigate this limitation, we propose a fiber photometry method based on spontaneous Raman scattering – which we call vibration

…observed in microglia following traumatic brain injury. NOX activation requires metabolic support, especially within the pentose-phosphate-pathway (PPP), to fulfil the heightened NADPH demand. Our objective was to identify key metabolic changes associated with NOX activation during pro-inflammatory stimulation in microglia. Using an immortalized microglia (IMG) cell line and PPP inhibitor, 6-aminonicotinamide (6-AN), we stimulated IMGs with LPS (100 ng/mL) and/or 6-AN for 24 hou

Traumatic brain injury (TBI) involves an acute injury (primary damage), which may evolve in the hours to days after impact (secondary damage). Cortical spreading depolarization (CSD) is a metabolically demanding processes that may worsen the secondary brain injury. Metabolic stress has been associated with mitochondrial dysfunction, including impaired calcium homeostasis and elevated ROS production. However, the association between mitochondrial impairment and vascular function after TBI is poorly understood. We therefore aimed to 1) Identify the role of CSD on neurological outcome after TBI,

…Grn-deficient mice after experimental traumatic brain injury (TBI). However, the relative contribution of neuronal or microglial PGRN in neuroprotective and anti-inflammatory effects is still elusive. Here, we tested the hypothesis that transgeni

Acquired brain injuries (ABIs), such as stroke and traumatic brain injury (TBI), represent global health challenges, stroke ranking as the third leading combined cause of death and disability, and TBI contributing to over 7 million disability-adjusted life years. Functional recovery in ABIs is influenced by age, older individuals showing poorer recovery. Axonal plasticity, a form of structural neuroplasticity, holds promise for understanding and promoting recovery. Injuries were carried out in 14-month-old male Wistar rats. Focal stroke was induced by unilateral intracerebral administration of

…adaptability of the mammalian brain. It remains elusive whether a traumatic brain injury (TBI) in a sensory cortex results in similar functional reorganization in spared sensory networks. We herein investigated global alterations in neuronal activity maps in the mouse brain subjected to a TBI in the visual cortex and delved into the underlying cellular mechanisms. Our data shows substantial differences in brain activity maps 2-3

Traumatic brain injury (TBI) is a cause of disability and a risk factor for the development of epilepsy, partially mediated by reactive gliosis. The aim of this project was to observe astroglial and microglial reactions to brain injury and identify sex differences in the process of glial scar formation.Penetrating cortical brain injury was induced on postnatal day 30 (P30) in male and female rats. The animals were perfused on P32, P38, P46, or P60. Brain tissue was sectioned and stained against glial fibrillary acidic protein (GFAP, astrocyte marker) and ionized calcium-binding adapter molecul

Traumatic brain injury (TBI) is an acute brain lesion representing one of the main causes of mortality and disability worldwide. Searching for therapeutic strategies that shrink the inflammatory response after TBI is key to prevent and/or ameliorate secondary brain injury and to improve patients outcome. After TBI, there is a fast activation of innate immunity, where microglia responds to damage-associated molecular patterns such as ATP by P2X7 purinergic receptors. The P2X7-NLRP3 inflammasome axis has been identified as one of the main actors in neuroinflammation. Thus, the aim of this study

…The brain is one of the most affected organs, making aging a key player in the development of neurodegenerative diseases, including Alzheimer's (AD) and Parkinson's disease (PD), the most prevalent ones.Understanding the processes occurring during aging may open up possibilities for new strategies to maintain good health throughout lifespan. Our research group has been working for years on the study of galectin

Aims: Post-injury physical exercise can reduce memory deficits associated to traumatic brain injury (TBI) in late adolescent and young adult rats, but both the effectiveness of this treatment and possible sex-dependent effects in late middle-aged injured rats are important issues still unsolved. The aim of the present work was to examine whether chronic object recognition memory (ORM) deficits associated to TBI can be alleviated by post-injury physical exercise in males and females late middle-aged rats. Methods: 14 months-old rats were submitted to a controlled cortical impact injury model of