CXCR4

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

Stem cell therapy has emerged as a promising strategy for treating stroke, but it still presents several challenges, such as the optimal administration route or safety concerns. In clinical practice, endovascular delivery of cells is preferred to intracerebral injection. However, circulating stem cells must cross the blood-brain barrier (BBB) and might get trapped in peripheral organs, resulting in an insufficient number of cells reaching the lesion. To optimize their migration across the BBB, we aimed to mimic immune cells as they extravasate into the brain parenchyma following injury. For in

Individuals affected by Primary immunodeficiency disorders (PIDDs), congenital disorders that severely compromise the immune system, frequently exhibit elevated levels of emotional distress, including depression and anxiety. However, their neurological manifestations are often considered a secondary effect of the patients’ poor quality of life and the potential underlying mechanisms linking genetic alterations in PIDDs to neurological conditions have not been explored so far. We aim to investigate whether genetic alterations in PIDD patients can directly contribute to affecting brain architect