Traumatic Brain Injury and Neurovascular Disturbances

This study uses in vivo imaging to track microvascular recovery and remodeling after cortical injury, showing dynamic vascular growth and functional recovery over time.

This study shows that DORA-22 treatment reduces posttraumatic seizures and restores sleep homeostasis after traumatic brain injury.

This paper develops a cold-protective treatment for traumatic optic neuropathy using a clinically relevant animal model, showing that combined hypothermia and cold protection reduces inflammation and metabolic stress without cellular damage.

This study shows that FHM1 mutations in CaV2.1 channels worsen outcomes after TBI by increasing CSDs, seizures, and brain edema in mice.

This study investigates the long-term cognitive and cerebrovascular effects of mild traumatic brain injury in rats, finding chronic cognitive dysfunction and altered vascular reactivity.

This study examines transcriptional changes in rat hippocampus after traumatic brain injury, identifying time-dependent gene expression patterns and epigenetic modifications.

This study identifies PD-L1-expressing astrocytes as regulators of neuroinflammation in TBI, showing their role in limiting excessive immune responses and improving outcomes.

This study shows that C1q mediates chronic neuron loss and inflammation after brain injury by targeting the corticothalamic circuit in mice.

The paper shows that brain edema from ischemic stroke impairs glutamate clearance, leading to widespread depolarization foci and neuronal death, suggesting osmotherapy could be beneficial.

This study identifies glial AP1 as a dual-factor promoting early TBI recovery but driving chronic tauopathy, with similar activation observed in aging brains.

This study examines the combined effects of mild traumatic brain injury and hemorrhagic shock in rats, showing increased neurological deficits and mortality, and introduces PET imaging with 18F-fluorodeoxyglucaric acid as a non-invasive injury marker.

This study shows that genetic inactivation of SARM1 reduces axonal damage and improves functional outcomes after traumatic brain injury.

The paper introduces an Axon-on-a-Chip model to mimic diffuse axonal injury and study its cellular responses under mechanical stress.

This study investigates visual impairment and neurodegeneration in adolescent mice after head trauma, showing retinal ganglion cell injury, axonal degeneration, and elevated ER stress markers.

This study shows that TLR4-pathway activation in astrocytes after TBI leads to synaptic loss and BBB damage, which can be mitigated by TLR4 inhibition.

This study shows that acute treatment with TrkB agonist LM22A-4 after pediatric TBI reduces tissue damage and preserves myelin integrity, with some behavioral improvements.

This study investigates how skull anatomy influences brain injury patterns in rodents, showing that temporal ridge thickening focuses mechanical forces and causes specific neuropathology.

This study investigates the role of meningeal lymphatic vessels in modulating the neuro-immune response after traumatic brain injury in mice, finding reduced CD4+ T cell infiltration in their absence.

This study examines sleep-wake patterns and epileptiform activity in a mouse model of severe traumatic brain injury (TBI) to determine if sleep features predict post-traumatic epilepsy (PTE).

This study compares non-suture and suture duraplasty in decompressive craniectomy for TBI, finding shorter operative time and less blood loss with non-suture duraplasty, but similar complication rates and outcomes.

This study monitors intracranial pressure in ESRD patients before and after hemodialysis using noninvasive waveform analysis, finding significant pre-to-postdialysis improvements in pressure parameters.

This study shows that traumatic brain injury causes severe and prolonged meningeal lymphatic dysfunction, leading to increased neuroinflammation and cognitive deficits.

This study evaluates the effect of transient IL-4 expression from engineered MSCs on M2-like macrophage enrichment after TBI, finding no improvement in functional or histological outcomes.

This study shows Drebrin is essential for astrocyte scar formation after brain injury by regulating actin dynamics and RAB8 membrane trafficking.

The paper develops a mathematical model to simulate intracranial pressure and provides a unified interpretation of several disease entities related to cerebrospinal fluid.

This study investigates how aging affects astrocyte responses to traumatic brain injury in mice, finding age-related impairments in homeostatic functions and altered reactive astrogliosis.

This study shows that removing microglia with a CSF1R inhibitor after TBI reduces neurodegeneration and improves neurological outcomes.

This study identifies CtBP1 and CtBP2 as drivers of inflammation in TBI and shows their inhibition reduces neuroinflammation and improves neurological outcomes in mice.

This study investigates how WNT3A expression is regulated during neuronal regeneration after traumatic brain injury by analyzing epigenetic changes in enhancers.