Neuroinflammation involving glial cell activation and BBB dysfunction has increasingly been recognized as a key feature of neuropsychiatric disorders. In vivo imaging methods, particularly translocator protein positron emission tomography (TSPO-PET) and dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI), have advanced our understanding of glial activation and BBB...
Pediatric acute-onset neuropsychiatric syndrome (PANS) is characterized by the sudden onset of obsessive-compulsive symptoms alongside a constellation of neuropsychiatric and somatic features. Disease progression typically includes flare and recovery states, with some patients exhibiting a persistent disease course (> 12 months of flare). We characterized circulating monocyte...
Healthy aging alone can lead to cognitive decline, decreased brain size, protein aggregation, accumulation of senescent cells and neuroinflammation. Furthermore, age is the primary risk factor for several neurodegenerative disorders such as Parkinson’s and Alzheimer’s disease. Age-related neuroinflammation, as known as inflammaging, is thought to restrict brain plasticity...
Acute ischemic stroke triggers immunosuppression, yet existing therapies struggle to balance neuroprotection with poststroke immunosuppression. We demonstrated that bone marrow mesenchymal stem cells (BM-MSC) reverse stroke-induced thymic atrophy by promoting T-cell differentiation and restoring peripheral T-cell populations. Bulk RNA sequencing of BM-MSC-treated thymuses...
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder where neuromuscular health is central to disease progression. The degeneration of motor neurons (MNs) leads to muscle weakness and paralysis, underscoring the critical importance of neuromuscular junctions (NMJs) and axonal integrity. Among the genetic contributors to ALS, mutations in the C9orf72...
Cardiac arrest (CA) is a life-threatening emergency with a global one-year survival rate of 2%-10%. Brain injury significantly impacts CA outcomes, and neuroinflammation is a key mediator of cerebral damage. Interleukin-17 (IL-17) has been implicated in multiple inflammatory disorders, yet its contribution to CA-induced cerebral damage remains undefined. To elucidate the role of...
Emerging evidence underscores the critical role of neuroinflammation and metabolism in the pathophysiology of epilepsy. Metabolic dysregulation and neuroinflammation exacerbate each other, creating a vicious cycle. Although this interplay offers novel insights into the mechanisms underlying neurological disorders and potential therapeutic approaches, its role in epilepsy remains...
Profilin 1 (Pfn1) expression decreases significantly in aged human microglia, suggesting that loss of cytoskeletal integrity may trigger microglial senescence and increased synaptic vulnerability. To test this hypothesis, we used an inducible, microglia-specific Pfn1 knockout in adult mice, a strategy designed to isolate the direct effects of acute Pfn1 loss at the cellular and...
As primary immune sentinels of the central nervous system (CNS), microglia respond rapidly to acute brain injury and engage in dynamic crosstalk with infiltrating peripheral immune cells. This interplay critically shapes the neuroinflammatory microenvironment—a key determinant of secondary brain injury (SBI) following intracerebral hemorrhage (ICH). Fatty acid-binding protein 4...
Traumatic brain injury (TBI) presents a major clinical burden, often resulting in both acute neurological impairment and pulmonary dysfunction, underscoring the complex and poorly understood brain–lung axis. Although dual-organ injury is well-documented, the mechanistic basis linking brain trauma to peripheral organ damage has remained elusive. In this study, we integrate...
Ischemic stroke is a leading cause of mortality and disability worldwide, yet its pathophysiological mechanisms remain poorly understood. In this study, we analyzed the coagulation function in 60 patients with acute ischemic stroke and found that their blood was in a hypercoagulable state. We confirmed this hematological change using a middle cerebral artery occlusion/reperfusion...
Neurotropic viruses, such as Japanese encephalitis virus (JEV), trigger central nervous system (CNS) inflammation primarily through disruption of the blood–brain barrier (BBB) and infiltration of peripheral immune cells. Although the gut microbiota is known to regulate diverse immunopathological processes, its contribution to CNS neuroinflammation and systemic immune responses...
Parkinson’s disease (PD) is a multisystem disorder frequently comorbid with non-motor symptoms like depressive disorder (DD) and gastrointestinal (GI) dysfunction. Chronic neuroinflammation and disruption of the gut-brain axis are implicated as shared pathological drivers, but the precise molecular mechanisms connecting these conditions remain elusive. We hypothesized that a...
Subarachnoid hemorrhage (SAH) is a critical cerebrovascular disease with high mortality and morbidity. Despite advances in treatments that have reduced mortality, survivors frequently suffer from persistent cognitive dysfunction. Border-associated macrophages (BAMs) play essential nutritional and immunoregulatory roles in neurological diseases; however, their dynamic alterations...
Postoperative neurocognitive impairment (PNCI) significantly affects the recovery and long-term outcomes of elderly patients, with central nervous system (CNS) inflammation serving as the key pathogenic driver of its development. As the resident immune cells of the CNS, microglia play a crucial role in regulating perioperative inflammation and maintaining homeostasis. However...
Ischemic stroke triggers excessive microglial activation and sustained neuroinflammation, driving secondary neuronal injury. Recent evidence suggests that dysfunction of the autophagy-lysosome system may be a crucial factor sustaining microglial pro-inflammatory responses, yet the underlying regulatory mechanisms remain unclear. NOD-like receptor family caspase recruitment domain...
SARS-CoV-2 infection is associated with long-lasting neuropsychiatric and cognitive symptoms, collectively referred to as neuro-PASC. Emerging studies indicates that accelerate brain aging and cellular senescence in COVID brain could lead to altered neuroimmune responses and neurodegenerative outcomes. However, little is known about how cellular senescence is development in neuro...
Aberrant and sustained activation of microglia is implicated in the progression and severity of multiple sclerosis (MS). However, whether intrinsic alterations in microglial function impact the pathogenesis of this disease remains unclear. We conducted transcriptomic and functional analyses of microglia-like cells (iMGLs) differentiated from induced pluripotent stem cells (iPSCs...
Diabetes mellitus (DM) could exacerbate experimental autoimmune myasthenia gravis (EAMG) by affecting both the innate and adaptive immune systems, although the specific mechanism remains unclear. GPR183, a G protein-coupled receptor predominantly expressed on immune cells, contributes to autoimmune disease development by directing immune cell migration to secondary lymphoid...
Neuronal intranuclear inclusion disease (NIID) is a group of neurodegenerative diseases caused by GGC repeat expansion and is characterized by diverse clinical manifestations that may characterize a spectrum of underlying pathologies. Extensive inflammatory cell infiltration has been observed in multiple tissues obtained from NIID patients, including the temporal lobe, skin...
The colony-stimulating factor 1 receptor (CSF1R) is a receptor tyrosine kinase essential for microglial development and homeostasis. While dysregulated CSF1R signaling has been implicated in Alzheimer’s disease (AD), the biological function of its soluble ectodomain (sCSF1R)—generated by a disintegrin and metalloproteinase 17 (ADAM17)-mediated cleavage—remains poorly understood...
T helper 17 (Th17) cells are a heterogeneous subset of CD4⁺ T cells that mediate host defense and drive autoimmune pathology. While phosphorylation of STAT3 at tyrosine 705 (Y705) is essential for Th17 differentiation, the functional role of serine 727 (S727) phosphorylation remains unresolved. Here, we show that STAT3 S727 phosphorylation is selectively required for the...
The delayed inflammatory response induced by stroke can cause secondary injury to peri-infarct tissue. Microglia and other immune cells that mediate this injury require increased glycolytic flux for pro-inflammatory activation. These cells, unlike neurons, astrocytes, and most other cell types, utilize hexokinase-2 (HK2) rather than hexokinase-1 for glycolysis. Accordingly, HK2...
Airway hyperresponsiveness (AHR) is often associated with mood disorders such as anxiety and depression which makes the airway symptoms more complicated and refractory. However, the underlying mechanisms remain unclear. This study investigated whether this was related to the activation of microglia in the hippocampus. Female Balb/c mice were randomly assigned into an AHR model...