Browse protocols, FAQs, guidelines, and technical articles tagged “neuroinflammation”, newest first. For research use only.
In amyotrophic lateral sclerosis, abnormally accumulated TDP-43 can damage mitochondria and promote the release of mitochondrial DNA into the cytoplasm. After recognizing this abnormal DNA, cGAS generates 2′,3′-cGAMP and activates STING, subsequently initiating TBK1–IRF3 and NF-κB ...
Microglia-containing human brain organoids (MC-HBOs) integrate neural cells, glial cells, and resident immune cells of the central nervous system within a three-dimensional culture system and can be used to analyze the roles of microglia in brain development, neuroinflammation, and ...
Alzheimer’s disease is jointly driven by Aβ deposition, Tau abnormalities, neuroinflammation, disrupted lipid metabolism, and synaptic injury. Defining the core targets at different pathological stages provides the basis for disease stratification, therapeutic monitoring, and the design of ...
Kallikrein-related peptidases regulate the skin barrier, neural plasticity, vascular homeostasis, and reproductive function through limited proteolysis. Dysregulated KLK expression, activation, or inhibition can remodel the extracellular matrix and receptor signaling and contribute to tumors, ...
The peripheral nervous system (PNS) participates in local immune regulation through sensory nerves, autonomic nerves, Schwann cells, and satellite glial cells. Immune cells and the cytokines, chemokines, and inflammatory mediators they release can also reciprocally affect neuronal excitability, ...
Neuroinflammation is an inflammatory response formed in the nervous system under conditions such as infection, injury, metabolic stress, abnormal protein deposition, or immune imbalance. Its core lies in the dynamic imbalance among microglia, astrocytes, peripheral immune cells, the blood-brain ...
In Alzheimer’s disease models, cholinergic detection should not focus only on measuring acetylcholine or acetylcholinesterase separately. The key is to assess the relationship among neurotransmitter levels, enzyme activity changes, cholinergic neuronal injury, and inflammatory responses. When ...
Cerebral infarction is focal ischemic injury of brain tissue caused by interruption or marked reduction of cerebral blood flow. Its core pathological process is not a single vascular occlusion event, but an ischemic cascade initiated after insufficient blood perfusion.
Neurosteroids are not merely steroid molecules delivered into brain tissue from the peripheral endocrine system, but rather a class of active steroids that can be synthesized locally within the central nervous system, further converted, and act on neurons, astrocytes, oligodendrocytes, and ...
The kinin system is a major molecular network linking tissue injury, inflammatory responses, vascular reactivity, and regulation of neural excitability. Through coordinated control of kinin generation, receptor stratification, ion-channel sensitization, and amplification of neuroinflammation, ...
Topics that share resources with this page.