Astrocytes are the most abundant cells in the central nervous system and play significant roles in normal brain. With cerebral infarction, astrocytes are activated as reactive astrocytes and form glial scars, which play an essential part in brain injury. According to their roles in neuroprotection after cerebral infarction, regulation of scar formation, nerve regeneration, maintenance of blood-brain barrier, promotion of angiogenesis and immune response, scholars have proposed a variety of therapeutic strategies based on targeting astrocytes. This article reviews the research progress on the changes in astrocyte signaling pathways before and after cerebral infarction and the related therapeutic strategies.
Astrocytes ; Cerebral Infarction ; physiopathology ; therapy ; Humans ; Neuroglia ; pathology ; Signal Transduction

UNLABELLED: A 14-year-old young man presented with a white oval mass on the right side of external auditory canal. PHYSICAL EXAMINATION Under ear endoscope, a size of 0.6 cm x 0.8 cm x 0.6 cm, smooth and unmovable mass was on the right side of external auditory canal. In surgery, a cystic neoplasm which is connected to neoplasm of the external auditory canal by bone defect was found in aditus of drum sinus, and local bone defect in the back wall of drum sinus. Tympanic membrane and auditory ossicle chain is complete. Postoperative pathologic findings were consistent with neuroglia choristoma. The diagnosis mainly relied on the postoperative pathological findings.
Adolescent ; Choristoma ; Ear, Middle ; pathology ; Humans ; Male ; Neuroglia

Female ; Humans ; Male ; Nervous System Neoplasms ; pathology ; Neuroglia ; pathology ; Neurons ; pathology

Multiple sclerosis (MS) is regarded as a chronic inflammatory disease that leads to demyelination and eventually to neurodegeneration. Activation of innate immune cells and other inflammatory cells in the brain and spinal cord of people with MS has been well described. However, with the innovation of technology in glial cell research, we have a deep understanding of the mechanisms of glial cells connecting inflammation and neurodegeneration in MS. In this review, we focus on the role of glial cells, including microglia, astrocytes, and oligodendrocytes, in the pathogenesis of MS. We mainly focus on the connection between glial cells and immune cells in the process of axonal damage and demyelinating neuron loss.
Humans ; Multiple Sclerosis ; Neuroglia ; Inflammation/pathology* ; Brain/pathology* ; Spinal Cord/pathology*

OBJECTIVETo study the clinical and pathologic features of gliosarcoma of cerebral hemispheres.

METHODSThe clinicopathologic features of 10 cases of gliosarcoma involving cerebral hemispheres were reviewed. Immunohistochemical study was carried out using EnVision method.

RESULTSThe mean age of the patients was 54 years and the male-to-female ratio was 6 to 4. Clinical symptoms included headache (6/10), nausea/vomiting (5/10), and sensory or motor impairment (4/10). Nine of the cases were primary gliosarcoma, with maximum diameter ranging from 2.4 to 5.5 cm (mean = 4.2 cm). The remaining case represented secondary gliosarcoma involving skull base and extracranial tissues. Histologic examination showed a biphasic pattern in all cases. Regarding the glial component, there were 9 cases of pleomorphic glioblastoma and 1 case of giant cell glioblastoma. Reticulin stain was positive in all cases. Immunohistochemical study showed that the tumor cells variably expressed GFAP (10/10), p16 (4/10), EGFR (1/10), CD68 (1/10) and p53 (6/10). The Ki-67 index ranged from 15% to 70% (mean = 34%). Six patients had follow-up data available. One patient was disease-free for 45 months and 5 patients died of the disease at 3 to 17 months after the operation (mean duration of survival = 9 months).

CONCLUSIONSGliosarcoma is a highly aggressive tumor, often locates in the deeper part cerebral hemispheres and has a relatively short duration of symptoms. It carries a poor prognosis. GFAP immunostain and reticulin stain are helpful in confirming the diagnosis. p53 and p16 are also expressed in some cases.

Adult ; Brain Neoplasms ; metabolism ; pathology ; Cerebrum ; pathology ; Female ; Glioblastoma ; metabolism ; pathology ; Gliosarcoma ; metabolism ; pathology ; Humans ; Male ; Middle Aged ; Neuroglia ; pathology

Diabetes patients tend to have the gastrointestinal motility disorder. Although the relationship between the motility disorder and both the neurons and Cajal cells in the enteric nervous system (ENS) is well established, little is known about the role of enteric glial cells (EGCs) in gastric motility in diabetes. This study aimed to examine the expression of the glial marker S100B and morphology of EGCs in gastric tissues and the relationship between activated EGCs and the damage of gastric emptying in diabetic models. The diabetic model of rat was induced with 1% streptozotocin (STZ). The model rats at 7-14 days and at 56-63 days were defined as early diabetic rats and advanced diabetic rats, respectively, and normal rats at the two time periods served as their corresponding controls. The gastric emptying rate of the rats was tested by using the phenol red solution. The ultrastructure of EGCs in the gastric antrum was observed by the transmission electron microscopy, and the expression of S100B in the myenteric plexus was immunohistochemically detected. The results showed that the gastric emptying rate was significantly increased in the early diabetic rats and decreased in the advanced diabetic rats when compared with their corresponding control rats (P<0.01 for both). The ultrastructure of EGCs was mostly normal in both the early diabetic and control groups. Vacuolization of mitochondria and expansion of endoplasmic reticulum occurred in both the advanced diabetic group and its control group, and even the structure of smooth muscle cells and intestinal neurons was destroyed in the advanced diabetic group. The expression level of S100B in the advanced diabetic group was significantly decreased compared with its control group (P<0.05). It was obviously increased in the early diabetic control group when compared with the advanced diabetic control group (P<0.05). However, there was no significant difference in the S100B expression between the early diabetic group and its control group (P>0.05). The findings suggested that the gastric motility dysfunction in diabetes may be associated with the changes of morphology and number of EGCs in the myenteric plexus.
Animals ; Diabetes Mellitus, Experimental ; pathology ; Gastrointestinal Motility ; physiology ; Male ; Neuroglia ; pathology ; Rats ; Rats, Sprague-Dawley

Chronic pain is challenging to treat due to the limited therapeutic options and adverse side-effects of therapies. Astrocytes are the most abundant glial cells in the central nervous system and play important roles in different pathological conditions, including chronic pain. Astrocytes regulate nociceptive synaptic transmission and network function via neuron-glia and glia-glia interactions to exaggerate pain signals under chronic pain conditions. It is also becoming clear that astrocytes play active roles in brain regions important for the emotional and memory-related aspects of chronic pain. Therefore, this review presents our current understanding of the roles of astrocytes in chronic pain, how they regulate nociceptive responses, and their cellular and molecular mechanisms of action.
Humans ; Astrocytes/pathology* ; Chronic Pain/pathology* ; Neuroglia/physiology* ; Neurons/physiology* ; Synaptic Transmission ; Chronic Disease

Accumulated evidence suggests that sporadic cases of Alzheimer's disease (AD) make up more than 95% of total AD patients, and diabetes has been implicated as a strong risk factor for the development of AD. Diabetes shares pathological features of AD, such as impaired insulin signaling, increased oxidative stress, increased amyloid-beta (Aβ) production, tauopathy and cerebrovascular complication. Due to shared pathologies between the two diseases, anti-diabetic drugs may be a suitable therapeutic option for AD treatment. In this article, we will discuss the well-known pathologies of AD, including Aβ plaques and tau tangles, as well as other mechanisms shared in AD and diabetes including reactive glia and the breakdown of blood brain barrier in order to evaluate the presence of any potential, indirect or direct links of pre-diabetic conditions to AD pathology. In addition, clinical evidence of high incidence of diabetic patients to the development of AD are described together with application of anti-diabetic medications to AD patients.
Alzheimer Disease ; Blood-Brain Barrier ; Encephalitis ; Humans ; Incidence ; Insulin ; Neuroglia ; Oxidative Stress ; Pathology ; Risk Factors ; Tauopathies

Mood disorder is a common psychiatric illness with a high lifetime prevalence in the general population. A serious problem such as suicide is commonly occurring in the patients with depression. Till now, the monoamine hypothesis has been the most popular theory of pathogenesis for depression. However, the more specific pathophysiology of depression and cellular molecular mechanism underlying action of commercial antidepressants have not been clearly defined. Several recent studies demonstrated that glial cells, especially astrocytes, are a promising answer to the pathophysiology of depression. In this article, current understanding of biology and molecular mechanisms of glial cells in the pathology of mood disorder and new research on the pathophysiology of depression will be discussed.
Antidepressive Agents ; Astrocytes ; Biology ; Depression ; Humans ; Mood Disorders* ; Neuroglia* ; Pathology ; Prevalence ; Suicide

Animals ; Brain Neoplasms ; genetics ; pathology ; Cell Differentiation ; Cell Transformation, Neoplastic ; genetics ; Glioma ; genetics ; pathology ; Humans ; Neoplastic Stem Cells ; pathology ; Neural Stem Cells ; pathology ; Neuroglia ; pathology ; Neurons ; pathology