Microglia, similar to peripheral macrophages, are the primary immune cells of the central nervous system (CNS). Microglia exist in the resting state in the healthy CNS, but can be activated and polarized into either M1 or M2 subtypes for immune defense and the maintenance of CNS homeostasis by multiple stimuli. Several long noncoding RNAs (lncRNAs) mediate human inflammatory diseases and neuropathologies by regulating their target genes. However, the function of common lncRNAs that contribute to microglial activation remains unclear. Thus, we used bioinformatic approaches to identify common lncRNAs involved in microglial activation in vitro. Our study identified several lncRNAs as common regulators of microglial activation. We identified 283 common mRNAs and 53 common lncRNAs during mouse M1 microglial activation processes, whereas 26 common mRNAs and five common lncRNAs were identified during mouse M2 microglial activation processes. A total of 648 common mRNAs and 274 common lncRNAs were identified during the activation of human M1 microglia. In addition, we identified 1,920 common co-expressed pairs in mouse M1 activation processes and 25 common co-expressed pairs in mouse M2 activation processes. Our study provides a comprehensive understanding of common lncRNA expression profiles in microglial activation processes in vitro. The list of common lncRNAs identified in this study provides novel evidence and clues regarding the molecular mechanisms underlying microglial activation.

Objectives: . Age-related hearing loss (ARHL), or presbycusis, is caused by disorders of sensory hair cells and auditory neurons. Many studies have suggested that the accumulation of mitochondrial DNA damage, the production of reactive oxygen species, noise, inflammation, and decreased antioxidant function are associated with subsequent cochlear senescence in response to aging stress. Long non-coding RNA (lncRNA) has been reported to play important roles in various diseases. However, the function of lncRNA in ARHL remains unclear. In this study, we analyzed the common expression profiles of messenger RNA (mRNA) and lncRNA through ARHL-related RNA-sequencing datasets. Methods: . We selected and downloaded three different sets of RNA-sequencing data for ARHL. We performed differential expression analysis to find common mRNA and lncRNA profiles in the cochleae of aged mice compared to young mice. Gene Ontology (GO) analysis was used for functional exploration. Real-time quantitative reverse-transcription polymerase chain reaction (qRT-PCR) was performed to validate mRNAs and lncRNAs. In addition, we performed trans target prediction analysis with differentially expressed mRNAs and lncRNAs to understand the function of these mRNAs and lncRNAs in ARHL. Results: . We identified 112 common mRNAs and 10 common lncRNAs in the cochleae of aged mice compared to young mice. GO analysis showed that the 112 upregulated mRNAs were enriched in the defense response pathway. When we performed qRT-PCR with 1 mM H2O2-treated House Ear Institute-Organ of Corti 1 (HEI-OC1) cells, the qRT-PCR results were consistent with the RNA-sequencing analysis data. lncRNA-mRNA networks were constructed using the 10 common lncRNAs and 112 common mRNAs in ARHL. Conclusion . Our study provides a comprehensive understanding of the common mRNA and lncRNA expression profiles in ARHL. Knowledge of ARHL-associated mRNAs and lncRNAs could be useful for better understanding ARHL and these mRNAs and lncRNAs might be a potential therapeutic target for preventing ARHL.

Cerebral hyperperfusion syndrome (CHS) is a rare, serious complication of carotid revascularization either after carotid endarterectomy or carotid stent placement. Although extensive effort has been devoted to reducing the incidence of CHS, little is known about the prevention. Postprocedural hypertension is very rare due to autoregulation of carotid baroreceptors but may occur if presented with autonomic dysfunction. We present two cases of CHS after cerebral revascularization that presented autonomic dysfunction.
Angioplasty ; Cerebral Revascularization ; Endarterectomy, Carotid ; Homeostasis ; Humans ; Hypertension ; Incidence ; Pressoreceptors ; Stents

Limbic-predominant age-related TDP-43 encephalopathy (LATE) is a recently established neurodegenerative disease entity. LATE neuropathological change (LATE-NC) is characterized by a TDP-43 proteinopathy that mainly involves the amygdala and medial temporal structures, with or without hippocampal sclerosis. LATE-NC is typically observed in individuals aged 80 years or older and manifests clinically as amnestic memory decline. Herein, we report a case of LATE diagnosed by brain autopsy in an 82-year-old male who had an 11-year history of memory impairment. Pathological examination revealed high Alzheimer disease neuropathological changes, as well as amygdala-predominant Lewy body pathology. In addition, immunohistochemistry for TDP-43 revealed neuronal and glial cytoplasmic inclusions in the dentate gyrus of the hippocampus, amygdala, and inferior temporal cortex. Increasing awareness of the newly defined entity LATE will enhance our understanding of the neurodegenerative processes that occur in the oldest individuals.

BACKGROUND: Herpes zoster (HZ) is caused by reactivation of latent varicella-zoster virus (VZV) infection. HZ-associated aseptic meningitis, a rare complication of HZ, can require hospitalization and a long treatment period. OBJECTIVE: A retrospective study was performed to identify potential factors associated with HZ-associated aseptic meningitis development. METHODS: We included all outpatients and patients admitted in the neurology and dermatology departments of a single tertiary center, who were diagnosed with HZ for two years. Among 818 patients, 578 patients were eligible for analysis. RESULTS: The demographics and potential risk factors were compared between the uncomplicated HZ group (n=554) and aseptic meningitis group (n=24). Among the potential factors, the dermatological distribution of skin rash and gender showed statistically significantly different between the two groups. Patients with craniocervical distribution of HZ accounted for 87.5% (n=21) of the aseptic meningitis group and 54.3% (n=301) of the uncomplicated HZ group (p=0.043). The aseptic meningitis group had more men (66.7%, n=16) than the uncomplicated HZ group (42.8%, n=237, p=0.033). Patients with craniocervical distribution had an odds ratio (OR) of 5.884 (p=0.001) for developing aseptic meningitis when compared with the other dermatome involvements. Additional logistic regression analysis resulted in a fading between gender difference (p=0.050) and craniocervical involvement having an OR of 5.667 for aseptic meningitis (p=0.006). CONCLUSION: In HZ patients, skin rash with craniocervical distribution and male gender were associated with a higher risk of aseptic meningitis.
Demography ; Dermatology ; Exanthema ; Herpes Zoster* ; Herpesvirus 3, Human ; Hospitalization ; Humans ; Logistic Models ; Male ; Meningitis ; Meningitis, Aseptic* ; Neurology ; Odds Ratio ; Outpatients ; Retrospective Studies ; Risk Factors*

BACKGROUND: Human infection with Streptococcus suis (S. suis), a zoonotic pathogen, has been reported mainly in pig-rearing and pork-consuming countries. Meningitis is the most-common clinical manifestation and is often associated with deafness and vestibular dysfunction. CASE REPORT: A 57-year-old man was referred to the hospital with headaches, fevers, chills, and hearing impairment. Meningitis was confirmed and S. suis was isolated from the cerebrospinal fluid. Spondylodiscitis occurred after 2 weeks of antibiotic treatment, and was successfully treated with a prolonged course of antibiotics for another 4 weeks. His hearing loss was irreversible despite the improvement of other symptoms. CONCLUSIONS: We report the first human case of S. suis infection in Korea. In patients presenting with meningitis, S. suis should be considered if the characteristic features of prominent and early hearing loss are present.
Anti-Bacterial Agents ; Chills ; Deafness ; Discitis ; Fever ; Headache ; Hearing Loss ; Humans ; Korea ; Meningitis ; Middle Aged ; Streptococcus ; Streptococcus suis

BACKGROUND: Recurrent seizures result in brain damage, but it is usually gradual, minimal, and difficult to observe by visual inspection of magnetic resonance images (MRIs). It is well known that hippocampal structure is vulnerable to seizure-associated brain damage. We measured the hippocampal volume in patients with epilepsy to evaluate the degree of damage to the hippocampus. METHODS: We recruited 33 patients with epilepsy and 21 healthy subjects from January 2007 to December 2008. We subclassified the patients into two groups: (1) 14 patients with intractable epilepsy and (2) 19 patients with drug-responsive epilepsy. In each group, the volumes of the left and right hippocampus were measured by manual drawing on brain MRIs. We compared the hippocampal volume in intractable epilepsy, drug-responsive epilepsy, and healthy subjects. The compounding effect of hippocampal sclerosis was ruled out by excluding eight patients with hippocampal sclerosis; we then compared the hippocampal volume in the two groups with epilepsy. RESULTS: The volume of the bilateral hippocampus on brain MRIs was smaller in patients with intractable epilepsy than in those with drug-responsive epilepsy and healthy subjects (left, p<0.004; right, p<0.03). After excluding the patients with hippocampal sclerosis by visual inspection, the hippocampal volumes were also found to be smaller in patients with intractable epilepsy than in those with drug-responsive epilepsy (left, p<0.04; right, p<0.05). CONCLUSIONS: While there is no definitive abnormality of the hippocampus on visual inspection of brain MRIs, we determined the degree of hippocampal atrophy and volume loss in patients with intractable epilepsy. Hippocampal volumetry will be helpful for the assessment of brain damage in patients with intractable epilepsy.
Atrophy ; Brain ; Epilepsy ; Hippocampus ; Humans ; Magnetic Resonance Spectroscopy ; Sclerosis ; Seizures

We report an unusual case of probable Creutzfeldt-Jakob disease (CJD) in hemodialysis patient. A woman 59 years of age with a past history of hypertension and end-stage renal disease presented with a stuporous state preceded by rapidly progressive cognitive dysfunction, myoclonus, and akinetic mutism. At first, the cause of the altered mental status was assumed to be uremic or hypertensive encephalopathy combined with fever. Proper managements, however, did not improve the neurologic symptoms. Diffusion-weighted magnetic resonance imaging revealed bilaterally asymmetric high signal intensity in both basal ganglia and cerebral cortices. Electroencephalography showed diffuse generalized theta-to-delta range slow wave and intermittent medium-to-high voltage complexes with a characteristic triphasic pattern on both hemispheres. Cerebrospinal fluid assay for the 14-3-3 protein was positive and diagnostic of CJD.
14-3-3 Proteins ; Akinetic Mutism ; Basal Ganglia ; Cerebral Cortex ; Creutzfeldt-Jakob Syndrome ; Dialysis ; Electroencephalography ; Female ; Fever ; Humans ; Hypertension ; Hypertensive Encephalopathy ; Kidney Failure, Chronic ; Magnetic Resonance Imaging ; Myoclonus ; Neurologic Manifestations ; Renal Dialysis ; Stupor

Excessive accumulation of beta-amyloid peptide (Abeta) is one of the major mechanisms responsible for neuronal death in Alzheimer's disease. Flavonoids, primarily antioxidants, are a group of polyphenolic compounds synthesized in plant cells. The present study aimed to identify flavonoid compounds that could inhibit Abeta-induced neuronal death by examining the effects of various flavonoids on the neurotoxicity of Abeta fragment 25-35 (Abeta25-35) in mouse cortical cultures. Abeta25-35 induced concentration- and exposure-time-dependent neuronal death. Neuronal death induced by 20 microM Abeta25-35 was significantly inhibited by treatment with either Trolox or ascorbic acid. Among 10 flavonoid compounds tested [apigenin, baicalein, catechin, epicatechin, epigallocatechin gallate (EGCG), kaempferol, luteolin, myricetin, quercetin, and rutin], all except apigenin showed strong 1,1-diphenyl-2-pycrylhydrazyl (DPPH) scavenging activity under cell-free conditions. The flavonoid compounds except apigenin at a concentration of 30 microM also significantly inhibited neuronal death induced by 20 microM Abeta25-35 at the end of 24 hours of exposure. Epicatechin, EGCG, luteolin, and myricetin showed more potent and persistent neuroprotective action than did the other compounds. These results demonstrated that oxidative stress was involved in Abeta-induced neuronal death, and antioxidative flavonoid compounds, especially epicatechin, EGCG, luteolin, and myricetin, could inhibit neuronal death. These findings suggest that these four compounds may be developed as neuroprotective agents against Alzheimer's disease.
Alzheimer Disease ; Animals ; Antioxidants ; Apigenin ; Ascorbic Acid ; Catechin ; Flavonoids ; Luteolin ; Mice ; Neurons ; Neuroprotective Agents ; Oxidative Stress ; Plant Cells ; Quercetin