Yilong Shan

Baicalein improves behavioral dysfunction induced by Alzheimer’s disease in rats

Background Alzheimer’s disease (AD) is considered to be a neurodegenerative disorder that is characterized by increased oxidative stress. Medicinal plants, with their antioxidant properties, have been used to cure several human diseases. The aim of the current study was to explore the protective and therapeutic effect of baicalein on AD-induced rats. Materials and methods Swiss Wistar rats were used in the study. The rats were divided into five groups. Group I: normal control group treated with water; Group II: disease control treated with AlCl3 to induce the mimicking AD for 4 successive weeks (SW); Group III: normal control group treated with baicalein (5 mg/kg) for 2 SW followed by combination of baicalein and AlCl3 for 4 SW; Group IV: normal control group treated with baicalein (10 mg/kg) for 2 SW followed by combination of baicalein and AlCl3 for 4 SW; Group V: normal control group treated with rivastigmine (0.3 mg/kg) for 2 SW followed by combination of rivastigmine and AlCl3 for 4 SW. Moreover, the therapeutic groups are as follows: Group VI: AD disease control treated with AlCl3 for 4 SW and serving as the therapeutic positive group; Group VII: AD disease control + baicalein (5 mg/kg) for 12 SW; Group VIII: AD disease control + baicalein (10 mg/kg) for 12 SW; Group IX: AD disease control + rivastigmine (0.3 mg/kg) for 12 SW. Behavioral test, T-maze, and rotarod test were also performed before and after the treatment. At the end of the experimental study, all the rats were sacrificed and their brains were removed and divided into two portions. The first portion was homogenated for estimating the level of acetylcholinesterase (AchE) and acetylcholine (Ach). Another portion was used for histopathological evaluation. Results The current investigation showed that baicalein significantly reduced the duration of revolving on the rotarod, cage activity, and T-maze activity in a dose-dependent manner compared with the AD control group rats. It also altered the AchE and Ach levels in the brain homogenates. The histopathology study also provides strength to the protective effect of baicalein. Conclusion The current study showed that baicalein significantly (P<0.05) improved the biochemical and histopathological condition of AD in rats.

High salt-induced activation and expression of inflammatory cytokines in cultured astrocytes

ABSTRACT Salt (sodium chloride, NaCl) accumulation in the brain is associated with various diseases of central nervous system (CNS). Activation of astrocytes is an important manifestation of pathophysiological processes in the CNS. However, the direct impact of high salt (HS) environment on astrocytes is unclear. In the current study, we found that high salt treatment can induce activation of astrocytes both in vivo and in vitro, manifested as morphological alteration coupled with increased expression of glial fibrillary acidic protein (GFAP). Additionally, HS upregulated the expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β) and vascular endothelial growth factor (VEGF); however, its effects on transforming growth factor-β (TGF-β) expression were not evident. Furthermore, HS treatment induced increased phosphorylation of signal transducer and activator transcription 3 (STAT 3). Inhibition of Janus kinase 2 (JAK 2) by specific pharmacological antagonists, AG490, attenuated the activation of JAK2/STAT3 pathway and induction of GFAP and other pro-inflammatory factors, respectively. The results suggest that the aforementioned multiple inflammatory cytokines and mediators that may be linked to the HS induced pathogenesis of CNS via the JAK2/STAT3 signaling pathways.

Serum 25-hydroxyvitamin D3 is associated with disease status in patients with neuromyelitis optica spectrum disorders in south China

Here, we investigated the relationship between serum 25-hydroxyvitamin D3 (25[OH]D3) levels and neuromyelitis optica spectrum disorder (NMOSD). Patients with NMOSD had lower 25(OH)D3 levels than healthy people, with lower levels in patients in the acute phase than those in remission. An inverse correlation was found between 25(OH)D3 and Expanded Disability Status Scale scores of patients during attacks. Higher serum 25(OH)D3 levels were associated with greater amelioration of symptoms during corticosteroid therapy. These results indicate that decreased vitamin D may be involved in NMOSD pathogenesis, and that 25(OH)D3 serum levels may reflect the severity of NMOSD in the acute phase.

Risk Factors and Clinical Manifestations of Juxtacortical Small Lesions: A Neuroimaging Study

Background and objective White matter hyperintensities can be easily identified by brain imaging. Juxtacortical small lesion (JCSL) is a special type of white matter lesion, defined as no greater than 5 mm in diameter and adjacent to the cerebral cortex in location. We notice lately that JCSLs alone may be associated to various neurological symptoms. Here, we design the present study to determine the risk factors for JCSLs and their clinical manifestations in patients in our neurology clinic. Methods 206 participants suffered from neurological disorders and completed magnetic resonance imaging (MRI) examinations were divided into two groups: patients with JCSLs and patients without lesions on MRI. Meanwhile, 129 age- and sex-matched healthy volunteers were also recruited. Laboratory examinations and the phenotypes and distributions of the symptoms of the three groups were compared. Results The serum levels of apoB and homocysteine (HCY) were independently related to the appearance of JCSLs and HCY level was also associated with the number of JCSLs. Patients with JCSLs might present with headache, insomnia, and/or anxiety/depression, which were related with the anatomical locations of the lesions. Conclusion These data suggest that JCSLs are symptomatic and might in result fromarteriole atherosclerosis, which should raise our attention.

Wnt5a Promotes Cortical Neuron Survival by Inhibiting Cell-Cycle Activation

β-Amyloid protein (Aβ) is thought to cause neuronal loss in Alzheimer’s disease (AD). Aβ treatment promotes the re-activation of a mitotic cycle and induces rapid apoptotic death of neurons. However, the signaling pathways mediating cell-cycle activation during neuron apoptosis have not been determined. We find that Wnt5a acts as a mediator of cortical neuron survival, and Aβ42 promotes cortical neuron apoptosis by downregulating the expression of Wnt5a. Cell-cycle activation is mediated by the reduced inhibitory effect of Wnt5a in Aβ42 treated cortical neurons. Furthermore, Wnt5a signals through the non-canonical Wnt/Ca2+ pathway to suppress cyclin D1 expression and negatively regulate neuronal cell-cycle activation in a cell-autonomous manner. Together, aberrant downregulation of Wnt5a signaling is a crucial step during Aβ42 induced cortical neuron apoptosis and might contribute to AD-related neurodegeneration.

Anti-thyroid antibodies and thyroid function in anti-N-methyl-d-aspartate receptor encephalitis

a Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, No 600 Tianhe Road, Guangzhou, Guangdong 510630, China b Department of Endocrinology and Metabolism, Shantou Central Hospital, No 114 Waima Road, Shantou, Guangdong 515031, China c Department of Neurology, The Affiliated Hospital of Wei Fang Medical University, No 2428 Yuhe Road, Weifang, Shandong 261031, China d Department of Neurology, The Fifth Affiliated Hospital of Sun Yat-sen University, No 52 Meihuadong Road, Zhuhai, Guangdong 519000, China

Cerebral small vessel disease: neuroimaging markers and clinical implication

Cerebral small vessel disease (CSVD) is a broad category of cerebrovascular diseases which primarily affect the perforating arterioles, capillaries and venules with multiple distinct etiologies. In spite of distinctive pathogenesis, CSVD shares similar neuroimaging markers, including recent small subcortical infarct, lacune of presumed vascular origin, white matter hyperintensity of presumed vascular origin, perivascular space and cerebral microbleeds. The radiological features of neuroimaging markers are indicative for etiological analysis. Furthermore, in sporadic arteriosclerotic pathogenesis associated CSVD, the total CSVD burden is a significant predictor for stroke events, global cognitive impairment, psychiatric disorders and later life quality. This review aims to summarize the radiological characteristics as well as the clinical implication of CSVD markers and neuroimaging interpretation for CSVD symptomatology.

Different Mechanisms of Two Subtypes of Perforating Artery Infarct in the Middle Cerebral Artery Territory: A High-Resolution Magnetic Resonance Imaging Study

Purpose: Perforating Artery Infarcts (PAIs) can be divided into two subtypes based on their etiologies: branch Atheromatous Disease (BAD) and Lacunar Infarct (LI). Recent studies have shown that while both subtypes can be caused by large artery lesions, the different mechanisms that underlie their development are not clear. This study was designed to use High-Resolution Magnetic Resonance Imaging (HRMRI) to explore the differences that contribute to the occurrence of these two subtypes in large artery lesions in the anterior circulation. Methods: Fifty patients with an acute PAI in the anterior circulation were enrolled (32 BAD and 18 LI patients). The ipsilateral middle cerebral artery (MCA) was scanned with HRMRI to analyze the atherosclerosis plaques. Artery remodeling and plaque characteristics of MCA lesions were compared between the two subtypes. Results: The rate of MCA lesions was significantly higher in BAD and substantially lower in LI (P = 0.033). LAs for the lumen areas in Bad, they were smaller than LI (P < 0.001), Additionally, the plaque area (P = 0.001) and plaque burden (P < 0.001) were superior in the BAD group. Most BAD patients displayed non-positive remodeling, while the great majority of LI patients showed positive remodeling (P < 0.001). Conclusion: In the anterior circulation, a considerable amount of BAD and LI share similarities with atherosclerotic plaques in large arteries. BAD patients mainly showed relatively large and stable atherosclerotic plaques in large arteries, while LI patients mainly exhibited relatively small and unstable atherosclerotic plaques. Clinical Trial Registration: This clinical trial is a retrospective study and therefore does not require registration.

Characteristics of paramedian pontine arteries disease and its association with hemoglobinA1c

The association of branch atherosclerotic disease (BAD) and diabetes mellitus (DM) in the territory of posterior circulation is rarely discussed. Intracranial BAD was divided into two different types: paramedian pontine arteries (PPA) disease (PPD) and lenticulostriate arteries (LSA) disease. The goal of the study was to evaluate the clinical characteristics of PPD and its association with hemoglobinA1c (HbA1c) in China.

Two Cases of Conus Medullaris Lesions with Neuromyelitis OpticaSpectrum Disorders

Abstract Neuromyelitis optica spectrum disorders (NMOSD), an autoimmune astrocytopathic disease associated with antiaquaporin- 4 (AQP4) antibody, is characterized by inflammatory lesions in the optic nerves, spinal cord, and central parts of the brain. These symptoms, urinary and fecal incontinence about conus medullaris involvement in NMOSD, are usually not appreciated as the possible manifestation of NMOSD. Missing diagnosis at this early stage will lead to a delay in the treatment, and hence, irreversible complications. We present two cases of conus medullaris involvements with neuromyelitis optica spectrum disorders