Subjects -> MEDICAL SCIENCES (Total: 8196 journals)
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ENDOCRINOLOGY (149 journals)                     

Showing 1 - 134 of 134 Journals sorted alphabetically
AACE Clinical Case Reports     Hybrid Journal   (Followers: 5)
Acta Diabetologica     Hybrid Journal   (Followers: 17)
Adipositas - Ursachen, Folgeerkrankungen, Therapie     Hybrid Journal   (Followers: 1)
Advances in Chronic Kidney Disease     Hybrid Journal   (Followers: 15)
Advances in Diabetes and Metabolism     Open Access   (Followers: 22)
Advances in Endocrinology     Open Access   (Followers: 7)
AJP Endocrinology and Metabolism     Hybrid Journal   (Followers: 25)
American Journal of Kidney Diseases     Hybrid Journal   (Followers: 53)
Annales d'Endocrinologie     Hybrid Journal   (Followers: 2)
Applied Physiology, Nutrition and Metabolism     Hybrid Journal   (Followers: 37)
Best Practice & Research Clinical Endocrinology & Metabolism     Hybrid Journal   (Followers: 15)
BMC Endocrine Disorders     Open Access   (Followers: 8)
Case Reports in Endocrinology     Open Access   (Followers: 3)
Clinical Diabetes     Full-text available via subscription   (Followers: 40)
Clinical Diabetes and Endocrinology     Open Access   (Followers: 20)
Clinical Endocrinology     Hybrid Journal   (Followers: 42)
Clinical Medicine Insights : Endocrinology and Diabetes     Open Access   (Followers: 29)
Clinical Nutrition Insight     Full-text available via subscription   (Followers: 13)
Clinical Reviews in Bone and Mineral Metabolism     Hybrid Journal  
Comprehensive Psychoneuroendocrinology     Open Access  
Current Opinion in Endocrine and Metabolic Research     Hybrid Journal   (Followers: 1)
Current Opinion in Endocrinology, Diabetes and Obesity     Hybrid Journal   (Followers: 48)
Dermato-Endocrinology     Open Access   (Followers: 3)
Diabesity     Open Access   (Followers: 3)
Diabetes & Metabolic Syndrome: Clinical Research & Reviews     Hybrid Journal   (Followers: 27)
Diabetes & Metabolism     Hybrid Journal   (Followers: 72)
Diabetes, Obesity and Metabolism     Hybrid Journal   (Followers: 261)
Diabetes/Metabolism Research and Reviews     Hybrid Journal   (Followers: 63)
Diabetology & Metabolic Syndrome     Open Access   (Followers: 8)
Discover Oncology     Open Access   (Followers: 1)
Domestic Animal Endocrinology     Hybrid Journal   (Followers: 6)
Dubai Diabetes and Endocrinology Journal     Open Access  
Egyptian Journal of Obesity, Diabetes and Endocrinology     Open Access   (Followers: 1)
Endocrine     Hybrid Journal   (Followers: 11)
Endocrine and Metabolic Science     Open Access   (Followers: 1)
Endocrine Connections     Open Access   (Followers: 4)
Endocrine Disruptors     Open Access  
Endocrine Journal     Open Access   (Followers: 13)
Endocrine Pathology     Hybrid Journal   (Followers: 7)
Endocrine Practice     Hybrid Journal   (Followers: 58)
Endocrine Regulations     Open Access  
Endocrine Research     Hybrid Journal   (Followers: 3)
Endocrine Reviews     Full-text available via subscription   (Followers: 44)
Endocrine, Metabolic & Immune Disorders - Drug Targets     Hybrid Journal   (Followers: 1)
Endocrine-Related Cancer     Full-text available via subscription   (Followers: 2)
Endocrinología, Diabetes y Nutrición (English Edition)     Hybrid Journal   (Followers: 2)
Endocrinology     Full-text available via subscription   (Followers: 50)
Endocrinology and Metabolism Clinics of North America     Full-text available via subscription   (Followers: 28)
Endocrinology, Diabetes & Metabolism     Open Access  
Endocrinology, Diabetes & Metabolism Case Reports     Open Access  
Endocrinology, Obesity and Metabolic Disorders     Full-text available via subscription   (Followers: 6)
Endokrynologia Polska     Open Access   (Followers: 2)
European Journal of Endocrinology     Full-text available via subscription   (Followers: 40)
European Thyroid Journal     Full-text available via subscription   (Followers: 3)
Experimental and Clinical Endocrinology & Diabetes     Hybrid Journal   (Followers: 24)
Experimental and Clinical Endocrinology & Diabetes Reports     Open Access   (Followers: 4)
Expert Opinion on Drug Metabolism & Toxicology     Hybrid Journal   (Followers: 15)
Expert Review of Endocrinology & Metabolism     Hybrid Journal   (Followers: 7)
Frontiers in Clinical Diabetes and Healthcare     Open Access  
Frontiers in Endocrinology     Open Access   (Followers: 5)
Frontiers in Neuroendocrine Science     Open Access  
Frontiers in Neuroendocrinology     Hybrid Journal   (Followers: 10)
General and Comparative Endocrinology     Hybrid Journal   (Followers: 5)
Growth Hormone & IGF Research     Hybrid Journal   (Followers: 14)
Gynakologische Endokrinologie     Hybrid Journal  
Gynecological Endocrinology     Hybrid Journal   (Followers: 5)
Hormone and Metabolic Research     Hybrid Journal   (Followers: 16)
Hormone Research in Paediatrics     Full-text available via subscription   (Followers: 16)
Hormones : International Journal of Endocrinology and Metabolism     Hybrid Journal  
Hormones and Behavior     Hybrid Journal   (Followers: 12)
Indian Journal of Endocrinology and Metabolism     Open Access   (Followers: 4)
International Journal of Clinical Endocrinology and Metabolism     Open Access   (Followers: 1)
International journal of endocrine oncology     Open Access  
International Journal of Endocrinology     Open Access   (Followers: 3)
International Journal of Endocrinology     Open Access   (Followers: 1)
International Journal of Endocrinology and Metabolism     Open Access   (Followers: 3)
International Journal of Obesity     Hybrid Journal   (Followers: 90)
International Journal of Osteoporosis and Metabolic Disorders     Open Access   (Followers: 1)
International Journal of Pediatric Endocrinology     Open Access   (Followers: 11)
JIMD Reports     Open Access  
Journal für Gynäkologische Endokrinologie/Österreich     Hybrid Journal  
Journal für Klinische Endokrinologie und Stoffwechsel : Austrian Journal of Clinical Endocrinology and Metabolism     Hybrid Journal  
Journal of Bone and Mineral Metabolism     Hybrid Journal   (Followers: 5)
Journal of Clinical and Translational Endocrinology     Open Access  
Journal of Clinical and Translational Endocrinology Case Reports     Open Access   (Followers: 2)
Journal of Clinical Endocrinology & Metabolism     Full-text available via subscription   (Followers: 139)
Journal of Developmental Origins of Health and Disease     Hybrid Journal   (Followers: 2)
Journal of Diabetes and Endocrinology     Open Access   (Followers: 7)
Journal of Diabetes and Endocrinology Assocation of Nepal     Open Access  
Journal of Diabetes and Metabolic Disorders     Open Access   (Followers: 8)
Journal of Diabetes Science and Technology     Hybrid Journal   (Followers: 13)
Journal of Diabetology     Open Access   (Followers: 1)
Journal of Endocrinological Investigation     Full-text available via subscription   (Followers: 7)
Journal of Endocrinology     Full-text available via subscription   (Followers: 13)
Journal of Endocrinology and Metabolism     Open Access   (Followers: 5)
Journal of Endocrinology and Reproduction     Hybrid Journal  
Journal of Endocrinology, Metabolism and Diabetes of South Africa     Open Access   (Followers: 8)
Journal of Inborn Errors of Metabolism and Screening     Open Access  
Journal of Molecular Endocrinology     Full-text available via subscription   (Followers: 5)
Journal of Neuroendocrinology     Hybrid Journal   (Followers: 8)
Journal of Pineal Research     Hybrid Journal   (Followers: 1)
Journal of Renal and Hepatic Disorders     Open Access  
Journal of Restorative Medicine     Open Access  
Journal of Social Health and Diabetes     Open Access   (Followers: 1)
Journal of the ASEAN Federation of Endocrine Societies     Open Access  
Kidney International     Hybrid Journal   (Followers: 52)
Kidney Research Journal     Open Access   (Followers: 6)
L'Endocrinologo     Hybrid Journal  
Metabolic Brain Disease     Hybrid Journal   (Followers: 1)
Metabolic Syndrome and Related Disorders     Hybrid Journal   (Followers: 5)
Metabolism     Hybrid Journal   (Followers: 11)
Molecular and Cellular Endocrinology     Hybrid Journal   (Followers: 8)
Molecular Metabolism     Open Access   (Followers: 9)
Nature Reviews Endocrinology     Full-text available via subscription   (Followers: 60)
Neuroendocrinology     Full-text available via subscription   (Followers: 8)
Nigerian Endocrine Practice     Full-text available via subscription  
Nutrition in Clinical Practice     Hybrid Journal   (Followers: 43)
Open Journal of Endocrine and Metabolic Diseases     Open Access   (Followers: 1)
Psychoneuroendocrinology     Hybrid Journal   (Followers: 15)
Reproductive Biology and Endocrinology     Open Access   (Followers: 3)
Reproductive Endocrinology     Open Access   (Followers: 1)
Reviews in Endocrine and Metabolic Disorders     Hybrid Journal   (Followers: 2)
Revista Argentina de Endocrinología y Metabolismo     Open Access  
Revista Cubana de Endocrinología     Open Access  
Revista Venezolana de Endocrinología y Metabolismo     Open Access  
Sri Lanka Journal of Diabetes Endocrinology and Metabolism     Open Access  
The Endocrinologist     Full-text available via subscription   (Followers: 6)
The Lancet Diabetes and Endocrinology     Full-text available via subscription   (Followers: 167)
Therapeutic Advances in Endocrinology and Metabolism     Open Access   (Followers: 5)
Thyroid     Hybrid Journal   (Followers: 11)
Thyroid Research     Open Access   (Followers: 3)
Thyroid Research and Practice     Open Access   (Followers: 3)
Trends in Endocrinology & Metabolism     Full-text available via subscription   (Followers: 19)
Vitamins & Hormones     Full-text available via subscription   (Followers: 1)

           

Similar Journals
Journal Cover
Metabolic Brain Disease
Journal Prestige (SJR): 0.909
Citation Impact (citeScore): 2
Number of Followers: 1  
 
  Hybrid Journal Hybrid journal (It can contain Open Access articles)
ISSN (Print) 1573-7365 - ISSN (Online) 0885-7490
Published by Springer-Verlag Homepage  [2469 journals]
  • The effect of chronic stress and its preconditioning on spatial memory as
           well as hippocampal LRP1 and RAGE expression in a streptozotocin-induced
           rat model of Alzheimer’s disease

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      Abstract: Abstract According to available evidence, prolonged or chronic exposure to stress is detrimental to various brain structures, including the hippocampus. The current study examined the expression of two critical blood–brain barrier receptors required for amyloid-beta clearance to understand better the mechanism by which chronic stress impairs learning and memory in patients with Alzheimer's disease (AD). Rats were randomly assigned to one of two groups in this study: experiment 1 and experiment 2. Each main group was then divided into four subgroups. Rats were bilaterally injected with streptozotocin (STZ, 3 mg/kg, twice) using the intracerebroventricular (ICV) technique to induce the Alzheimer's model. Additionally, they were subjected to foot shock (1 mA, 1 Hz) for 10 s every 60 s (1 h/day) for ten consecutive days prior to and following STZ injection. The Morris Water Maze (MWM) test was used to assess spatial learning and memory. Real-time PCR was used to determine Low-density lipoprotein receptor-related protein-1 (LRP1) and receptor for advanced glycation end-products (RAGE) mRNA levels in the hippocampus. Moreover, the animals' body weights were determined as physiological parameters in all groups. The results indicated that 10-day chronic electric foot shock stress reduced body weight, impaired spatial learning and memory, decreased hippocampal LRP1 mRNA expression, and increased hippocampal RAGE mRNA expression in a rat AD model. It can be concluded that chronic stress in conjunction with AD alters the expression of LRP1 and RAGE in the hippocampus. The findings pave the way for scientists to develop novel treatment strategies for AD.
      PubDate: 2022-08-05
       
  • Gold nanoparticles application to the treatment of brain dysfunctions
           related to metabolic diseases: evidence from experimental studies

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      Abstract: Abstract Nanotechnology is an emerging and expanding technology worldwide. The manipulation of materials on a nanometric scale generates new products with unique properties called nanomaterials. Due to its significant expansion, nanotechnology has been applied in several fields of study, including developing materials for biomedical applications, i.e., nanomedicine. The use of nanomaterials, including nanoparticles, in nanomedicine, is promising and has been associated with pharmacokinetics, bioavailability, and therapeutic advantages. In this regard, it is worth mentioning the Gold Nanoparticles (AuNPs). AuNPs’ biomedical application is extensively investigated due to their high biocompatibility, simple preparation, catalytic, and redox properties. Experimental studies have pointed out critical therapeutic actions related to AuNPs in different pathophysiological contexts, mainly due to their anti-inflammatory and antioxidant effects. Thus, in this review, we will discuss the main experimental findings related to the therapeutic properties of AuNPs in metabolic, neurodegenerative diseases, and ultimately brain dysfunctions related to metabolic diseases.
      PubDate: 2022-08-04
       
  • An aqueous macerate of Ziziphus jujuba reduces long-term spatial memory
           impairment in D-galactose treated rats: role of anti-inflammatory pathways
           

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      Abstract: Abstract Pharmacological treatments against Alzheimer disease provide only symptomatic relief and are associated with numerous side effects. Previous studies showed that a concoction of Ziziphus jujuba leaves possesses anti-amnesic effects in scopolamine-treated rats. More recently, an aqueous macerate of Z. jujuba leaves has been shown to reduce short-term memory impairment in D-galactose-treated rats. However, no study on the effect of an aqueous macerate of Z. jujuba on long-term memory impairment was performed. Therefore, this study evaluates the effect of an aqueous macerate of Z. jujuba on long-term spatial memory impairment in D-galactose-treated rats. Long-term spatial memory impairment was induced in rats by administering D-galactose (350 mg/kg/day, s.c.), once dailyfor 21 days. On the 22nd day, the integrity of this memory was assessed using the Morris water maze task. Rats that developed memory impairment were treated with tacrine (10 mg/kg, p.o.), or aspirin (20 mg/kg, p.o.), or extract (41.5, 83, and 166 mg/kg, p.o.), once daily, for 14 days. At the end of the treatment, memory impairment was once more assessed using the same paradigm. Animals were then euthanized, and some pro-inflammatory cytokine markers were analyzed in the hippocampus or blood. The extract at all doses significantly reduced the latency to attain the platforming of the water maze test. The extract (83 mg/kg) also increased the time spent in the target quadrant during the retention phase. The extract markedly reduced the concentration of pro-inflammatory cytokine markers in the hippocampus and blood. Together, these results suggest that this aqueous extract Z. jujuba reduces long-term spatial memory impairment. This effect may be mediated in part by its anti-inflammatory activity.
      PubDate: 2022-08-04
       
  • Anti-Caspr-conjugated gold nanoparticles emergence as a novel approach in
           the treatment of EAE animal model

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      Abstract: Abstract Multiple sclerosis (MS) is a chronic autoimmune disorder of central nervous system which is increasing worldwide. Although immunosuppressive agents are used for the treatment of MS disease, nevertheless the lack of non-toxic and efficient therapeutic method is perceptible. Hence, this study aims to evaluate the effect of Contactin-associated protein (Caspr) antibody-, poly ethylene glycol (PEG)- and exosome combined gold nanoparticles (GNPs) in comparison to Glatiramer acetate as a selective treatment of MS disease in the experimental autoimmune encephalomyelitis (EAE) mouse model. EAE was induced in female C57BL/6 mice and 25-day treatment with anti-Caspr-, PEG- and exosome combined GNPs was evaluated. Histopathological examination of spinal cord, regulatory T cells as well as inflammatory pathway including IFN-ɣ and IL-17 and mir-326 were investigated. The results showed the severity of MS symptoms was significantly decreased in all treated groups. Histological examination of the spinal cord indicated the reduced demyelination and immune cell infiltration. Besides, regulatory T cells were significantly increased following all treatments. Remarkably, the cytokine levels of IFN-ɣ and IL-17 as well as mir-326 is altered in treated groups. Taken together, the obtained findings demonstrate that the administration of anti-Caspr-, PEG- and exosome combined GNPs can be considered a potential treatment in MS disease.
      PubDate: 2022-08-04
       
  • Circ_0000011 promotes cerebral ischemia/reperfusion injury via
           miR-27a-3p-dependent regulation of NRIP1

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      Abstract: Background Cerebral ischemia/reperfusion (I/R) can result in brain function impairments. Circular RNAs (circRNAs) have emerged as vital regulators in cerebral I/R injury. However, the functions of mmu_circ_0000011 in cerebral I/R injury are still unclear. Thus, in this study, we aimed to explore the effect of mmu_circ_0000011 on cerebral I/R injury. Methods Oxygen-glucose deprivation and reperfusion (OGD/R)-induced HT-22 cells were used to mimic the condition of cerebral I/R injury in vitro. Cell Counting Kit-8 (CCK-8) assay, lactate dehydrogenase (LDH) assay, 5’-ethynyl-2’-deoxyuridine (EdU) assay and flow cytometry analysis were utilized to assess cell viability, LDH release, proliferation and apoptosis, respectively. qRT-PCR and western blot were performed to determined the levels of circ_0000011, miR-27a-3p and NRIP1. Dual-luciferase reporter assay and RNA pull-down assay were utilized to analyze the targeting relation of circ_0000011, miR-27a-3p and NRIP1. Results OGD/R treatment inhibited HT-22 cell viability and promoted LDH release, cell apoptosis and inflammation. Circ_0000011 level was increased in OGD/R-induced HT-22 cells. Silencing of circ_0000011 promoted cell proliferation and inhibited LDH release, apoptosis and inflammation in OGD/R-treated HT-22 cells. For mechanism analysis, circ_0000011 was demonstrated to sponge miR-27a-3p, which directly targeted NRIP1. MiR-27a-3p inhibition or NRIP1 overexpression ameliorated the impacts of circ_0000011 silencing on cell proliferation, LDH release, apoptosis and inflammation in OGD/R-treated HT-22 cells. Conclusions Circ_0000011 promotes OGD/R-induced HT-22 cell impairments by elevating NRIP1 through sponging miR-27a-3p.
      PubDate: 2022-08-04
       
  • Rolipram and pentoxifylline combination ameliorates experimental diabetic
           neuropathy through inhibition of oxidative stress and inflammatory
           pathways in the dorsal root ganglion neurons

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      Abstract: Abstract Diabetic neuropathy (DN) is the most challenging microvascular complication of diabetes and there is no suitable treatment for it, so the development of new agents to relieve DN is urgently needed. Since oxidative stress and inflammation play an essential role in the development of DN, clearance of these factors are good strategies for the treatment of this disease. According to key role of cyclic adenosine monophosphate (cAMP) in the regulation of oxidative stress and inflammatory pathways, it seems that phosphodiesterase inhibitors (PDEIs) can be as novel drug targets for improving DN through enhancement of cAMP level. The aim of this study was to evaluate the effects of rolipram, a selective PDE4 inhibitor, and pentoxifylline, a general PDE inhibitor on experimental model of DN and also to determine the possible mechanisms involved in the effectiveness of these agents. We investigated the effects of rolipram (1 mg/kg) and pentoxifylline (100 mg/kg) and also combination of rolipram (0.5 mg/kg) and pentoxifylline (50 mg/kg), orally for five weeks in rats that became diabetic by STZ (55 mg/kg, i.p.). After treatments, motor function was evaluated by open-field test, then rats were anesthetized and dorsal root ganglion (DRG) neurons isolated. Next, oxidative stress biomarkers and inflammatory factors were assessed by biochemical and ELISA methods, and RT-PCR analysis in DRG neurons. Rolipram and/or pentoxifylline treatment significantly attenuated DN – induced motor function deficiency by modulating distance moved and velocity. Rolipram and/or pentoxifylline treatment dramatically increased the cAMP level, as well as suppressed DN – induced oxidative stress which was associated with decrease in LPO and ROS and increase in TAC, total thiol, CAT and SOD in DRG neurons. On the other hand, the level of inflammatory factors (TNF-α, NF-kB and COX2) significantly decreased following rolipram and/or pentoxifylline administration. The maximum effectiveness was with rolipram and/or pentoxifylline combination on mentioned factors. These findings provide novel experimental evidence for further clinical investigations on rolipram and pentoxifylline combination for the treatment of DN.
      PubDate: 2022-08-04
       
  • Protective effects of isofraxidin against scopolamine-induced cognitive
           and memory impairments in mice involve modulation of the BDNF-CREB-ERK
           signaling pathway

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      Abstract: Background Isofraxidin is a coumarin compound mainly isolated from several traditional and functional edible plants beneficial for neurodegenerative diseases, including Sarcandra glabra and Apium graveolens, and Siberian Ginseng. Objective This study aimed to assess effects of isofraxidin against memory impairments and cognition deficits in a scopolamine-induced mouse model. Materials & methods Animals were randomly divided into 6 groups, control, vehicle, donepezil (10 mg/kg, p.o.), and isofraxidin (3, 10, and 30 mg/kg, p.o.). Isofraxidin or donepezil was administered for 44 days, once per day. The scopolamine insults (1 mg/kg, i.p.) was given from the 21st day, once per day. Morris water maze test and Y-maze test were used for the behavioral test. After that, brain samples were collected for analysis. Results Firstly, isofraxidin significantly improved scopolamine-induced behavioral impairments and cognition deficits in Morris water maze and Y-maze test. Then, isofraxidin facilitated cholinergic activity via inhibiting acetylcholinesterase (AChE) activity. Besides, isofraxidin decreased lipid peroxidation level but enhanced levels of glutathione, glutathione peroxidase, and superoxide dismutase. Moreover, isofraxidin suppressed the expression of inflammatory mediators and cytokines. Further investigations showed that isofraxidin up-regulated expression of brain-derived neurotrophic factor (BDNF), and promoted phosphorylation of tropomyosin-related kinase B (TrkB), cyclic AMP-response element-binding protein (CREB), and extracellular signal-regulated kinase (ERK). Discussion & Conclusions These results suggested that isofraxidin ameliorated scopolamine-induced cognitive and memory impairments, possibly through regulating AChE activity, suppressing oxidative stress and inflammatory response, and modulating BDNF-CREB-ERK pathways.
      PubDate: 2022-08-03
       
  • Adiponectin, the adiponectin paradox, and Alzheimer’s Disease: Is this
           association biologically plausible'

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      Abstract: Abstract Dementia, especially Alzheimer’s Disease (AD) and vascular dementia, is a major public health problem that continues to expand in both economically emerging and hegemonic countries. In 2017, the World Alzheimer Report estimated that over 50 million people were living with dementia globally. Metabolic dysfunctions of brain structures such as the hippocampus and cerebral cortex have been implicated as risk factors for dementia. Several well-defined metabolic risk factors for AD include visceral obesity, chronic inflammation, peripheral and brain insulin resistance, type 2 diabetes mellitus (T2DM), hypercholesterolemia, and others. In this review, we describe the relationship between the dysmetabolic mechanisms, although still unknown, and dementia, particularly AD. Adiponectin (ADPN), the most abundant circulating adipocytokine, acts as a protagonist in the metabolic dysfunction associated with AD, with unexpected and intriguing dual biological functions. This contradictory role of ADPN has been termed the adiponectin paradox. Some evidence suggests that the adiponectin paradox is important in amyloidogenic evolvability in AD. We present cumulative evidence showing that AD and T2DM share many common features. We also review the mechanistic pathways involving brain insulin resistance. We discuss the importance of the evolvability of amyloidogenic proteins (APs), defined as the capacity of a system for adaptive evolution. Finally, we describe potential therapeutic strategies in AD, based on the adiponectin paradox.
      PubDate: 2022-08-03
       
  • An aqueous extract of Syzygium cumini protects against kainate-induced
           status epilepticus and amnesia: evidence for antioxidant and
           anti-inflammatory intervention

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      Abstract: Abstract Temporal lobe epilepsy is the most common drug-resistant epilepsy. To cure epilepsy, drugs must target the mechanisms at the origin of seizures. Thus, the present investigation aimed to evaluate the antiepileptic- and anti-amnesic-like effects of an aqueous extract of Syzygium cumini against kainate-induced status epilepticus in mice, and possible mechanisms of action. Mice were divided into 7 groups and treated as follows: normal group or kainate group received po distilled water (10 mL/kg), four test groups received Syzygium cumini (28.8, 72, 144, and 288 mg/kg, po), and the positive control group treated intraperitoneally (ip) with sodium valproate (300 mg/kg). An extra group of normal mice was treated with piracetam (200 mg/kg, po). Treatments were administered 60 min before the induction of status epilepticus with kainate (15 mg/kg, ip), and continued daily throughout behavioral testing. Twenty-four hours after the induction, T-maze and Morris water maze tasks were successively performed. The animals were then sacrificed and some markers of oxidative stress and neuroinflammation were estimated in the hippocampus. The extract significantly prevented status epilepticus and mortality. In the T-maze, the aqueous extract markedly increased the time spent and the number of entries in the discriminated arm. In the Morris water maze, the extract significantly increased the time spent in the target quadrant during the retention phase. Furthermore, the aqueous extract induced a significant reduction of oxidative stress and neuroinflammation. These results suggest that the aqueous extract of Syzygium cumini has antiepileptic- and anti-amnesic-like effects, likely mediated in part by antioxidant and anti-inflammatory activities.
      PubDate: 2022-08-02
       
  • p-Coumaric acid protects against D-galactose induced neurotoxicity by
           attenuating neuroinflammation and apoptosis in mice brain

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      Abstract: Abstract D-galactose (D-gal) induced senescence in rodents is a widely used model for assessment of molecules affecting brain ageing. Chronic administration of D-gal causes neuroinflammation leading to cognitive deficit and memory impairment which represent Alzheimer’s dementia. In present study, we investigated the neuroprotective effects of the natural phenol, p-Coumaric acid (PCA) and its underlying mechanism in the chronic D-gal treated mice. Subcutaneous administration of D-gal (150 mg/kg) to Swiss albino mice for 42 consecutive days resulted in cognitive impairment as observed in Morris water maize (MWM) and Y maze test, which was ameliorated by concurrent treatment with PCA (80 mg/kg, and 100 mg/kg, p.o.). Importantly, PCA treatment attenuated the D-gal induced oxidative stress and significantly inhibited acetylcholinesterase (AChE) activity in mice brain. Furthermore, PCA treatment significantly lowered levels of inflammatory marker nuclear factor kappa B (NFκB) and reduced levels of proapoptotic enzyme caspase3. We also observed that PCA treatment exhibited β-secretase enzyme (BACE1) inhibitory effect. However, our results revealed that PCA treatment failed to decrease the level of advanced glycation end products both in vitro and in vivo. Taken together, current study demonstrated the significant neuroprotective effect of PCA against D-gal induced oxidative stress, neuroinflammation, cognitive impairment and apoptosis.
      PubDate: 2022-08-01
       
  • Retraction Note to: Long non-coding RNA SNHG7 upregulates FGF9 to
           alleviate oxygen and glucose deprivation-induced neuron cell injury in a
           miR-134-5p-dependent manner

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      PubDate: 2022-08-01
       
  • Altered glucose metabolism and its association with carbonic anhydrase 8
           in Machado-Joseph Disease

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      Abstract: Abstract Machado-Joseph disease (MJD), also known as spinocerebellar ataxia type 3 (SCA3), is an autosomal dominant neurodegenerative disease. This disorder is caused by polyglutamine (polyQ)-containing mutant ataxin-3, which tends to misfold and aggregate in neuron cells. We previously demonstrated a protective function of carbonic anhydrase 8 (CA8) in MJD disease models and a decreased glycolytic activity associated with down-regulated CA8 in a human osteosarcoma (OS) cell model. Given that a reduction in body weight accompanied by gait and balance instability was observed in MJD patients and transgenic (Tg) mice, in this study, we aimed to examine whether metabolic defects are associated with MJD and whether CA8 expression is involved in metabolic dysfunction in MJD. Our data first showed that glucose uptake ability decreases in cells harboring mutant ataxin-3, but increases in cells overexpressing CA8. In addition, the expressions of glucose transporter 3 (GLUT3) and phosphofructokinase-1 (PFK1) were significantly decreased in the presence of mutant ataxin-3. Consistently, immunohistochemistry (IHC) showed that GLUT3 was less expressed in cerebella of aged MJD Tg mice, indicating that the dysfunction of GLUT3 may be associated with late-stage disease. On the other hand, transient down-regulation of CA8 revealed decreased expressions of GLUT3 and PFK1 in HEK293 cells harboring wild-type (WT) ataxin-3, but no further reduction of GLUT3 and PFK1 expressions were observed in HEK293 cells harboring mutant ataxin-3. Moreover, immunoprecipitation (IP) and immunofluorescence (IF) demonstrated that interactions exist between ataxin-3, CA8 and GLUT3 in MJD cellular and Tg models. These lines of evidence suggest that CA8 plays an important role in glucose metabolism and has different impacts on cells with or without mutant ataxin-3. Interestingly, the decreased relative abundance of Firmicutes/Bacteroidetes (F/B) ratio in the feces of aged MJD Tg mice coincided with weight loss and metabolic dysfunction in MJD. Taken together, our results are the first to demonstrate the effects of CA8 on glucose metabolism and its involvement in the metabolic defects in MJD disease. Further investigations will be required to clarify the underlying mechanisms for the metabolic defects associated with MJD.
      PubDate: 2022-08-01
       
  • Basal metabolic rate and risk of multiple sclerosis: a Mendelian
           randomization study

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      Abstract: Abstract To determine the relationship between basal metabolic rate (BMR) and multiple sclerosis (MS) susceptibility, we analyzed genome-wide association study (GWAS) summary statistics data from the International Multiple Sclerosis Genetics Consortium on a total of 115,803 participants of European descent, including 47,429 patients with MS and 68,374 controls. We selected 378 independent genetic variants strongly associated with BMR in a GWAS involving 454,874 participants as instrumental variables to examine a potential causal relationship between BMR and MS. A genetically predicted higher BMR was associated with a greater risk of MS (odds ratio [OR]: 1.283 per one standard deviation increase in BMR, 95% confidence interval [CI]: 1.108–1.486, P = 0.001). Moreover, we used the lasso method to eliminate heterogeneity (Q statistic = 384.58, P = 0.370). There was no pleiotropy in our study and no bias was found in the sensitivity analysis using the leave-one-out test. We provide novel evidence that a higher BMR is an independent causal risk factor in the development of MS. Further work is warranted to elucidate the potential mechanisms.
      PubDate: 2022-08-01
       
  • PI3K/AKT/mTOR signalling inhibitor chrysophanol ameliorates
           neurobehavioural and neurochemical defects in propionic acid-induced
           experimental model of autism in adult rats

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      Abstract: Abstract Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder marked by social and communication deficits as well as repetitive behaviour. Several studies have found that overactivation of the PI3K/AKT/mTOR signalling pathways during brain development plays a significant role in autism pathogenesis. Overexpression of the PI3K/AKT/mTOR signalling pathway causes neurological disorders by increasing cell death, neuroinflammation, and oxidative stress. Chrysophanol, also known as chrysophanic acid, is a naturally occurring chemical obtained from the plant Rheum palmatum. This study aimed to examine the neuroprotective effect of CPH on neurobehavioral, molecular, neurochemical, and gross pathological alterations in ICV-PPA induced experimental model of autism in adult rats. The effects of ICV-PPA on PI3K/AKT/mTOR downregulation in the brain were studied in autism-like rats. Furthermore, we investigated how CPH affected myelin basic protein (MBP) levels in rat brain homogenate and apoptotic biomarkers such as caspase-3, Bax, and Bcl-2 levels in rat brain homogenate and blood plasma samples. Rats were tested for behavioural abnormalities such as neuromuscular dysfunction using an actophotometer, motor coordination using a beam crossing task (BCT), depressive behaviour using a forced swim test (FST), cognitive deficiency, and memory consolidation using a Morris water maze (MWM) task. In PPA-treated rats, prolonged oral CPH administration from day 12 to day 44 of the experimental schedule reduces autistic-like symptoms. Furthermore, in rat brain homogenates, blood plasma, and CSF samples, cellular, molecular, and cell death markers, neuroinflammatory cytokines, neurotransmitter levels, and oxidative stress indicators were investigated. The recent findings imply that CPH also restores abnormal neurochemical levels and may prevent autism-like gross pathological alterations, such as demyelination volume, in the rat brain.
      PubDate: 2022-08-01
       
  • Circular RNA circ_0021001 regulates miR-148b-3p/GREM1 axis to modulate
           proliferation and apoptosis of vascular smooth muscle cells

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      Abstract: Abstract Intracranial aneurysm (IA) is an abnormal expression in the intracranial arteries, which is related to the growth and apoptosis of vascular smooth muscle cells (VSMCs). Circular RNA (circRNA) circ_0021001 (also named circARFIP2) has been identified to mediate the regulation of VSMCs proliferation. However, the molecular mechanism of circ_0021001 involved in VSMC dysfunction in IA is poorly defined. The expression levels of circ_0021001, microRNA-148b-3p (miR-148b-3p), and Gremlin 1 (GREM1) were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell viability, proliferation, cell cycle progression, and apoptosis were detected by Cell Counting Kit-8 (CCK-8), 5-ethynyl-2’-deoxyuridine (EdU), and flow cytometry assays. Protein levels of proliferating cell nuclear antigen (PCNA), p21, B-cell lymphoma-2 (Bcl-2), Bcl-2 related X protein (Bax), and GREM1 were examined by western blot assay. The binding relationship between miR-148b-3p and circ_0021001 or GREM1 was predicted by StarBase and then verified using a dual-luciferase reporter assay. The expression levels of circ_0021001 and GREM1 were increased, and that of miR-148b-3p was decreased in IA tissues and HUASMCs. Moreover, the downregulation of circ_0021001 could repress proliferation ability and induce apoptosis of HUASMCs. The mechanical analysis uncovered that circ_0021001 served as a sponge of miR-148b-3p to regulate GREM1 expression. Circ_0021001 silencing could suppress cell growth and induce apoptosis of HUASMCs partially through modulating the miR-148b-3p/GREM1, presented circ_0021001 as a promising therapeutic target for IA.
      PubDate: 2022-08-01
       
  • Emerging urinary alpha-synuclein and miRNA biomarkers in Parkinson’s
           disease

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      Abstract: Abstract Parkinson’s disease (PD) is one of the most common neurodegenerative diseases after Alzheimer’s disease (AD), afflicting adults above the age of sixty irrespective of gender, race, ethnicity, and social status. PD is characterized by motor dysfunctions, displaying resting tremor, rigidity, bradykinesia, and postural imbalance. Non-motor symptoms, including rapid eye movement (REM) behavior disorder, constipation, and loss of sense of smell, typically occur many years before the appearance of the PD motor symptoms that lead to a diagnosis. The loss of dopaminergic neurons in the substantia nigra, which leads to the motor symptoms seen in PD, is associated with the deposition of aggregated, misfolded α-Synuclein (α-Syn, SNCA) proteins forming Lewy Bodies. Additionally, dysregulation of miRNA (a short form of mRNA) may contribute to the developing pathophysiology in PD and other diseases such as cancer. Overexpression of α-Syn and miRNA in human samples has been found in PD, AD, and dementia. Therefore, evaluating these molecules in urine, present either in the free form or in association with extracellular vesicles of biological fluids, may lead to early biomarkers for clinical diagnosis. Collection of urine is non-invasive and thus beneficial, particularly in geriatric populations, for biomarker analysis. Considering the expression and function of α-Syn and miRNA, we predict that they can be used as early biomarkers in the diagnosis and prognosis of neurodegenerative diseases.
      PubDate: 2022-08-01
       
  • Putative involvement of sirtuin modulators in LPS-induced sickness
           behaviour in mice

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      Abstract: Abstract NAD+—dependent histone deacetylases (sirtuins 1–7) have been shown to be involved in various pathophysiological conditions including their involvement in cardiovascular, cancerous, neurodegenerative, immune dysregulation and inflammatory conditions. This study investigates the inflammomodulatory potential of resveratrol (RES), a sirtuin activator and sirtinol (SIR), a sirtuin inhibitor in lipopolysaccharide (LPS)-induced model of sickness behaviour in mice. Male Swiss albino mice were divided into five groups (n = 6) consisting of saline (SAL), LPS, RES, SIR, and fluoxetine (FLU) respectively, each group except LPS was prepared by intraperitoneally (i.p.) administration of SAL (10 mL/kg), RES (50 mg/kg), SIR (2 mg/kg) and FLU (10 mg/kg). Thirty minutes after the treatments, all the groups, except SAL were administered LPS (2 mg/kg, i.p.). The behavioural assays including, open field test, forced swim test, and tail suspension tests were conducted 1 h after LPS challenge. LPS administration significantly reduced the locomotor activity along with inducing a state of high immobility and that was prevented by pretreatment with RES and SIR. Further, various proinflammatory cytokines (TNF-α, IL-6, and IL-1β), and oxidative stress markers (MDA and GSH) were found to be significantly elevated in the brain homogenates after LPS treatment. SIR pretreatment abrogated the LPS-induced neuroinflammatory and oxidative stress changes, whereas RES was only effective in reducing the oxidative stress and TNF-α levels. The results of this study speculate that the role of SIRT modulators in neuroinflammatory conditions could vary with their dose, regimen and chemical properties. Further studies with detailed molecular and pharmacokinetic profiling will be needed to explore their therapeutic potentials.
      PubDate: 2022-08-01
       
  • Drug delivery for neuronopathic lysosomal storage diseases: evolving roles
           of the blood brain barrier and cerebrospinal fluid

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      Abstract: Abstract Whereas significant strides have been made in the treatment of lysosomal storage diseases (LSDs), the neuronopathy associated with these diseases remains impervious mainly because of the blood-brain barrier (BBB), which prevents delivery of large molecules to the brain. However, 100 years of research on the BBB since its conceptualization have clarified many of its functional and structural characteristics, spurring recent endeavors to deliver therapeutics across it to treat central nervous system (CNS) disorders, including neuronopathic LSDs. Along with the BBB, the cerebrospinal fluid (CSF) also functions to protect the microenvironment of the CNS, and it is therefore deeply involved in CNS disorders at large. Recent research aimed at developing therapeutics for neuronopathic LSDs has uncovered a number of critical roles played by the CSF that require further clarification. This review summarizes the most up-to-date understanding of the BBB and the CSF acquired during the development of therapeutics for neuronopathic LSDs, and highlights some of the associated challenges that require further research.
      PubDate: 2022-08-01
       
  • Exogenous hydrogen sulfide restores CSE and CBS but no 3-MST protein
           expression in the hypothalamus and brainstem after severe traumatic brain
           injury

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      Abstract: Abstract Hydrogen sulfide (H2S) is a gasotransmitter endogenously synthesized by cystathionine-γ-lyase (CSE), cystathionine-β-synthase (CBS), and 3-mercaptopiruvate sulfurtransferase (3-MST) enzymes. H2S exogenous administration prevents the development of hemodynamic impairments after traumatic brain injury (TBI). Since the hypothalamus and the brainstem highly regulate the cardiovascular system, this study aimed to evaluate the effect of NaHS subchronic treatment on the changes of H2S-sythesizing enzymes in those brain areas after TBI and in physiological conditions. For that purpose, animals were submitted to a lateral fluid percussion injury, and the changes in CBS, CSE, and 3-MST protein expression were measured by western blot at days 1, 2, 3, 7, and 28 in the vehicle group, and 7 and 28 days after NaHS treatment. After severe TBI induction, we found a decrease in CBS and CSE protein expression in the hypothalamus and brainstem; meanwhile, 3-MST protein expression diminished only in the hypothalamus compared to the Sham group. Remarkably, i.p. daily injections of NaHS, an H2S donor, (3.1 mg/kg) during seven days: (1) restored CBS and CSE but no 3-MST protein expression in the hypothalamus at day 28 post-TBI; (2) reestablished only CSE in brainstem 7 and 28 days after TBI; and (3) did not modify H2S-sythesizing enzymes protein expression in uninjured animals. Mainly, our results show that the NaHS effect on CBS and CSE protein expression is observed in a time- and tissue-dependent manner with no effect on 3-MST expression, which may suggest a potential role of H2S synthesis in hypothalamus and brainstem impairments observed after TBI.
      PubDate: 2022-06-27
       
  • Clonidine ameliorates cerebral ischemia–reperfusion injury by
           up-regulating the GluN3 subunits of NMDA receptor

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      Abstract: Abstract This study aimed to investigate the protective effects of the alpha-2 adrenergic receptor (α2-AR) agonist, clonidine, on the cerebral ischemia–reperfusion (I/R) injury and elaborate the underlying mechanisms. Cerebral I/R model was established by middle cerebral artery occlusion (MCAO) for 2 h followed by reperfusion for 4 h in adult male SD rats. Saline, clonidine and yohimbine (an α2-AR antagonist) were intraperitoneally administered each day for one week before surgery. Neurological deficit was evaluated just before decapitation. TTC staining was applied for correlation of cerebral infarction volume. HE staining was performed to observe the neuron morphology. Immunohistochemical staining was performed to detect the localization and expression of GluN3 proteins. Western blot analysis also was used to detect the expression levels of GluN3 proteins. Our data showed that clonidine ameliorated neurological deficit and reduced the cerebral infarction volume of the rats with cerebral I/R. It is worth noting that treatment with clonidine up-regulated the protein expression of GluN3 in the rats with the cerebral I/R, especially in the cell membrane. Moreover, clonidine also up-regulated the transposition from cytoplasm to cell membrane of GluN3 after cerebral I/R. In addition, yohimbine abolished the neuroprotective effects of clonidine. The results indicated that clonidine played a protective role in cerebral I/R injury through regulation of the protein expression of GluN3 subunits of N-methyl-D-aspartate (NMDA) receptor.
      PubDate: 2022-06-21
       
 
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