Neurochemistry international最新文献

{"title":"Structural fingerprinting of pleiotropic flavonoids for multifaceted Alzheimer's disease","authors":"Amisha Punmiya,&nbsp;Arati Prabhu","doi":"10.1016/j.neuint.2023.105486","DOIUrl":"10.1016/j.neuint.2023.105486","url":null,"abstract":"<div><p><span><span>Alzheimer's disease<span><span> has emerged as one of the most challenging neurodegenerative diseases associated with dementia, loss of cognitive functioning and memory impairment. Despite enormous efforts to identify disease modifying technologies, the repertoire of currently approved drugs consists of a few symptomatic candidates that are not capable of halting </span>disease progression. Moreover, these single mechanism drugs target only a small part of the pathological cascade and do not address most of the etiological basis of the disease. Development of therapies that are able to simultaneously tackle all the multiple interlinked causative factors such as </span></span>amyloid protein<span> aggregation, tau hyperphosphorylation, </span></span>cholinergic<span> deficit, oxidative stress<span><span><span>, metal dyshomeostasis and neuro-inflammation has become the focus of intensive research in this domain. Flavonoids are natural </span>phytochemicals that have demonstrated immense potential as medicinal agents due to their multiple beneficial therapeutic effects. The polypharmacological profile of flavonoids aligns well with the multifactorial pathological landscape of Alzheimer's disease, making them promising candidates to overcome the challenges of this neurodegenerative disorder. This review presents a detailed overview of the pleiotropic biology of flavonoids favourable for Alzheimer therapeutics and the structural basis for these effects. Structure activity trends for several flavonoid classes such as </span>flavones<span>, flavonols<span>, flavanones<span><span>, isoflavones, </span>flavanols<span> and anthocyanins are comprehensively analyzed in detail and presented.</span></span></span></span></span></span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"163 ","pages":"Article 105486"},"PeriodicalIF":4.2,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9258551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of nonalcoholic fatty liver disease-related metabolic state on depression","authors":"Smaragda Ntona ,&nbsp;Apostolis Papaefthymiou ,&nbsp;Jannis Kountouras ,&nbsp;Dimitra Gialamprinou ,&nbsp;Georgios Kotronis ,&nbsp;Marina Boziki ,&nbsp;Stergios A. Polyzos ,&nbsp;Maria Tzitiridou ,&nbsp;Dimitrios Chatzopoulos ,&nbsp;Tharshika Thavayogarajah ,&nbsp;Ioanna Gkolia ,&nbsp;Georgios Ntonas ,&nbsp;Elisabeth Vardaka ,&nbsp;Michael Doulberis","doi":"10.1016/j.neuint.2023.105484","DOIUrl":"10.1016/j.neuint.2023.105484","url":null,"abstract":"<div><p><span><span>Nonalcoholic fatty liver disease<span> (NAFLD), also recently referred as metabolic (dysfunction)-associated fatty liver disease (MAFLD), is characterized by hepatocyte steatosis<span><span><span> in the setting of metabolic risk conditions and in the absence of an underlying precursor, for instance alcohol consumption, hepatotropic viruses and hepatotoxic drugs. A possible association between NAFLD and depression has been proposed, owing to intersecting pathophysiological pathways. This narrative review aimed to summarize the current evidence that illustrate the potential pathophysiological and clinical linkage between NAFLD-related metabolic state and depression. Prefrontal cortex lesions are suggested to be a consequence of liver steatosis-associated systematic hyperinflammatory state, a phenomenon also occurring in depression. In addition, depressive symptoms are present in </span>neurotransmitter imbalances. These abnormalities seem to be correlated with NAFLD/MAFLD, in terms of insulin resistance (IR), ammonia and gut dysbiosis’ impact on serotonin, dopamine, </span>noradrenaline levels and </span></span></span>gamma aminobutyric acid receptors. Furthermore, reduced levels of nesfatin-1 and copine-6-associated BDNF (brain-derived neurotrophic factor) levels have been considered as a probable link between NAFLD and depression. Regarding NAFLD-related gut </span>dysbiosis<span><span>, it stimulates mediators including lipopolysaccharides, short-chain fatty acids and </span>bile acids<span><span>, which play significant role in depression. Finally, western diet and IR, which are mainstay components of NAFLD/MAFLD, are, also, substantiated to affect neurotransmitters in hippocampus and produce neurotoxic </span>lipids<span> that contribute to neurologic dysfunction, and thus trigger emotional disturbances, mainly depressive symptoms.</span></span></span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"163 ","pages":"Article 105484"},"PeriodicalIF":4.2,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10690991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pregnenolone enhances the proliferation of mouse neural stem cells and promotes oligodendrogenesis, together with Sox10, and neurogenesis, along with Notch1 and Pax6","authors":"Kourosh Negintaji ,&nbsp;Amir Ghanbari ,&nbsp;Mohsen frozanfar ,&nbsp;Mojtaba Jafarinia ,&nbsp;Kazem Zibara","doi":"10.1016/j.neuint.2023.105489","DOIUrl":"10.1016/j.neuint.2023.105489","url":null,"abstract":"<div><h3>Background</h3><p>Pregnenolone<span><span> is a precursor of various steroid hormones involved in osteoblast proliferation, </span>microtubules polymerization<span><span> and cell survival protection. Previous reports focused on the effects of pregnenolone metabolites on stem cell proliferation and differentiation; however, the effects of pregnenolone itself has not been well explored. The present study aimed to investigate the role of pregnenolone on </span>NSC proliferation and to determine the doses required for NSC differentiation as well as the various genes involved in its mechanism of action.</span></span></p></div><div><h3>Methods</h3><p><span>NSCs were isolated from the embryonic cortex of E14 mice, incubated for 5 days, and then treated with pregnenolone doses of 2, 5, 10, 15 and 20 μM for another 5 days. The number of neurospheres and neurosphere derived cells were then counted. Flow cytometry was used to evaluate the differentiation of NSCs into </span>oligodendrocytes<span>, astrocytes, and neurons. The expression level of Notch1, Pax6 and Sox10 genes were also measured by Real Time PCR after 5 days of treatment.</span></p></div><div><h3>Results</h3><p>Our data suggest that treatment with 10 μM pregnenolone is optimal for NSC proliferation. In fact, this concentration caused the highest increase in the number of neurospheres and neurosphere derived cells, compared to the control group. In addition, treatment with low doses of pregnenolone (5 and 10 μM) caused a significant increase in NSC differentiation towards immature (Olig2⁺) and mature (MBP⁺) oligodendrocyte cell populations, compared to controls. However, NSC differentiation into neurons (beta <em>III</em> tubulin ⁺<span> cells) increased in all treatment groups, with the highest and most significant increase obtained at 15 μM concentration. It is worth noting that pregnenolone at the highest concentration of 15 μM decreased the number of astrocytes (GFAP+). Furthermore, there was an increase of Sox10 expression with low pregnenolone doses, leading to oligodendrogenesis, whereas Notch1 and Pax6 gene expression increased in pregnenolone groups with more neurogenesis.</span></p></div><div><h3>Conclusion</h3><p>Pregnenolone regulates NSCs proliferation <em>in vitro</em>. Treatment with low doses of pregnenolone caused an increase in the differentiation of NSCs into mature oligodendrocytes while higher doses increased the differentiation of NSCs into neurons. Oligodendrogenesis was accompanied by Sox10 while neurogenesis occurred together with Notch1 and Pax6 expression.</p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"163 ","pages":"Article 105489"},"PeriodicalIF":4.2,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10821729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influence of anti-obesity strategies on brain function in health and review: A review","authors":"Keila Rufatto de Souza,&nbsp;Nicole Alessandra Engel,&nbsp;Ana Beatriz Costa,&nbsp;Hevylin Jacintho Soares,&nbsp;Catarina Barbosa Chaves Bressan,&nbsp;Mariana Pacheco de Oliveira,&nbsp;Larissa Marques Dela Vedova,&nbsp;Larissa Espindola da Silva,&nbsp;Talita Farias Mendes,&nbsp;Mariella Reinol da Silva,&nbsp;Gislaine Tezza Rezin","doi":"10.1016/j.neuint.2022.105468","DOIUrl":"10.1016/j.neuint.2022.105468","url":null,"abstract":"<div><p>The aim of this review was to investigate in the literature the application of strategies such as low carbohydrate diet (LCD), ketogenic diet<span> (KD) and intermittent fasting (IF) and their effects on the CNS. We performed a narrative review of the literature. The search was specifically carried out in PubMed, selecting articles in English, which had the following keywords: obesity, central nervous system, low carb diet, ketogenic diet and intermittent fasting, using the narrative review methodology. The studies found show that the benefits of the LCD, KD and IF strategies, at the CNS level, have a strong influence on the mechanisms of hunger and satiety, as well as on the reduction of food reward and show improvement in memory and mood influenced by the interventions.</span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"163 ","pages":"Article 105468"},"PeriodicalIF":4.2,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9258539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Blockade of receptor for advanced glycation end-products with azeliragon ameliorates streptozotocin-induced diabetic neuropathy","authors":"Simeng Ma ,&nbsp;Yoki Nakamura ,&nbsp;Kazue Hisaoka-Nakashima,&nbsp;Norimitsu Morioka","doi":"10.1016/j.neuint.2022.105470","DOIUrl":"10.1016/j.neuint.2022.105470","url":null,"abstract":"<div><p><span><span>Treatment options for diabetic neuropathy are suboptimal, so development of a new therapeutic strategy is urgent. We focused on the role of receptor for advanced glycation end-products (RAGE) in diabetic neuropathy. We elaborated the effects of </span>azeliragon<span><span> (orally available small-molecule antagonist of RAGE) on streptozotocin (STZ)-induced mechanical hypersensitivity in mice. A reduction in mechanical nociceptive threshold observed 28 days after STZ treatment was improved by </span>single administration of azeliragon (10 and 30 mg/kg) at 3 h, but this effect disappeared at 24 h. Conversely, repeat administration (three times; days 28, 30, and 32) of azeliragon (30 mg/kg) enhanced the antinociceptive effect significantly compared with that obtained upon single administration, and this effect persisted at least up to 24 h. The antinociceptive effect of azeliragon (30 mg/kg) was almost comparable with that of </span></span>pregabalin<span> (30 mg/kg). These drug treatments had no effect on blood glucose levels. Our findings suggest that RAGE might be an effective target for diabetic neuropathy treatment.</span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"163 ","pages":"Article 105470"},"PeriodicalIF":4.2,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10701081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anxiolytic- and antidepressant-like effects of Bacillus coagulans Unique IS-2 mediate via reshaping of microbiome gut-brain axis in rats","authors":"Srilakshmi Satti ,&nbsp;Mani Surya Kumar Palepu ,&nbsp;Aditya A. Singh ,&nbsp;Yash Jaiswal ,&nbsp;Surya Prakash Dash ,&nbsp;Siva Nageswara Rao Gajula ,&nbsp;Sowmya Chaganti ,&nbsp;Gananadhamu Samanthula ,&nbsp;Rajesh Sonti ,&nbsp;Manoj P. Dandekar","doi":"10.1016/j.neuint.2023.105483","DOIUrl":"10.1016/j.neuint.2023.105483","url":null,"abstract":"<div><h3>Background</h3><p><span>Due to the rising cases of treatment-refractory affective disorders, the discovery of newer therapeutic approaches is needed. In recent times, probiotics have garnered notable attention in managing stress-related disorders. Herein, we examined the effect of </span><span><em>Bacillus coagulans</em></span><span> Unique IS-2® probiotic on anxiety- and depression-like phenotypes employing maternal separation (MS) and chronic-unpredictable mild stress (CUMS) model in rats.</span></p></div><div><h3>Methods</h3><p>Both male and female Sprague-Dawley rats were subjected to MS + CUMS. Probiotic treatment was provided for 6 weeks via drinking water. Anxiety- and depression-like phenotypes were assessed using sucrose-preference test (SPT), forced-swimming test (FST), elevated-plus maze test (EPM), and open-field test (OFT). Blood, brain, intestine, and fecal samples were obtained for biochemical and molecular studies.</p></div><div><h3>Results</h3><p><span>Stress-exposed rats drank less sucrose solution, showed increased passivity, and explored less in open-arms in SPT, FST, and EPM, respectively. These stress-generated neurobehavioral aberrations were alleviated by 6-week of </span><em>Bacillus coagulans</em><span> Unique IS-2 treatment. The overall locomotor activity in OFT remained unchanged. The decreased levels of BDNF<span> and serotonin and increased levels of C-reactive protein, TNF-α, IL-1β, and dopamine, in the hippocampus and/or frontal cortex of stress-exposed rats were reversed following probiotic treatment. Administration of probiotic also restored the systemic levels of L-tryptophan, L-kynurenine, kynurenic-acid, and 3-hydroxyanthranilic acid, villi/crypt ratio, goblet-cell count, </span></span><span><em>Firmicutes</em></span> to <span><em>Bacteroides</em></span><span><span> ratio, and levels of acetate, propionate, and </span>butyrate<span> in fecal samples. These results indicate remodeling of the microbiome gut-brain axis in </span></span><em>Bacillus coagulans</em><span> Unique IS-2 recipient rats. However, protein levels of doublecortin, GFAP, and zona occludens in the hippocampus and occludin-immunoreactivity in the intestine remained unchanged. No prominent sex-specific changes were noted.</span></p></div><div><h3>Conclusion</h3><p>Anxiolytic- and antidepressant-like effects of <em>Bacillus coagulans</em> Unique IS-2 in MS + CUMS rat model may be mediated via reshaping the microbiome gut-brain axis.</p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"163 ","pages":"Article 105483"},"PeriodicalIF":4.2,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9258550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-inflammatory effects of dopamine on microglia and a D1 receptor agonist ameliorates neuroinflammation of the brain in a rat delirium model","authors":"Yuki Nishikawa ,&nbsp;Mohammed E. Choudhury ,&nbsp;Kanta Mikami ,&nbsp;Taisei Matsuura ,&nbsp;Madoka Kubo ,&nbsp;Masahiro Nagai ,&nbsp;Satoru Yamagishi ,&nbsp;Tomomi Doi ,&nbsp;Manami Hisai ,&nbsp;Haruto Yamamoto ,&nbsp;Chisato Yajima ,&nbsp;Tasuku Nishihara ,&nbsp;Naoki Abe ,&nbsp;Hajime Yano ,&nbsp;Toshihiro Yorozuya ,&nbsp;Junya Tanaka","doi":"10.1016/j.neuint.2023.105479","DOIUrl":"10.1016/j.neuint.2023.105479","url":null,"abstract":"<div><p><span><span>Microglia play a central role in neuroinflammatory processes by releasing proinflammatory mediators. This process is tightly regulated along with </span>neuronal activities<span>, and neurotransmitters may link neuronal activities to the microglia. In this study, we showed that primary cultured rat microglia express the dopamine (DA) D1 receptor (D1R) and D4R, but not D2R, D3R, or D5R. In response to a D1R-specific agonist SKF-81297 (SKF), the cultured microglia exhibited increased intracellular cAMP levels. DA and SKF suppressed </span></span>lipopolysaccharide<span><span> (LPS)-induced expression of interleukin-1β (IL-1β) and tumor necrosis α (TNFα) in cultured microglia. Microglia in the normal mature rat prefrontal cortex (PFC) were sorted and significant expression of D1R, D2R, and D4R was observed. A delirium model was established by administering LPS intraperitoneally to mature male </span>Wistar rats<span><span>. The model also displayed sleep-wake disturbances as revealed by electroencephalogram and electromyogram recordings as well as increased expression of IL-1β and TNFα in the PFC. DA levels were increased in the PFC 21 h after LPS administration. Increased cytokine expression was observed in sorted microglia from the PFC of the delirium model; however, TNFα, but not IL-1β expression, was abruptly decreased 21 h after LPS administration in the delirium model, whereas DA levels were increased. A D1R antagonist SCH23390 partially abolished the TNFα expression change. This suggests that endogenous DA may play a role in suppressing </span>neuroinflammation<span>. Administration of the DA precursor L-DOPA or SKF to the delirium model rats inhibited the expression of IL-1β and TNFα. The simultaneous administration of clozapine, a D4R antagonist, strengthened the suppressive effects of L-DOPA. These results suggest that D1R mediates the suppressive effects of LPS-induced neuroinflammation, in which microglia may play an important role. Agonists for D1R may be effective for treating delirium.</span></span></span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"163 ","pages":"Article 105479"},"PeriodicalIF":4.2,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10701903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pulsed electric fields stimulate microglial transmitter release of VEGF, IL-8 and GLP-1 and activate endothelial cells through paracrine signaling","authors":"Frederikke Hyldahl,&nbsp;Elisabeth Hem-Jensen,&nbsp;Ulrik L. Rahbek,&nbsp;Katerina Tritsaris,&nbsp;Steen Dissing","doi":"10.1016/j.neuint.2022.105469","DOIUrl":"10.1016/j.neuint.2022.105469","url":null,"abstract":"<div><p><span><span>As action potentials propagate along an axon, pulsed extracellular electric fields (E-fields) are induced. We investigated the role of E-fields in activating microglia cells and affecting capillary function and found that E-fields control human microglia secretions in concert with purinergic factors. We generated E-fields by applying transcranial pulsed </span>electromagnetic fields<span><span><span> (T-PEMF) identical to those appearing outside neurons as action potentials propagate. T-PEMF alone enhanced mRNA synthesis for VEGF, IL-8, IL-6 and the </span>proglucagon<span> gene as well as the PC1/3 enzyme that cleaves the proglucagon protein to </span></span>glucagon<span> and GLP-1 proteins. We found that T-PEMF enhanced secretion from microglia of VEGF, IL-8 and GLP-1 proteins having angiogenic and proliferative profiles. Interestingly, T-PEMF and purinergic transmitters together enhanced secretions confirming synergy between their actions. ATP also induced nitric oxide (NO) syntheses in distinct locations in the nucleus and the mRNA synthesis for the responsible iNOS was reduced by T-PEMF. When the microglia-secretory fluid was added to brain endothelial cells we saw vivid Ca</span></span></span>²⁺<span> signaling and enhanced transcription of mRNA for IL-8 and VEGF. Our previous work shows that applying T-PEMF to the human brain provides up to 60% remission for patients with refractory depressions within 8 weeks and improvements for Parkinson patients. Thus, physiological E-fields activate microglia, work synergistically with neurotransmitters, and cause paracrine secretions which cause activation of capillaries. Application of these E-Fields is effective for treating refractory depressions and appear promising for treating neurodegenerative brain diseases.</span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"163 ","pages":"Article 105469"},"PeriodicalIF":4.2,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9258540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"microRNA as a therapeutic for ischemic stroke","authors":"Raluca Todoran ,&nbsp;Sarina R. Falcione ,&nbsp;Michael Clarke ,&nbsp;Twinkle Joy ,&nbsp;Roobina Boghozian ,&nbsp;Glen C. Jickling","doi":"10.1016/j.neuint.2023.105487","DOIUrl":"10.1016/j.neuint.2023.105487","url":null,"abstract":"<div><p><span>microRNA (miRNA) are important regulators of gene expression. miRNA have the potential as a treatment to modulate genes, pathways and cells involved in </span>ischemic stroke<span><span>. In this review, we specifically present miRNA in stroke as a treatment to decrease thrombosis, reduce blood brain barrier<span> (BBB) disruption and hemorrhagic transformation (HT), modulate inflammation, and modify angiogenesis. miRNA as a treatment for stroke is an emerging area with evidence from animal studies demonstrating its potential. While no miRNA is currently approved for human use, several have shown promise in </span></span>clinical trials to treat medical conditions, such as miR-122 for hepatitis C. The role of miRNA as a treatment for specific applications in ischemic stroke is presented including a discussion of the benefits and barriers of miRNA as a treatment, and directions for future advancement.</span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"163 ","pages":"Article 105487"},"PeriodicalIF":4.2,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10689771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selectively compromised inner retina function following hypoxic-ischemic encephalopathy in mice: A noninvasive measure of severity of the injury","authors":"Onur E. Taparli ,&nbsp;Pawan K. Shahi ,&nbsp;Nur Sena Cagatay ,&nbsp;Nur Aycan ,&nbsp;Burak Ozaydin ,&nbsp;Sefer Yapici ,&nbsp;Xinying Liu ,&nbsp;Ulas Cikla ,&nbsp;Dila Zafer ,&nbsp;Jens C. Eickhoff ,&nbsp;Peter Ferrazzano ,&nbsp;Bikash R. Pattnaik ,&nbsp;Pelin Cengiz","doi":"10.1016/j.neuint.2022.105471","DOIUrl":"10.1016/j.neuint.2022.105471","url":null,"abstract":"<div><p>The intricate system of connections between the eye and the brain implies that there are common pathways for the eye and brain that get activated following injury. Hypoxia-ischemia (HI) related encephalopathy is a consequence of brain injury caused by oxygen and blood flow deprivation that may result in visual disturbances and neurodevelopmental disorders in surviving neonates. We have previously shown that the tyrosine<span><span> receptor kinase B (TrkB) agonist/modulator improves neuronal survival and long-term neuroprotection in a sexually differential way. In this study, we tested the hypotheses that; 1) TrkB agonist therapy improves the visual function in a sexually differential way; 2) Visual function detected by electroretinogram (ERG) correlates with severity of brain injury detected by magnetic resonance (MRI) imaging following neonatal HI in mice. To test our hypotheses, we used C57/BL6 mice at postnatal day (P) 9 and subjected them to either Vannucci's rodent model of neonatal HI or sham surgery. ERG was performed at P 30, 60, and 90. MRI was performed following the completion of the ERG. ERG in these mice showed that the a-wave is normal, but the b-wave amplitude is severely abnormal, reducing the b/a wave amplitude ratio. Inner retina function was found to be perturbed as we detected severely attenuated </span>oscillatory potential after HI. No sex differences were detected in the injury and severity pattern to the retina as well as in response to 7,8-DHF therapy. Strong correlations were detected between the percent change in b/a ratio and percent hemispheric/hippocampal tissue loss obtained by MRI, suggesting that ERG is a valuable noninvasive tool that can predict the long-term severity of brain injury.</span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"163 ","pages":"Article 105471"},"PeriodicalIF":4.2,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9258541","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}