Journal of neurogenetics最新文献

{"title":"TERT distal promoter GC islands are critical for telomerase and together with DNMT3B silencing may serve as a senescence-inducing agent in gliomas.","authors":"Naz Şerifoğlu,&nbsp;Begün Erbaba,&nbsp;Michelle M Adams,&nbsp;Ayça Arslan-Ergül","doi":"10.1080/01677063.2022.2106371","DOIUrl":"https://doi.org/10.1080/01677063.2022.2106371","url":null,"abstract":"<p><p>Telomerase is reactivated in the majority of cancers. For instance, in gliomas, it is common that the TERT promoter is mutated. Research on telomere promoter GC islands have been focused primarily on proximal TERT promoter but little is known about the distal promoter. Therefore, in this study, we investigated the proximal and distal TERT promoter, in terms of DNA methylation. We did bisulfite sequencing in zebrafish tissue samples for the distal tert promoter. In the zebrafish brain tissues, we identified a hypomethylation site in the tert promoter, and found that this hypomethylation was associated with aging and shortened telomeres. Through site directed mutagenesis in glioma cell lines, we changed 10 GC spots individually, cloned into a reporter vector, and measured promoter activity. Finally, we silenced DNMT3B and measured telomerase activity along with vidaza and adriamycin treatments. Site directed mutagenesis of glioma cell lines revealed that each of the 10 GC spots are critical for telomerase activity. Changing GC to AT abolished promoter activity in all spots when transfected into glioma cell lines. Then, through silencing of DNMT3B, we observed a reduction in hTERT expression levels, while hTR remained the same, and a major increase in senescence-associated beta-galactosidase activity. Finally, we propose a model regarding the efficacy of two chemotherapeutic drugs, adriamycin and azacytidine, on gliomas. Here, we show that distal TERT promoter is critical; changing even one GC to AT abolishes TERT promoter activity. DNMT3B, a de novo methyltransferase, together with GC islands in distal TERT promoter plays an important role in regulation of telomerase expression and senescence.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":"36 4","pages":"89-97"},"PeriodicalIF":1.9,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10477786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An expansion of phenotype: novel homozygous variant in the <i>MED17</i> identified in patients with progressive microcephaly and global developmental delay.","authors":"Rafiullah Rafiullah,&nbsp;Alia M Albalawi,&nbsp;Sultan R Alaradi,&nbsp;Majed Alluqmani,&nbsp;Muhammad Mushtaq,&nbsp;Abdul Wali,&nbsp;Sulman Basit","doi":"10.1080/01677063.2022.2149748","DOIUrl":"https://doi.org/10.1080/01677063.2022.2149748","url":null,"abstract":"<p><p>Global developmental delay (GDD) is a lifelong disability that affects 1-3% of the population around the globe. It is phenotypically variable and highly heterogeneous in terms of the underlying genetics. Patients with GDD are intellectually disabled (ID) manifesting cognitive impairment and deficient adaptive behavior. Here, we investigated a two-looped consanguineous family segregating severe ID, seizure, and progressive microcephaly. Magnetic resonance imaging (MRI) of the brain showed mild brain atrophy and myelination defect. Whole exome sequencing (WES) was performed on the DNA samples of two patients and a novel homozygous missense variant (Chr11:g0.93528085; NM_004268.5_c.871T > C; p. Trp291Gly) was identified in the MED17 gene. Sanger sequencing revealed that the identified variant is heterozygous in both parents and healthy siblings. This variant is conserved among different species, causes a non-conserved amino acid change, and is predicted deleterious by various in silico tools. The variant is not reported in population variant databases. MED17 (OMIM: 613668) encodes for the mediator of RNA polymerase II transcription complex subunit 17. Structure modeling of MED17 protein revealed that Trp291 is involved in different inter-helical interactions, providing structural stability. Replacement of Trp291Gly, a less hydrophobic amino acid loses the inter-helical interaction leading to a perturb variant of MED17 protein.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":"36 4","pages":"108-114"},"PeriodicalIF":1.9,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10484594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Possible association between the <i>lrrk2</i> gene and anxiety behavior: a systematic literature review.","authors":"R E Moreira-Júnior,&nbsp;R M Souza,&nbsp;J G de Carvalho,&nbsp;J P Bergamini,&nbsp;A L Brunialti-Godard","doi":"10.1080/01677063.2022.2144293","DOIUrl":"https://doi.org/10.1080/01677063.2022.2144293","url":null,"abstract":"<p><p>Alterations to the <i>LRRK2</i> gene have been associated with Parkinson's disease and alcohol consumption in animals and humans. Furthermore, these disorders are strongly related to anxiety disorders (ADs). Thus, we investigated how the <i>LRRK2</i> gene might influence anxiety in humans and mice. We elaborated a systematic review based on the <i>PRISMA</i> Statement of studies that investigated levels of anxiety in animal or human models with alterations in the <i>LRRK2</i> gene. The search was conducted in the PubMed, Scopus, and Web of Science databases, and in reference lists with descriptors related to ADs and the <i>LRRK2</i>. From the 62 articles assessed for eligibility, 16 were included: 11 conducted in humans and seven, in mice. <i>Lrrk2</i> KO mice and the <i>LRRK2</i> G2019S, <i>LRRK2 R1441G</i>, and <i>LRRK2</i> R1441C variants were addressed. Five articles reported an increase in anxiety levels concerning the <i>LRRK2</i> variants. Decreased anxiety levels were observed in two articles, one focusing on the <i>LRRK2</i> G2019S and the other, on the <i>Lrrk2</i> KO mice. Eight other articles reported no differences in anxiety levels in individuals with <i>Lrrk2</i> alterations compared to their healthy controls. This study discusses a possible influence between the <i>LRRK2</i> gene and anxiety, adding information to the existing knowledge respecting the influence of genetics on anxiety.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":"36 4","pages":"98-107"},"PeriodicalIF":1.9,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10845372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Knockdown of PHLDA2 promotes apoptosis and autophagy of glioma cells through the AKT/mTOR pathway.","authors":"Chengyong Guo,&nbsp;Shuo Liu,&nbsp;Tao Zhang,&nbsp;Jipeng Yang,&nbsp;Zhaohui Liang,&nbsp;Shengkui Lu","doi":"10.1080/01677063.2022.2096023","DOIUrl":"https://doi.org/10.1080/01677063.2022.2096023","url":null,"abstract":"<p><p>Pleckstrin homology like domain family A member 2 (PHLDA2) is an imprinted gene expressed in placenta and has been shown to be associated with tumor progression. However, the effect of PHLDA2 on glioma cell growth has not been reported yet. Data based on TCGA database showed that PHLDA2 was up-regulated in glioma tissues. Moreover, PHLDA2 was also elevated in glioma cells. Functional assays showed that siRNA-mediated knockdown of PHLDA2 reduced cell viability of glioma cells and suppressed the cell proliferation. Cell apoptosis of glioma cells was promoted by silencing of PHLDA2 with increased Bax and decreased Bcl-2. Silencing of PHLDA2 reduced protein expression of p62, enhanced LC3 and Beclin1 to promote autophagy. Phosphorylated AKT and mTOR were down-regulated in glioma cells by interference of PHLDA2. In conclusion, downregulation of PHLDA2 inhibited glioma cell proliferation, and promoted cell apoptosis and autophagy through inactivation of AKT/mTOR signaling.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":"36 2-3","pages":"74-80"},"PeriodicalIF":1.9,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10339877","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The light-activated TRP channel: the founding member of the TRP channel superfamily.","authors":"Baruch Minke,&nbsp;William L Pak","doi":"10.1080/01677063.2022.2121824","DOIUrl":"https://doi.org/10.1080/01677063.2022.2121824","url":null,"abstract":"<p><p>The <i>Drosophila</i> light-activated Transient Receptor Potential (TRP) channel is the founding member of a large and diverse family of channel proteins. The <i>Drosophila</i> TRP (dTRP) channel, which generates the electrical response to light has been investigated in a great detail two decades before the first mammalian TRP channel was discovered. Thus, dTRP is unique among members of the TRP channel superfamily because its physiological role and the enzymatic cascade underlying its activation are established. In this article we outline the research leading to elucidation of dTRP as the light activated channel and focus on a major physiological property of the dTRP channel, which is indirect activation via a cascade of enzymatic reactions. These detailed pioneering studies, based on the genetic dissection approach, revealed that light activation of the <i>Drosophila</i> TRP channel is mediated by G-Protein-Coupled Receptor (GPCR)-dependent enzymatic cascade, in which phospholipase C β (PLC) is a crucial component. This physiological mechanism of <i>Drosophila</i> TRP channel activation was later found in mammalian TRPC channels. However, the initial studies on the mammalian TRPV1 channel indicated that it is activated directly by capsaicin, low pH and hot temperature (>42 °C). This mechanism of activation was apparently at odds with the activation mechanism of the TRPC channels in general and the <i>Drosophila</i> light activated TRP/TRPL channels in particular, which are target of a GPCR-activated PLC cascade. Subsequent studies have indicated that under physiological conditions TRPV1 is also target of a GPCR-activated PLC cascade in the generation of inflammatory pain. The <i>Drosophila</i> light-activated TRP channel is still a useful experimental paradigm because its physiological function as the light-activated channel is known, powerful genetic techniques can be applied to its further analysis, and signaling molecules involved in the activation of these channels are available.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":"36 2-3","pages":"55-64"},"PeriodicalIF":1.9,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10709524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The force-from-lipid principle and its origin, a '<i>what is true for E. coli is true for the elephant'</i> refrain.","authors":"Boris Martinac,&nbsp;Ching Kung","doi":"10.1080/01677063.2022.2097674","DOIUrl":"https://doi.org/10.1080/01677063.2022.2097674","url":null,"abstract":"<p><p>The force-from-lipid (FFL) principle states that it is the lateral stretch force from the lipid membrane that ultimately opens mechanosensitive (MS) channels, not the external tether nor the internal cytoskeleton. Piezo channels for certain touch or proprioception and the hair-cell channels for hearing or balance apparently obey this principle, which is based on the idea that the lipid bilayer is an amphipathic compartment with a distinct internal force-distribution profile. Physical stretch or insertion of chemical impurities alters this profile, driving channel shape change to conform to the new environment. Thus, FFL governs all dynamic proteins embedded in membrane, including Kv's and TRPs. This article retraces the humble origin of the FFL concept. <i>Paramecium</i> research first created the mind set and the resources to electrically explore other microbial membranes. Patch clamp revealed MS-channel activities from yeast and <i>E. coli</i> spheroplasts. Despite formidable obstacles against interdisciplinary research, the <i>E. coli</i> MS-channel protein, MscL, was purified through fractionation by following its activity, much like enzyme purification. Reconstituted into a simple lipid bilayer, pure MscL retains mechanosensitivity, thus firmly establishing the FFL principle in 1994. The relatively simple MscL and its functional cousin MscS soon became ideal models for detailed analyses. Like the DNA-RNA-protein 'central dogma' or ATP synthesis, FFL is a fundamental principle, which appeared early in evolution, retained in all cellular life forms, and is expected to contribute to future molecular research on sensations, homeostasis, and embryonic development.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":"36 2-3","pages":"44-54"},"PeriodicalIF":1.9,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10707764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Abnormal larval neuromuscular junction morphology and physiology in <i>Drosophila</i> prickle isoform mutants with known axonal transport defects and adult seizure behavior.","authors":"Atsushi Ueda,&nbsp;Tristan C D G O'Harrow,&nbsp;Xiaomin Xing,&nbsp;Salleh Ehaideb,&nbsp;J Robert Manak,&nbsp;Chun-Fang Wu","doi":"10.1080/01677063.2022.2093353","DOIUrl":"https://doi.org/10.1080/01677063.2022.2093353","url":null,"abstract":"<p><p>Previous studies have demonstrated the striking mutational effects of the <i>Drosophila</i> planar cell polarity gene <i>prickle (pk)</i> on larval motor axon microtubule-mediated vesicular transport and on adult epileptic behavior associated with neuronal circuit hyperexcitability. Mutant alleles of the <i>prickle</i>-<i>prickle</i> (<i>pk^pk</i>) and <i>prickle</i>-<i>spiny-legs</i> (<i>pk^sple</i>) isoforms (hereafter referred to as <i>pk</i> and <i>sple</i> alleles, respectively) exhibit differential phenotypes. While both <i>pk</i> and <i>sple</i> affect larval motor axon transport, only <i>sple</i> confers motor circuit and behavior hyperexcitability. However, mutations in the two isoforms apparently counteract to ameliorate adult motor circuit and behavioral hyperexcitability in heteroallelic <i>pk^pk/pk^spl</i>^e flies. We have further investigated the consequences of altered axonal transport in the development and function of the larval neuromuscular junction (NMJ). We uncovered robust dominant phenotypes in both <i>pk</i> and <i>sple</i> alleles, including synaptic terminal overgrowth (as revealed by anti-HRP and -Dlg immunostaining) and poor vesicle release synchronicity (as indicated by synaptic bouton focal recording). However, we observed recessive alteration of synaptic transmission only in <i>pk/pk</i> larvae, i.e. increased excitatory junctional potential (EJP) amplitude in <i>pk/pk</i> but not in <i>pk</i>/+ or <i>sple</i>/<i>sple</i>. Interestingly, for motor terminal excitability sustained by presynaptic Ca²⁺ channels, both <i>pk</i> and <i>sple</i> exerted strong effects to produce prolonged depolarization. Notably, only <i>sple</i> acted dominantly whereas <i>pk</i>/+ appeared normal, but was able to suppress the <i>sple</i> phenotypes, i.e. <i>pk/sple</i> appeared normal. Our observations contrast the differential roles of the <i>pk</i> and <i>sple</i> isoforms and highlight their distinct, variable phenotypic expression in the various structural and functional aspects of the larval NMJ.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":"36 2-3","pages":"65-73"},"PeriodicalIF":1.9,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10689881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Abnormalities of neural stem cells in Lesch-Nyhan disease.","authors":"Ashok R Dinasarapu, Diane J Sutcliffe, Fatemeh Seifar, Jasper E Visser, H A Jinnah","doi":"10.1080/01677063.2022.2129632","DOIUrl":"10.1080/01677063.2022.2129632","url":null,"abstract":"<p><p>Lesch-Nyhan disease (LND) is a neurodevelopmental disorder caused by variants in the <i>HPRT1</i> gene, which encodes the enzyme hypoxanthine-guanine phosphoribosyl transferase (HGprt). HGprt deficiency provokes numerous metabolic changes which vary among different cell types, making it unclear which changes are most relevant for abnormal neural development. To begin to elucidate the consequences of HGprt deficiency for developing human neurons, neural stem cells (NSCs) were prepared from 6 induced pluripotent stem cell (iPSC) lines from individuals with LND and compared to 6 normal healthy controls. For all 12 lines, gene expression profiles were determined by RNA-seq and protein expression profiles were determined by shotgun proteomics. The LND lines revealed significant changes in expression of multiple genes and proteins. There was little overlap in findings between iPSCs and NSCs, confirming the impact of HGprt deficiency depends on cell type. For NSCs, gene expression studies pointed towards abnormalities in WNT signaling, which is known to play a role in neural development. Protein expression studies pointed to abnormalities in the mitochondrial F₀F₁ ATPase, which plays a role in maintaining cellular energy. These studies point to some mechanisms that may be responsible for abnormal neural development in LND.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":"36 2-3","pages":"81-87"},"PeriodicalIF":1.9,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9847586/pdf/nihms-1862228.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9464385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The origins of the force-from-lipid principle and the founding member of the TRP channel superfamily.","authors":"Chun-Fang Wu","doi":"10.1080/01677063.2022.2132104","DOIUrl":"https://doi.org/10.1080/01677063.2022.2132104","url":null,"abstract":"The 2021 Nobel Prize in Medicine and Physiology recognized the seminal work of David Julius, who established the temperature and pain sensory mechanisms based on the TRPV channel, and Ardem Patapoutian, who resolved the stretch activation mechanism for touch and proprietary sensation via Piezo channels. We are fortunate and proud to publish a special section on the force-from-lipid principle underlining Piezo channel activation and the origin of the first TRP channel, prepared by the pioneers who initiated the early work that led to the discoveries (Martinac & Kung, 2022; Minke & Pak, 2022). Professors Baruch Minke and William Pak recount the story of their early endeavor to reveal the phototransduction process mediated by the TRP channel in the fruit fly Drosophila. This light-sensitive TRP channel is now recognized as the founding member of the TRP channel superfamily, which encompasses a large category of channels underpinning different sensory mechanisms, including visual, auditory, thermal, and mechanosensory transduction. The functioning of Piezo channels turns out to be based on the same force-from-lipid principle, originating from lipid membrane lateral force without involving any cytoskeletal or cell adhesion molecules. As professors Ching Kung and Boris Martinac recount in their article, the initial finding actually originated from studies on a special strain of giant E. coli. Indeed, ‘what is true for E. coli is true for the elephant’.","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":"36 2-3","pages":"43"},"PeriodicalIF":1.9,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10709528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"lncRNA XIST induces Aβ accumulation and neuroinflammation by the epigenetic repression of NEP in Alzheimer's disease.","authors":"Xi-Wu Yan,&nbsp;Huai-Jun Liu,&nbsp;Yu-Xing Hong,&nbsp;Ting Meng,&nbsp;Jun Du,&nbsp;Cheng Chang","doi":"10.1080/01677063.2022.2028784","DOIUrl":"https://doi.org/10.1080/01677063.2022.2028784","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is the leading cause of dementia globally, but effective treatment is lacking. We aimed to explore lncRNA XIST role in AD and the mechanisms involved in the effect of changes in lncRNA XIST on the expression of Aβ-degrading enzymes. The mouse model of AD and the cell model induced by Aβ were established. LncRNA XIST, IDE, NEP, Plasmin, ACE, EZH2 expressions and distribution of XIST in the nucleus and cytoplasm were detected by qRT-PCR. Inflammatory cytokines IL-6, IL-1β, TNFα, IL-8, and Aβ42 levels were detected by ELISA. TUNEL was used to measure brain tissue damage. Cell proliferation was detected by CCK-8 assay. Flow cytometry detected cell apoptosis. RIP validated the combination of XIST and EZH2. ChIP verified that XIST recruits EZH2 to mediate enrichment of HEK27me3 in the NEP promoter region. The protein expression in brain tissues and cells was detected by Western blot. The expression of lncRNA XIST was increased in AD mice and cell models. Inflammation and injury of nerve cells occurred in AD mice and cell models. The knockdown of lncRNA XIST alleviated Aβ-induced neuronal inflammation and damage. LncRNA XIST affected the expression of Aβ-degrading enzyme NEP, and lncRNA XIST was negatively correlated with NEP expression in AD mice. LncRNA XIST regulated NEP expression partly through epigenetic regulation by binding with EZH2. LncRNA XIST mediated neuronal inflammation and injury through epigenetic regulation of NEP. Overall, our study found that lncRNA XIST induced Aβ accumulation and neuroinflammation by the epigenetic repression of NEP in AD.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":"36 1","pages":"11-20"},"PeriodicalIF":1.9,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39751382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}