LncRNA NEAT1 Inhibits Neuronal Apoptosis and Induces Neuronal Viability of Depressed Rats Via microRNA-320-3p/CRHR1 Axis.

Long noncoding RNA nuclear enriched abundant transcript 1 (NEAT1) has been reported to be involved in depression. This study aims to investigate the mechanism of NEAT1/microRNA (miR)-320-3p/Corticotropin-releasing hormone receptor 1 (CRHR1) axis in depressed rats. Rats with depression-like behaviors were prepared by exposing the rats to chronic unpredictable mild stress. Behavioral functions, pathological damage, neuronal apoptosis and monoamine neurotransmitter were examined in depressed rats . Primary hippocampal neurons were injured through simulation with corticosterone(CORT). Cell viability and apoptosis were measured in CORT-Induced hippocampal neurons. The binding relationship between NEAT1 and miR-320-3p and the targeting relationship between miR-320-3p and CRHR1 were detected. Elevated NEAT1, CRHR1 and reduced miR-320-3p exhibited in depressed rats and CORT-treated hippocampal neurons, NEAT1 bound to miR-320-3p to target CRHR1. Silencing NEAT1 or elevating miR-320-3p improved behavioral functions, attenuated pathological damage and apoptosis in the hippocampus, and increased monoamine neurotransmitter in depressed rats. Repression of NEAT1 or promotion of miR-320-3p enhanced viability and suppressed apoptosis of CORT-treated hippocampal neurons. The study highlights that NEAT1 competitively binds to miR-320-3p to up-regulate CRHR1 expression, thereby promoting hippocampal damage of depressed rats.

TDP-43 transports ribosomal protein mRNA to regulate axonal local translation in neuronal axons.

Mislocalization and abnormal deposition of TDP-43 into the cytoplasm (TDP-43 proteinopathy) is a hallmark in neurons of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). However, the pathogenic mechanism of the diseases linked to TDP-43 is largely unknown. We hypothesized that the failure of mRNA transport to neuronal axons by TDP-43 may contribute to neurodegeneration in ALS and FTLD, and sought to examine the function of TDP-43 by identifying its target mRNA for axonal transport. We found that mRNAs related to translational function including ribosomal proteins (RPs) were decreased by shRNA-based TDP-43 knock-down in neurites of cortical neurons. TDP-43 binds to and transports the RP mRNAs through their 5' untranslated region, which contains a common 5' terminal oligopyrimidine tract motif and a downstream GC-rich region. We showed by employing in vitro and in vivo models that the RP mRNAs were translated and incorporated into native ribosomes locally in axons to maintain functionality of axonal ribosomes, which is required for local protein synthesis in response to stimulation and stress to axons. We also found that RP mRNAs were reduced in the pyramidal tract of sporadic ALS cases harboring TDP-43 pathology. Our results elucidated a novel function of TDP-43 to control transport of RP mRNAs and local translation by ribosomes to maintain morphological integrity of neuronal axons, and proved the influence of this function of TDP-43 on neurodegeneration in ALS and FTLD associated with TDP-43 proteinopathy.

Generation of induced pluripotent stem cell(iPSC)line CJUHi001-A derived peripheral blood mononuclear cells of spinocerebellar ataxia type 1(SCA1) the CAG repeat mutation in ATXN1 gene.

Spinocerebellar ataxia type 1 (SCA1) is an autosomal dominant neurodegenerative disorder caused by CAG repeat mutations in the ATXN1 gene. In this study, we generated an induced pluripotent stem cell line (iPSC) by using non-integrating Sendai virus (SeV) from peripheral blood mononuclear cells(PBMCs)of SCA1 patient harboring a CAG repeat mutation in the ATXN1 gene. The induced patient-specific iPSC line with a normal karyotype and expresses pluripotent markers, it also shows differentiation totipotency and tridermogenesis in vitro. It may be an excellent model for studying spinocerebellar ataxia type 1 (SCA1) in vitro and will be beneficial for studying SCA1 pathogenesis and therapeutic intervention strategies.

A Neural Network Model of Smart Aging Combining Family Structure Change Factors.

In this paper, we analyze the changes in family structure and explore the changes in detail, based on which we construct a neural network model of smart aging. Based on the gender perspective, the individual growth model in the multilayer linear model is used to examine the effects of family structure changes on the elderly in terms of economic exchange, daily care, and emotional support. The results show that there is no significant gender difference in the family structure changes on the elderly in terms of economic exchange and daily care, but there is a significant gender difference in terms of emotional support. To solve the problem of data imbalance in the daily activity categories of the elderly, this paper resamples the data and uses different neural network models for activity recognition of the sensor data generated from the daily activities of the elderly. In this paper, the daily behavior patterns of the elderly over a while are studied by correlating three conditions of time distance, optimal path, and sensor distance to discover the daily behavior patterns of the elderly, while the abnormal behavior patterns can be well separated by EM clustering algorithm. The daily behavior of the elderly is a coarse-grained representation of their daily activities. It is not limited to a specific activity and does not require the sensor ID, trigger time, and location triggered by the activity to be consistent, but in long-term daily activity data, it abstracts the general behavior rules of the elderly activities. Through the research of this paper, the existing system is improved, and the multifaceted needs of the elderly are fully considered, from housing needs to spiritual needs, to face the current elderly care problems with a positive attitude, create a good social elderly care environment for the elderly, and realize the real elderly care.

Proteolipid protein 1 gene sequencing of hereditary spastic paraplegia.

PCR amplification and sequencing of whole blood DNA from an individual with hereditary spastic paraplegia, as well as family members, revealed a fragment of proteolipid protein 1 (PLP1) gene exon 1, which excluded the possibility of isomer 1 expression for this family. The fragment sequence of exon 3 and exon 5 was consistent with the proteolipid protein 1 sequence at NCBI. In the proband samples, a PLP1 point mutation in exon 4 was detected at the basic group of position 844, T→C, phenylalanine→leucine. In proband samples from a male cousin, the basic group at position 844 was C, but gene sequencing signals revealed mixed signals of T and C, indicating possible mutation at this locus. Results demonstrated that changes in PLP1 exon 4 amino acids were associated with onset of hereditary spastic paraplegia.

A linear trinuclear mixed valence vanadium(V/IV/V) complex: synthesis, characterization, and solution behavior.

The reaction between vanadium(III) acetylacetonate and N-hexanoylsalicylhydrazide (H3hshz) yields a linear trinuclear mixed valence vanadium(V/IV/V) complex, V3O3(hshz)2(OEt)2, 1 (where hshz3- is a triply deprotonated trianionic N-hexanoyl salicylichydrazidate), with a pseudo C2 symmetry. A V(IV)O2+ group is at the center of complex 1 and is spanned by two terminal vanadium(V) ions with a square pyramidal geometry bridged via hydrazido ligands. In the crystalline form, the oxo group of the central vanadium(IV) ion is weakly coordinated to one of the terminal square pyramidal vanadium(V) ions of the neighboring trinuclear complex to form a dimeric structure. These dimers are linked via bis mu-alkoxo bridges to form a one-dimensional zigzag chain structure. In chloroform or methylene dichloride, the weak linkages between the trinuclear complexes present in the crystalline form are broken, and only the mixed valence trinuclear complex can be identified. In dimethyl sulfoxide or dimethylformamide, the trinuclear complex partially dissociates, and the unligated ligands remain in equilibrium with the trinuclear complex.