Provided herein non-human transgenic animals comprising a genome that: i) under-expresses, or is inducible to under-express, Hu Antigen R (HuR) in at least some neurons of said transgenic animal; ii) does not express HuR, or is inducible to not express HuR, in at least some neurons of said transgenic animal; or iii) does not express functional HuR, or is inducible to not express functional HuR in at least some neurons of said transgenic animal, as well as methods of screening drugs and therapies (e.g., useful in treating ALS) using such animals.

The present invention relates to a composition for treating neuroinflammatory disease comprising a complement component 8 gamma protein or a fragment thereof, and more particularly, to use for treating neuroinflammatory disease of a complement component 8 gamma protein or a fragment thereof which exhibits an effect of reducing the expression of inflammatory cytokines in microglia. The composition of the present invention has effects of reducing Alzheimer's abnormal behavior patterns and reducing the secretion of neuroinflammatory cytokines in brain microglia and thus can be very usefully used for development of an agent for preventing or treating neuroinflammatory disease.

The present disclosure relates to a method for restoring brainwave impairment in Alzheimer's brain using optogenetic technology. The method for restoring brainwave impairment in Alzheimer's brain according to the present disclosure can restore brainwave impairment in Alzheimer's brain to a normal level by specifying inhibitory neurons associated with brainwave impairment in Alzheimer's disease and selectively activating impaired neurons through optical stimulation rather than electrical stimulation.

The present invention relates to microglial or myeloid expressed Alzheimer's disease associated (ME-AD) gene reporter constructs, cell lines and transgenic animals and their use for identifying agents that modulate the level or expression of ME-AD genes.

A system is provided comprising a plurality of C. elegans cultures, where each culture comprises a transgenic C. elegans strain that models a mammalian disease or condition. Methods of using a system, e.g., for characterizing microbial strains of a mammalian microbiome and determining whether such microbial strains affect a mammalian disease or disorder.

This invention is generally related to novel compositions and methods for treating or preventing fibrosis, diseases or disorders associated with fibrosis, neurodegeneration, diseases or disorders associated with neurodegeneration and cardiovascular disease or disorders.

The present disclosure relates to a method for preparing an Alzheimer's disease (AD) animal model, including: selecting healthy male human ApoE4 transgenic mice, and intraperitoneally injecting a 4 mmol/L Al(mal).sub.3 solution at a volume of 10 ml/kg, with aluminum exposure for 60 days, and interval time of 2 days for every 5 days, to obtain an AD animal model co-induced by genetic and environmental factors which are interacted without being simply superimposed. The AD animal model established according to the method of the examples in the present disclosure can express the characteristic pathological changes of AD and has the characteristics of learning and memory impairment. The AD animal model provided by the present disclosure can be used for drug screening and AD mechanism research, and has the advantages of stable properties, prominent reproducibility, easy operation, and low cost.

Provided herein, in some embodiments, are methods for modulating expression and/or activity of disks large-associated protein 2 (DLGAP2), as well as methods of treating age-related cognitive decline, such as Alzheimer's disease.

The present invention provides a transgenic invertebrate model for Alzheimer's disease and a method for screening a therapeutic agent for Alzheimer's disease using the model. The present invention provides a transgenic invertebrate, in which genes encoding enzymes involved in production of a ganglioside are introduced and the ganglioside is expressed.

The present invention provides a tau exon 10 skipping-promoting antisense oligonucleotide containing at least one 2′-O, 4′-C-ethylene-bridged nucleic acid, and a nucleotide sequence complementary to a sequence consisting of at least 10 continuous nucleotides in a region consisting of the nucleotide sequence shown in SEQ ID NO: 44 in exon 10 of a tau mRNA precursor. In addition, the present invention provides a tau exon 10 skipping-suppressing antisense oligonucleotide containing at least one 2′-O, 4′-C-ethylene-bridged nucleic acid, and a nucleotide sequence complementary to a sequence consisting of at least 10 continuous nucleotides in a region consisting of the nucleotide sequence shown in SEQ ID NO: 45 in intron 10 of a tau mRNA precursor.