Method for controlling for the appearance of seizures in the mammalian brain comprising modifying the abundance of a specific miRNA—miR-211, for uses in preventing seizures and providing a model system to examine the effect of a drug or a treatment to seizures.

Methods of treating a subject for a neurodegenerative disorder are provided. Aspects of the methods include administering to a subject in need thereof an effective amount of an agent that reduces the prevalence of lipid droplet accumulating microglia (LAM) to treat the subject for the neurodegenerative disorder. A variety of neurodegenerative disorders may be treated by practice of the methods. Also provided are methods of identifying lipid droplet-associated target genes, including target genes that are positive and negative regulators of lipid droplet formation, as well as methods of treating a neurodegenerative disorder in a subject by administering to the subject an antagonist of a positive regulator of lipid droplet formation and/or an agonist of a negative regulator of lipid droplet formation.

The present invention pertains to novel analgesics useful for treating mechanical pain. The invention suggests the use of inhibitors of α-tubulin acetylation for inhibition of neurological sensations that are mediated by sensory neurons. The perception of mechanical pain is can be modulated by altering the α-tubulin acetylation, in context of the invention in particular by modulation of the expression and/or activity of the enzyme α-tubulin acetyltransferase (Atat). The invention provides the medical application of α-tubulin acetyltransferase inhibitors as analgesics and a screening method for the identification of compounds useful in the treatment of pain.

Provided are a transgenic non-human mammal expressing a fusion protein, wherein the fusion protein comprises an ε subunit of an ATP synthase and two distinct fluorescent proteins as a donor and an acceptor for FRET, one of the fluorescent proteins being placed at an amino terminal moiety of the ε subunit and the other being placed at a carboxyl terminal moiety of the ε subunit, and a method of screening for an agent for preventing or treating diseases in a mammal in need thereof, comprising using an above transgenic non-human mammal.

The present disclosure provides a kit and method for constructing a long-acting depression animal model. The present disclosure adopts Bacille Calmette-Guerin (BCG) (or Mycobacterium bovis (M. bovis)) and low-dose pertussis toxin (PTX) for combined induction, which greatly reduces modeling cost. A mouse model constructed by the method of the present disclosure can clearly distinguish a time interval of pathological behaviors from a time interval of depression-like behaviors and has prominent face validity and predictive validity. The method of the present disclosure is simple and convenient and does not require a large number of tedious daily operations as the depression model construction by chronic unpredictable stress, chronic restraint stress, social defeat, mother-child separation, or the like. The mouse model of the present disclosure can provide a valuable long-term intervention window for research on antidepressant therapy.

The present invention relates to a method for producing animal models of cerebrovascular disease, comprising ligation of the common carotid artery (CCA) and administration of a nitric oxide (NO) inhibitor, animal models of cerebrovascular disease produced thereby, and a method for producing animals having small individual differences in susceptibility to the onset of cerebrovascular disease by using the same. The method for producing animal models of cerebrovascular disease according to the present invention can overcome the conventional problems of complexity and low yield. Particularly, the production method of the present invention can produce animal models of cerebrovascular disease with a high yield by a simple method. Moreover, the animal models produced by the production method may be used in studies to verify the effectiveness and safety of substances for the diagnosis, prevention or treatment of cerebrovascular disease or methods for treatment of cerebrovascular disease, and make it possible to study genes that cause differences in the level of cerebrovascular disease between the animal models. In addition, it is possible to provide offspring animals having uniform susceptibility to the onset of cerebrovascular disease by mating the animal models having similar susceptibilities to the onset of cerebrovascular disease according to the present invention.

A method for preventing or treating a neurodegenerative disease or condition by administering to a subject in need thereof an effective amount of an amylase or maltose is provided, wherein the amylase or maltose reduces aggregation-associated or misfolded protein- associated proteotoxicity, induces transcription of chaperones and proteases, promotes degradation of proteasome substrates, or preserves protein quality under stress conditions in a subject.

A chimeric non-human mammal disease model, wherein (1) at least 30% of all the glial cells in the corpus callosum of the chimeric non-human mammal are human glial cells, and/or (2) at least 5% of all of the glial cells in the white matter of the brain and/or brain stem of the chimeric non-human mammal are human glial cells, and wherein the human glial cells comprise a combination of a first group of human glial cells tagged with a first label and a second group of human glial cells tagged with a second label that is distinguishable from the first label.

The present invention concerns non-human animals with cells having a genome that is lacking the entire E3 ubiquitin ligase (Ube3a) gene (including all isoforms and alternative promoters). These animals are useful for modeling Angelman Syndrome. The invention also includes methods for assessing the effect of an agent, such as potential therapeutics, on an animal model by exposing the animal or cells, tissues, or organs isolated therefrom, to an agent of interest.

The present invention relates to nucleic acid constructs, viral vectors and viral particles comprising a transgene encoding GAT-1; and use of such viral particles for treating diseases mediated by SLC6A1-impairment.