Described herein is a multiplexed and high content screening assay using primary neurons for identifying small molecule modulators of neuronal mitochondrial mitostasis (MnMs). Also described is a high throughput screening assay using primary neurons for identifying small molecules that increase mitochondrial function, identified by measuring the electrochemical potential across the inner mitochondrial membrane and ATP generation. Most MnMs that increased mitochondrial content, length and/or health also increased mitochondrial function without altering neurite outgrowth. Some MnMs protect mitochondria in primary neurons from Aβ(1-42) toxicity, glutamate toxicity, increased oxidative stress and the toxic cellular environment associated with Alzheimer's disease. Some MnMs target mitochondria directly. An MnM also increases the synaptic activity of hippocampal neurons and is potent in vivo, increasing the respiration rate of brain mitochondria after administering the compound to mice. The MnMs were demonstrated to protect the mitochondrial population in neurons in an in vivo model of Alzheimer's Disease. Also described is a method for treating a patient suffering from a disorder characterized by dysfunction of neuronal mitostasis, comprising administering to the patient a therapeutically effective amount of a compound (MnM), or a pharmaceutically acceptable salt thereof.

The present invention provides methods for assessing a compound's potential toxicity.

The present disclosure relates to compounds that bind to flavin-containing enzymes and inhibit mitochondrial function, referred to herein as mitoflavoscins. Methods of screening compounds for mitochondrial inhibition and anti-cancer properties are disclosed. Also described are methods of using mitoflavoscins to prevent or treat cancer, bacterial infections, and pathogenic yeast, as well as methods of using mitoflavoscins to provide anti-aging benefits. Specific mitoflavoscin compounds are also disclosed.

Disclosed herein are methods and systems for evaluating the bioenergetic poise and bioenergetic capacity of living cells in a single assay.

Systems and methods for automated optical tweezer (OT)-based mitochondrial transfer are provided. The system for automated optical tweezer-based mitochondrial transfer includes a microfluidic device and an optical tweezer micromanipulation system. The microfluidic device includes one or more confinement means for confining cells and a channel for flowing mitochondria near the confinement means. The optical tweezer micromanipulation system is configured to trap at least one of the mitochondria within the channel of the microfluidic device for transport of the mitochondria to one of the confined cells.

The present invention relates to a real-time fluorescence imaging sensor for measuring glutathione in cell organelles and a method for fabricating the same. More specifically, the present invention relates to a novel compound for measuring glutathione in cell organelles, a method for preparing the novel compound, a real-time fluorescence imaging sensor for measuring glutathione in cell organelles, which comprises the novel compound, a method for fabricating the imaging sensor, and a method of measuring glutathione in cell organelles by use of the imaging sensor. When the composition comprising the compound according to the present invention is used, it can measure the antioxidant activity of the organelle mitochondria or Golgi apparatus in living cells, particularly stem cells, and can screen highly active stem cells based on the results obtained by measuring the antioxidant activity of the cell organelle.

Provided herein are methods and compositions related to the treatment of cancer using copper ionophores.

The present invention relates to a method for screening an activator of mitochondrial activity by using gypenoside-treated cells, to a composition for screening an activator of mitochondrial activity, comprising the gypenoside, and to a kit comprising the composition. By using the method for screening an activator of mitochondrial activity of the present invention, it is possible to effectively discover a preparation which can substantially promote the mitochondrial activity, and thus the method is expected to be widely used in developing a therapeutic agent for diseases caused by mitochondrial activity inhibition.

The present invention encompasses the use of compounds for a novel approach to treat and prevent diseases, conditions, and disorders such as diabetes and ischemic reperfusion injury. Compounds of the invention, including but not limited to BAM15 ((2-fluorophenyl){6-[(2-fluorophenyl)amino](1,2,5-oxadiazolo[3,4-e]pyrazin-5-yl)}amine), a mitochondrial uncoupler, can improve glucose tolerance, increases cellular oxygen consumption, treat or prevent kidney ischemia reperfusion injury reverse insulin resistance, reverse or treat hyperinsulinemia, and reverse or treat hyperlipidemia. The present invention further provides novel compounds as well as methods for identifying compounds with the same or similar properties as BAM15.

Compositions and methods for screening for a disease or a disorder associated with a deficiency in frataxin in a subject using biomarkers for diseases or disorders associated with a deficiency in frataxin are disclosed. The compositions and methods include determining the acetylation status of mitochondrial proteins. Also disclosed are methods of detecting progression of a disease or a disorder associated with a deficiency in frataxin in a subject and methods of monitoring effectiveness of a therapy for diseases or disorders associated with a deficiency in frataxin.