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This invention includes the generation and use of monoclonal antibodies that specifically recognize either arginine vasopressin (AVP) or oxytocin (OT) when bound to neurophysins. The neurophysins (NPs) are a family of proteins that bind to hormones as they are released from the hypothalamus and make their way to the pituitary gland. Monoclonal antibodies were generated that specifically recognize vasopressin bound to a neurophysin (NP-AVP) or oxytocin bound to a neurophysin (NP-OT). Seven monoclonal antibodies were characterized.

This technology relates to the creation and use of newly identified ligands to the D1 dopamine receptor (D1R). The D1 dopamine receptor is linked to a variety of neuropsychiatric disorders and represents an attractive drug target for the enhancement of cognition in schizophrenia, Alzheimer disease, and other disorders. These ligands are positive allosteric modulators (PAMs) that bind to the dopamine receptor at a site other than where dopamine binds and causes the receptor to have an increased response.

The technology relates to therapeutic approaches that inhibit and block the replication of the endogenous HERV-K retrovirus. Previous work has shown that patients with Amyotrophic Lateral Sclerosis (ALS) can have HERV-K activation. In animal models, activation of HERV-K can lead to neurodegenerative symptoms similar to those exhibited by ALS patients. Work in these animal models has allowed the identification of the responsible transcription factor (TDP-43) as well as the corresponding positions of the HERV-K promoter binding sites.

The technology includes USP30 knockout HeLa cells that were generated using CRISPR technology. Parkin and Pink1 are key master genes for triggering the degradation of mitochondria (mitophagy). In contrast, USP30 has been found to be localized in the mitochondria and have a role in antagonizing Parkin function, thereby impeding mitophagy.

This invention relates to methods and algorithms that incorporate information from multiple imaging modalities to identify, estimate the size, and track the time course of brain lesions. Subjects develop brain lesions over the natural course of a disease. Currently, lesions are measured and tracked by a trained neuroradiologist using slice-by-slice inspection, a slow process that is prone to human error and hard to generalize to large observational studies.

This technology includes a cell line that stably expresses YFP-Parkin and mt-mKeima that can be used to study mitochondrial degradation, mitophagy, using flow cytometry (FACS). Compromised mitophagy is implicated in Parkinson disease. The effects of any compounds or genetic alteration on Parkin-mediated mitophagy can be monitored.

This technology involves the generation and use of a mouse model for studying hypogonadism in humans and a cell line to study cellular and molecular properties of gonadotropin-releasing hormone (GnRH) cells. The mouse model expresses the simian virus 40 T antigen driven by the GnRH promoter, resulting in hypogonadism due to an arrest in neuronal migration during development and tumor formation along the migratory pathway. Olfactory bulb tumors in this model animal were dispersed, and GnRH-secreting neuronal cell line (GN/NLT cell line) was established.

This technology includes the generation and use of HeLa cell lines that have the TANK-binding kinase 1 (TBK1) gene knocked out solely or in combination with either the genes NDP52 or OPTN. Both NDP52 and OPTN are receptors involved in the degradation of mitochondria, mitophagy. The TBK1 kinase has a role in enhancing the effect of mitophagy on these receptors. Mutations in TBK1 have been shown to be associated with neurodegenerative diseases such as Parkinson, frontotemporal dementia, and amyotrophic lateral sclerosis (ALS).

This technology is an improvement on the ability to visualize cortical lesions in neurological diseases that cause focal tissue damage to the cortex, including multiple sclerosis (MS). Two approaches are used. The first approach includes optimization of routinely available diffusion-weighted sequences to maximize resolution and contrast, both of which are required to differentiate small cortical lesions from normal-appearing cortex.

This technology includes the combination of an induced pluripotent stem cell (iPSC) line that can inducibly be differentiated into neurons (using an inducible Neurogenin 2, Ngn2, cassette) and enable CRISPR inhibition gene knockdown (via stable expression of dCas9-BFP-KRAB). The combination of these elements in a cell line enables multiple lines of research, including small molecule screens for drug development in neuronal disease models, as well as studying stem cell biology in an iPSC neuronal cell model.