This invention includes the generation and use of polyclonal antibodies that specifically recognize the glutamate receptor 1 protein that has been phosphorylated at Serine 567 (GluA1 pS567). Glutamate receptors are ligand-gated ion channels and are the predominant excitatory neurotransmitter receptor type in humans. A peptide sequence on the gene was selected surrounding the phosphorylation site. This peptide was then generated and injected into rabbits to create an immune response. Serum was then collected from the rabbit and the antibodies were affinity purified.

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.

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.

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 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 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 includes the creation and use of five human embryonic stem cell (hESC) lines with reporter genes integrated at safe harbor sites. These cell lines can be used to study the biology of stem cell development, including their use as an assay for small molecules.

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 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 includes multiple cells with various combinations of autophagy receptors knocked out. The cell lines include knockouts of the OPTN, NDP52, and TAX1BP1 genes that are involved in cargo selective autophagy. These lines may be used to explore how cell biology debris is catabolized, which may be relevant to neurodegenerative diseases like amyotrophic lateral sclerosis (ALS).