Highly-sensitive and Dynamic Biomarkers for Intrathecal Inflammation for Neuroimmunological Diseases

The technology relates to the identification and validation of eight biomarkers for active central nervous system (CNS) intrathecal inflammation. The management of neuroimmunological diseases is severely hindered by an inability to reliably measure intrathecal inflammation. Current laboratory tests, that were developed over 40 years ago, do not capture low to moderate levels of CNS inflammation and provide limited information about its phenotype.

Development of a Rabbit Polyclonal Antibody for the pT707 Phosphorylated Site of Neuroligin-4 (NLHN4)

This technology includes the creation and use of a polyclonal antibody for Neuroligin-4, NLGN4, that was created by injecting a peptide surrounding the pT707 phosphorylation site into rabbits and affinity purifying the resulting serum. Neuroligin-4 is a member of the neuroligin family of cell adhesion proteins. This family has been shown to play a role in the maturation and function of the neuronal synapse and has been implicated in patients with autism and intellectual disability.

Diagnosing and Treating Collagen type VI-related Dystrophies Based on a New COL6A1 Mutation

This invention includes the identification of a new mutation in the collagen type VI (COL6A1) gene, including a method for diagnosing and treating patients with this mutation. Collagen type VI-related dystrophies (COL6-RD) are devastating neuromuscular disorders that manifest with progressive generalized muscle weakness, contractures, and respiratory failure. Currently, no cure exists for COL6-RD.

Treatment of Immune-mediated Brain Swelling with Combined Anti-LFA1/VLA4 Therapy

This technology includes a therapeutic approach to prevent secondary edema after cerebrovascular hemorrhage. Using an animal model, we found that edema is triggered by massive extravasation of myelomonocytic cells from the blood into the brain in response to hemorrhaging vessels. Administration of anti-LFA1 and anti-VLA4 antibodies resulted in an inhibition of extravasation of the myelomonocytic cells. This single dose treatment prevented secondary edema and markedly improved functional outcomes if administered within the first six hours following cerebrovascular hemorrhage.

Nanobody Therapeutics for SARS-CoV2

This technology includes the design and use of several nanobodies that bind to the SARS-CoV2 spike protein receptor binding domain and block spike protein interaction with the angiotensin converting enzyme 2 (ACE2) receptor. Nanobodies are 12-15 kDa single-domain antibody fragments that are more stable and easier to produce in large quantities compared to conventional antibodies. SARS-CoV2 is the virus responsible for the COVID19 pandemic. The SARS-CoV2 spike protein is responsible for viral entry into human cells via interaction with ACE2 on the cell surface.

Design of Switch-Mode Amplifier to Transform Single Transmit Hardware for Multi-Nuclear MRI

This technology includes the design and implementation for 1H-nuclear magnetic resonance imaging (MRI) that allows single transmit hardware to be "transformed" for another nucleus excitation to perform multi-nuclear MR. A radiofrequency (RF) optically controlled switch-mode amplifier prototype is tuned for excitation of two nuclei. The amplifier received the nuclei carrier signals optically through a single fiber.

Targeting the 5’UTR of Survival Motor Neuron 2 (SMN2) with Antisense Oligonucleotides to Increase Expression for the Treatment of Spinal Muscular Atrophy

This technology includes the identification and use of antisense oligonuclecotides (ASOs) complimentary to the 5’UTR of SMN2 (Survival of motor neuron 2) for the treatment of spinal muscular atrophy (SMA). SMA is an autosomal-recessive motor neuron disease caused by the loss of both copies of the SMN1 gene. Copies of the similar gene SMN2 decrease the severity of this disease in a dose-dependent manner. Thus, increasing expression levels of the SMN2 transcript can be used to treat SMA.