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Development of a Method to Treat Alzheimer’s Disease by Protection of Synapses

NMDA receptors (NMDARs) are principal regulators of synaptic signaling in the brain. Modulation of NMDARs’ function and trafficking is important for the regulation of synaptic transmission and several forms of synaptic plasticity. Postsynaptic density protein 95 (PSD-95) acts as a scaffolding protein and stabilizes the surface and synaptic expression of NMDARs. NMDA receptors (NMDARs) are ionotropic glutamate receptors that are expressed throughout the nervous system and play crucial roles in neuronal development, synaptic plasticity, learning and memory. PSD-95 (Post Synaptic Density protein) or SAP90, a membrane-associated guanylate kinase (MAGUK), is the major scaffolding protein in the excitatory postsynaptic density (PSD) and a potent regulator of synaptic strength. It is almost exclusively located in the post synaptic density of neurons and is involved in anchoring synaptic proteins. Its direct and indirect binding partners include neuroligin, NMDA receptors, AMPA receptors, and potassium channels. Postsynaptic loss does not precede obvious Aβ (beta-amyloid or amyloid beta) and Tau deposition, but instead appears to occur as Aβ and Tau pathologies advance. This indicates that PSD-95 is an excellent intrinsic biomarker for post synaptic mechanisms and its expression is reduced in brain tissue from patients with Alzheimer’s Disease (AD) as well as in mouse models of AD.

Using Bacteria for Gut Health Improvement and Weight Management

Researchers at the University of California, Davis have developed a method of using bacteriocin peptides to reduce gut inflammation, improve gut barrier function, and reduce obesity in humans.

Use Of Non-Ionic Copolypeptide Hydrogels For Cell Suspension And Cell And Molecule Delivery

UCLA researchers in the Departments of Bioengineering, Chemistry and Biochemistry, and Neurobiology have developed novel copolypeptide hydrogel formulations for the delivery of cells and molecules to locations throughout the body, including the central nervous system.

Nell-1 As An Anti-Osteoinflammatory, Disease-Modifying Anti-Arthritis Agent

UCLA researchers in the Department of Plastic Surgery and the School of Dentistry have developed a novel anti-osteoinflammatory agent for the prevention and suppression of arthritis disease progression.

Identification of a New Molecular Target and Methods for Treating Pancreatic Cancer

Pancreatic cancer is an aggressive disease with limited treatment options and a high mortality rate. Pancreatic cancer is the 3rd leading cause of cancer death in the United States; despite some recent advances in systemic therapy, survival remains dismal in large part due to its profound drug resistance and its propensity for early metastasis. Typically, diagnosis of pancreatic cancer occurs only with advanced stages of the disease since there are currently no early markers for detection. Individuals with pancreatic cancer have a poor prognosis due to the late diagnosis, the extent of metastasis, and ineffective treatments. Survival rates are dismal, with a one-year survival rate of 25% and a 5-year survival rate of 6%. Currently, approximately 20% of pancreatic cancer patients are able to undergo the Whipple procedure; this surgical procedure involves removal of the affected portion of the pancreas, leading to an increased survival rate. However, the remaining 80% of pancreatic cancer patients cannot undergo this treatment because their tumors or the extent of metastasis are too severe. In addition, pancreatic cancer is not typically responsive to radiation and chemotherapy. An alternative approach for the treatment of pancreatic cancer is a complete pancreatectomy followed by continual supplementation with digestive enzymes and insulin. Thus, more effective drugs are needed to increase the survival rate of pancreatic cancer patients. Targeting RORγ may lead to the design of a new class of therapeutics that can be used to treat this devastating disease.

Small Molecules Against IRE1 To Prevent Pd-L1 Upregulation

The strategy to treat cancer by modulating the immune response has been the subject of research for the last twenty years, including the use of vaccines or activating cytokine therapies. Recently, in the last few years, a breakthrough was achieved by the discovery of immune checkpoints, particularly the cytotoxic T lymphocyte-associated molecule-4 (CTLA-4), programed cell death receptor-1 (PD-1), or programed cell death ligand-1 (PD-L1).   The blockade of the pathway for PD-L1 and PD-1 has been used therapeutically for the treatment of a variety of cancers and has achieved long-term remissions in some patients and there are a number of active clinical trials ongoing that target PD-1 and PD-L1. However, a number of cancers are resistant to checkpoint inhibitor-based immunotherapy. The majority of the drugs used for the blockade of the PD-1 and PD-L1 pathways are humanized antibodies. The fact that there have been immune related toxicities associated with PD pathway blockade using the current technologies suggests that an alternative approach may be necessary.

A Method to Prevent the Myelin Abnormalities Associated with Arginase Deficiency

UCLA researchers in the Department of Surgery have developed a gene therapy to prevent dysmyelination (and other CNS abnormalities) as a result of arginase deficiency.

Exercise In A Pill: Compounds That Reproduce The Effects Of Exercise On Muscle Metabolism And Growth

UCLA researchers in the Department of Neurology have identified and synthesized small molecule analogs that activate skeletal muscle growth, mediated by calcium calmodulin kinase II signaling.

Treatment for Restoring Ureagenesis in Carbamoyl Phosphate Synthetase 1 Deficiency

UCLA researchers in the Department of Surgery have developed a gene therapy to treat carbamoyl phosphate synthetase 1 deficiency.

Pharmacological Mitigation of Late-Stage Toxemia

Anthrax disease, caused by Bacillus anthracis, is a highly lethal infection with patient fatality rate between 45-85% during fulminant, toxemia-related late-stages of infection. Systemic release of anthrax edema toxin during late-stage infection induces vascular collapse through endothelial barrier disruption, culminating in fatal hypovolemic shock, a hallmark of systemic anthrax infection. Existing therapeutic strategies to mitigate the effects of anthrax infections only target early-stage infection vis-à-vis bacterial clearance (antibiotics) and toxin-host cell interactions (anti-toxin antibodies), but are ineffective in preventing toxemic-shock which is induced even after pathogen clearance. In fact, patients with fulminant infection require aggressive, continuous fluid drainage and assisted breathing, and no effective therapeutic interventions exist currently for this critical stage of infection. Pathogen induced cell-cell barrier disruption (anthrax, cholera, traveler’s diarrhea, gastroenteritis, pertussis, pneumonia) account for significant socio-economic impacts each year. Stand-alone antitoxin therapies such as those mentioned here can fulfill the unmet medical need for measures that significantly improve the survival rate of patients with severe infections, and lower the risk for development of antibiotic resistance.   High fatality rate of anthrax infections, despite intense antibiotic and supportive therapies, are primarily due to the continuing activities of anthrax exotoxins (ET and LT) released in the patient's circulatory system. Edema toxin or ET, a highly active adenylate cyclase that induces uncontrolled, pathological elevation in cellular levels of the second messenger cAMP is a major virulence protein of Bacillus anthracis and mediates significant lethality during fulminant stages of infection. ET induces rapid disruption of the endothelial barrier, resulting in irreversible tissue damage and lethality due massive fluid loss resulting in cardiovascular collapse and hypovolemic shock. It is therefore imperative that new therapeutic measures be developed that effectively blocks the intracellular function of ET (i.e. cellular proteins/pathways co-opted to induce barrier instability), to reduce fatalities associated with anthrax toxemia.

A New Approach To Treat/Manage Inflammatory Bowel Disease

Researchers at UCI have developed a safe, inexpensive drug for the treatment of inflammatory bowel diseases.

Drug Repurposing To Explore Novel Treatment For Cushing Disease

UCLA researchers in the Department of Medicine and the Department of Molecular and Medicinal Pharmacology have identified several small molecule reagents to treat Cushing disease.

Prevention Of The Late Complications Of Acute Pancreatitis

UCLA researchers in the Department of Medicine and Surgery have developed a novel therapeutic for the prevention of late inflammatory complications in severe acute pancreatitis patients.

Novel Non-Antibody-Based Chimeric Antigen Receptor Against HIV That Also Protects Cells From Infection

UCLA researchers in the Department of Medicine have developed a novel chimeric antigen receptor (CAR) that targets T cells against HIV while protecting T cells from HIV infection.

HSC-Engineered Off-The-Shelf iNKT Cell Therapy For Cancer

UCLA researchers in the Department of Microbiology, Immunology, and Molecular Genetics, and the Department of Pathology & Laboratory Medicine have developed novel methods to produce invariant natural killer T (iNKT) cells from hematopoietic stem cells (HSCs) at high efficiency and yield for the development of off-the-shelf universal HSC-engineered iNKT cell therapy for cancer.

Hair Regeneration By Small Molecules That Activate Autophagy

UCLA researchers in the Department of Molecular and Medical Pharmacology, and the Department of Pathology & Laboratory Medicine have identified small molecules allowing stimulation of hair regeneration.

Novel Protease for Oncology and Inflammatory Diseases

The technology is a novel protease that reduces the ability of cells to respond to the inflammatory cytokine Tumor Necrosis Factor (TNF). High TNF levels have been linked to rheumatoid arthritis, Crohn’s disease and many types of cancers.

Treatment Of Lysosomal Storage Disorders

UCLA researchers in the Departments of Neurology have developed a novel treatment for Lysosomal-storage diseases (LSDs) with neurological impairment.

Microporous membranes for the separation of enantiomers

Current methods used to separate racemic compounds on a large scale have limitations in cost, energy efficiency, and discontinuous processing. UCI researchers have synthesized a membrane made of chiral porous polymers that can separate enantiomers from racemic mixtures through continuous processing.

New Drug Class for Treating Multiple Sclerosis

UCLA researchers from the Department of Molecular & Medical Pharmacology have developed a novel drug class for the treatment of multiple sclerosis.

In Vitro Reconstituted Plant Virus Capsids For Delivering Rna Genes To Mammalian Cells

UCLA researchers in the Department of Chemistry & Biochemistry have developed a method for using in vitro reconstituted plant virus-derived vectors to package and deliver RNA genes for targeted delivery of vaccines, MRI contrast agents, and therapeutic proteins in RNA form.

Plod3-Targeted Anti-Cancer Treatment

UCLA researchers in the department of Dentistry have developed a novel anti-cancer treatment that directly targets enzyme expression necessary to sustain cancer growth.

Engineered Biomaterial to Prevent Endothelial Inflammation

Researchers at the University of California, Davis have developed a biocompatible material to mimic the glycocalyx, the natural layer of molecules that coats the outside of endothelial cells. This technology can be used to treat inflammation in diseases characterized by dysfunction in leukocyte-endothelial cell interactions.

CRF Signaling And Hair Growth

UCLA researchers in the department of Medicine have developed a novel method to treat hair loss and potentially circumvent the common complications that rise from current treatments.

Novel Methods To Enhance Immunity

Myeloid cells are recruited to damaged tissues where they can resolve infections and tumor growth or stimulate wound healing and tumor progression. Recruitment of these cells is regulated by integrins, a family of adhesion receptors that includes integrin CD11b. Previous studies on tumor inflammation revealed that immune cell adhesion receptors play unique but critical roles during tumor progression. CD11b/CD18 has been shown to mediate macrophage adhesion, migration, chemotaxis and accumulation during inflammation. Accordingly, a need exists for novel methods of treating cancer that utilize the role that integrin CD11b plays during inflammation.

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