My first postdoctoral work was carried out with Prof. Eran Elinav at the Weizmann Institute of Science, Immunology Department. I found the first proofs of the microbiome involvement in Amyotrophic Lateral Sclerosis (ALS) pathogenesis and identified its mechanism by defined commensal strains and their biochemical activity. I utilized these findings for the first successful microbiome treatment in murine ALS, consisting of defined live bacterial therapy and metabolite supplementation. I also demonstrated similar findings in human ALS patients, including skewed metabolite levels in their nervous system that can serve as a basis for new human postbiotic therapy. This study was published in Nature.

During my Ph.D. I have designed experimental approaches aimed at establishing CD38 targeting as a novel therapeutic strategy for brain pathologies, including cancer and Alzheimer’s disease. I showed that genetic loss of CD38 attenuated glioma progression and enhanced the lifespan of glioma-bearing mice. Additionally, I identified a novel small molecule CD38 inhibitor that effectively phenocopied my previous findings in vivo and attenuated glioma and metastatic melanoma progression. Since up today there is no effective treatment against glioma, my findings are very important as they suggest that CD38 targeting may be used as therapeutic approach.

During my undergraduate and first graduate years I studied basic cell-biology questions that can be translated to potential cancer therapies. I sought to understand the interplay between resident brain cells such as astrocytes and cancer cells that can be located in remote areas of the body, yet metastasize to the brain. I was involved in studies testing chemical derivation of known chemotherapy drugs to improve its efficacy and bioavailability and reduce potential side-effects. As understanding the molecular basis of programmed cell death is one of the fundamental processes in developing novel strategies to treat cancer, I studied also the redistribution of nuclear proteins after stress induced by chemotherapy agents, and discovered a novel function for the pro-apoptotic proteins Bak and Bax in regulating this controlled release of nuclear proteins prior cell-death.