My pre- and post-doctoral work at Columbia Medical was funded by the Parkinson Disease Foundation whose Chair was Melvin Yahr MD. With my mentor Flory Bowen PhD, I was trained to test patients on L-DOPA and was part of collaborative work with Robert Katzman MD Chief of Neurology at Albert Einstein. My doctoral research was done in the Division of Neuroscience whose Chief was Maurice Rapport PhD, discoverer of the structure of serotonin and a global leader in lipid immunology and neurochemistry. My PhD research showed that antibodies to synaptic membrane proteins could induce epilepsy and alter behavior.
After becoming a faculty member at Columbia I would show that antibodies to GM1 ganglioside could induce epileptic activity. After publishing that work in Science I was awarded NIH and NSF support. The lab space assigned to be had been the space of Houston Merritt MD, discoverer of the anticonvulsant Dilantin, and a Neurologist with a historic reputation. Adjoining my labs was a small room where the Columbia-Greystone Topectomy Project occurred. A few floors below was housed the Library of Sigmund Freud and a few floors above was the primate colony.
The first decade of my research focused on the immunological base of epilepsy and behavioral alterations. I was fortunate to have interactions with Elvin Kabat MD at Columbia, renowned quantitative immunochemist. My research attracted enormous interest. I was in a department that was populated by highly skilled neurochemists and immunologists who provided extraordinary scientific support for my work. I became conversant and knowledgeable about CNS glycosphingolipids, especially GM1 ganglioside and the antibodies against it. My Chief, Dr. Rapport was a demanding mentor who gave me the opportunity to be a scientist and to teach me the rigors of scientific writing.
My research with both polyclonal and monoclonal antibodies to lipids would morph into studies of the ability of gangliosides to enhance recovery after neural damage. Many studies showed such enhancement in the peripheral nervous system. I would show enhancement of recovery after CNS damage, especially after CNS ischemia - stroke. With NIH funding, I developed a microsurgical model of CNS middle cerebral artery stroke in the rodent and used it to assess the efficacy of GM1 ganglioside. Interest in my work was enormous. I was invited to meetings and to give rounds around the world. Our work was the basis for clinical trials assessing the efficacy of gangliosides. As my research advanced I found that the lipids were not causing neuronal recovery after brisn damage. Rather, they were causing reduced levels of edema and celluialr Ca++ influx.
My research experience at Columbia was extraordinary. I would learn to grow cell cultures, how to raise and harvest monoclonal antibodies, use cholera toxin, fund a surgeon from Xian China to help finish the stroke model, to fund many pre and post-docs from the USA and globally, and to be invited to the former Soviet Union to lecture along with Nobel Laureate Levi Montalcini. At one point I had a lab staff of 18 with my co-PI SB Mahadik PhD. I had sufficient funding to purchase and maintain high cost laboratory equipment reflecting the cutting edge of science.
Columbia University Medical Center
Epileptiform activity induced by antiserum to synaptic membrane. Karpiak, Bowen, Rapport. Brain Res 1973; 59:303-310
Antiserum to brain gangliosides produces recurrent epileptiform activity. Karpiak, Graf, Rapport. Science (New York, NY) 1976; 194(4266):735--737.
Ganglioside receptors and induction of epileptiform activity: cholera toxin and choleragenoid (B subunits). Karpiak, Mahadik, Rapport. Exp Neurol 1978; 62(1):256-259.
GM1 ganglioside treatment reduces functional deficits associated with cortical focal ischemia. Bharucha, Wakade, Mahadik, Karpiak. Exp Neurol 1991; 114(1):136-139.
An immunological model of epilepsy: seizures induced by antibodies to GM1 ganglioside. Karpiak, Mahadik, Graf, Rapport. Epilepsia 1981; 22(2):189-196.
Immunological model of epilepsy. Epileptiform activity induced by fragments of antibody to GM1 ganglioside. Karpiak, Huang, Mahadik. J Neuroimmunol 1982; 3(1):15-21.
Antibodies to GM1 ganglioside inhibit morphine analgesia. Karpiak. Pharmacol Biochem Behav 1982; 16(4):611-613.
Gangliosides reduce mortality due to global ischemia: membrane protection. Karpiak, Li, Mahadik. Clinical neuropharmacology 1986; 9 Suppl 4:338--340.
Gangliosides (GM1 and AGF2) reduce mortality due to ischemia: protection of membrane function. Karpiak, Mahadik. Stroke 1987; 18(1):184--187.
Enhanced cortical maturation: gangliosides in CNS plasticity. Karpiak, Mahadik. Prog Brain Res 1990; 85:299-308.
An in vitro study on increased neuronal and astrocytic vulnerability to neurotoxic injury after in utero cocaine exposure: the reversal effects of GM1 treatment. Stadlin, Tsang, MacDonall, Mahadik, Karpiak. Prog Brain Res 1992; 94:339-350.
Reduction of cerebral edema with GM1 ganglioside. Karpiak, Mahadik. J Neurosci Res 1984; 12(2-3):485-492.
Temporal changes in edema, Na+, K+, and Ca++ in focal cortical stroke: GM1 ganglioside reduces ischemic injury. Karpiak, Wakade, Tagliavia, Mahadik. J Neurosci Res 1991; 30(3):512-520.
Loss and recovery of activities of alpha+ and alpha isozymes of (Na(+) + K+)-ATPase in cortical focal ischemia: GM1 ganglioside protects plasma membrane structure and function. Mahadik, Bharucha, Stadlin, Ortiz, Karpiak. J Neurosci Res 1992; 32(2):209-220.
Significant Publications **
**A complete listing of all my publications which includes over 140 peer reviewed articles.can be found in my CV upon request, and most are on the 2 publication pages of this site.