CAP Profiles

Bio

Bio

Neal D. Amin, MD, PhD received his bachelors in Biochemistry from Columbia University where he studied the structure-function relationship of neurexins and neuroligins, proteins implicated in familial autism. He continued his research interests as a medical and doctoral student at the University of California, San Diego in the Medical Scientist Training Program (MD/PhD). Dr. Amin's doctoral research was conducted at the Salk Institute for Biological Studies in the laboratory of Howard Hughes Medical Investigator Samuel Pfaff, where he studied spinal cord development and neurodegenerative disease. He used transcriptomics, mouse genetics, and deep phenotyping to uncover novel gene regulatory pathways driving the establishment of neuronal identity and function. Dr. Amin is currently a resident physician in the research track in the Department of Psychiatry and Behavioral Sciences at Stanford University with a particular interest in neurobiology and understanding molecular mechanisms behind neuropsychiatric disease.

Contact

Publications

All Publications

  • Loss of motoneuron-specific microRNA-218 causes systemic neuromuscular failure SCIENCE Amin, N. D., Bai, G., Klug, J. R., Bonanomi, D., Pankratz, M. T., Gifford, W. D., Hinckley, C. A., Sternfeld, M. J., Driscoll, S. P., Dominguez, B., Lee, K., Jin, X., Pfaff, S. L. 2015; 350 (6267): 1525-1529

    Abstract

    Dysfunction of microRNA (miRNA) metabolism is thought to underlie diseases affecting motoneurons. One miRNA, miR-218, is abundantly and selectively expressed by developing and mature motoneurons. Here we show that mutant mice lacking miR-218 die neonatally and exhibit neuromuscular junction defects, motoneuron hyperexcitability, and progressive motoneuron cell loss, all of which are hallmarks of motoneuron diseases such as amyotrophic lateral sclerosis and spinal muscular atrophy. Gene profiling reveals that miR-218 modestly represses a cohort of hundreds of genes that are neuronally enriched but are not specific to a single neuron subpopulation. Thus, the set of messenger RNAs targeted by miR-218, designated TARGET(218), defines a neuronal gene network that is selectively tuned down in motoneurons to prevent neuromuscular failure and neurodegeneration.

    View details for DOI 10.1126/science.aad2509

    View details for Web of Science ID 000366591100058

    View details for PubMedID 26680198

    View details for PubMedCentralID PMC4913787

  • Speed and segmentation control mechanisms characterized in rhythmically-active circuits created from spinal neurons produced from genetically-tagged embryonic stem cells ELIFE Sternfeld, M. J., Hinckley, C. A., Moore, N. J., Pankratz, M. T., Hilde, K. L., Driscoll, S. P., Hayashi, M., Amin, N. D., Bonanomi, D., Gifford, W. D., Sharma, K., Goulding, M., Pfaff, S. L. 2017; 6

    Abstract

    Flexible neural networks, such as the interconnected spinal neurons that control distinct motor actions, can switch their activity to produce different behaviors. Both excitatory (E) and inhibitory (I) spinal neurons are necessary for motor behavior, but the influence of recruiting different ratios of E-to-I cells remains unclear. We constructed synthetic microphysical neural networks, called circuitoids, using precise combinations of spinal neuron subtypes derived from mouse stem cells. Circuitoids of purified excitatory interneurons were sufficient to generate oscillatory bursts with properties similar to in vivo central pattern generators. Inhibitory V1 neurons provided dual layers of regulation within excitatory rhythmogenic networks - they increased the rhythmic burst frequency of excitatory V3 neurons, and segmented excitatory motor neuron activity into sub-networks. Accordingly, the speed and pattern of spinal circuits that underlie complex motor behaviors may be regulated by quantitatively gating the intra-network cellular activity ratio of E-to-I neurons.

    View details for DOI 10.7554/eLife.21540

    View details for Web of Science ID 000394260700001

    View details for PubMedID 28195039

    View details for PubMedCentralID PMC5308898