Professional Education

  • PhD, Max-Planck-Institute for Experimental Medicine, Germany, Clinical Neuroscience (2019)
  • Master of Science, University Of Pune (2011)
  • Bachelor of Science, University Of Pune (2009)

Stanford Advisors

All Publications

  • Functional hypoxia drives neuroplasticity and neurogenesis via brain erythropoietin. Nature communications Wakhloo, D. n., Scharkowski, F. n., Curto, Y. n., Javed Butt, U. n., Bansal, V. n., Steixner-Kumar, A. A., Wüstefeld, L. n., Rajput, A. n., Arinrad, S. n., Zillmann, M. R., Seelbach, A. n., Hassouna, I. n., Schneider, K. n., Qadir Ibrahim, A. n., Werner, H. B., Martens, H. n., Miskowiak, K. n., Wojcik, S. M., Bonn, S. n., Nacher, J. n., Nave, K. A., Ehrenreich, H. n. 2020; 11 (1): 1313


    Erythropoietin (EPO), named after its role in hematopoiesis, is also expressed in mammalian brain. In clinical settings, recombinant EPO treatment has revealed a remarkable improvement of cognition, but underlying mechanisms have remained obscure. Here, we show with a novel line of reporter mice that cognitive challenge induces local/endogenous hypoxia in hippocampal pyramidal neurons, hence enhancing expression of EPO and EPO receptor (EPOR). High-dose EPO administration, amplifying auto/paracrine EPO/EPOR signaling, prompts the emergence of new CA1 neurons and enhanced dendritic spine densities. Single-cell sequencing reveals rapid increase in newly differentiating neurons. Importantly, improved performance on complex running wheels after EPO is imitated by exposure to mild exogenous/inspiratory hypoxia. All these effects depend on neuronal expression of the Epor gene. This suggests a model of neuroplasticity in form of a fundamental regulatory circle, in which neuronal networks-challenged by cognitive tasks-drift into transient hypoxia, thereby triggering neuronal EPO/EPOR expression.

    View details for DOI 10.1038/s41467-020-15041-1

    View details for PubMedID 32152318

    View details for PubMedCentralID PMC7062779

  • Uncoupling the widespread occurrence of anti-NMDAR1 autoantibodies from neuropsychiatric disease in a novel autoimmune model MOLECULAR PSYCHIATRY Pan, H., Oliveira, B., Saher, G., Dere, E., Tapken, D., Mitjans, M., Seidel, J., Wesolowski, J., Wakhloo, D., Klein-Schmidt, C., Ronnenberg, A., Schwabe, K., Trippe, R., Maetz-Rensing, K., Berghoff, S., Al-Krinawe, Y., Martens, H., Begemann, M., Stoecker, W., Kaup, F., Mischke, R., Boretius, S., Nave, K., Krauss, J. K., Hollmann, M., Luhder, F., Ehrenreich, H. 2019; 24 (10): 1489–1501


    Autoantibodies of the IgG class against N-methyl-D-aspartate-receptor subunit-NR1 (NMDAR1-AB) were considered pathognomonic for anti-NMDAR encephalitis. This view has been challenged by the age-dependent seroprevalence (up to >20%) of functional NMDAR1-AB of all immunoglobulin classes found in >5000 individuals, healthy or affected by different diseases. These findings question a merely encephalitogenic role of NMDAR1-AB. Here, we show that NMDAR1-AB belong to the normal autoimmune repertoire of dogs, cats, rats, mice, baboons, and rhesus macaques, and are functional in the NMDAR1 internalization assay based on human IPSC-derived cortical neurons. The age dependence of seroprevalence is lost in nonhuman primates in captivity and in human migrants, raising the intriguing possibility that chronic life stress may be related to NMDAR1-AB formation, predominantly of the IgA class. Active immunization of ApoE-/- and ApoE+/+ mice against four peptides of the extracellular NMDAR1 domain or ovalbumin (control) leads to high circulating levels of specific AB. After 4 weeks, the endogenously formed NMDAR1-AB (IgG) induce psychosis-like symptoms upon MK-801 challenge in ApoE-/- mice, characterized by an open blood-brain barrier, but not in their ApoE+/+ littermates, which are indistinguishable from ovalbumin controls. Importantly, NMDAR1-AB do not induce any sign of inflammation in the brain. Immunohistochemical staining for microglial activation markers and T lymphocytes in the hippocampus yields comparable results in ApoE-/- and ApoE+/+ mice, irrespective of immunization against NMDAR1 or ovalbumin. These data suggest that NMDAR1-AB of the IgG class shape behavioral phenotypes upon access to the brain but do not cause brain inflammation on their own.

    View details for DOI 10.1038/s41380-017-0011-3

    View details for Web of Science ID 000487241400009

    View details for PubMedID 29426955

    View details for PubMedCentralID PMC6756099

  • Lactobacillus plantarum Shows More Probiotic Potential than S. cremoris JOURNAL OF PURE AND APPLIED MICROBIOLOGY Wakhloo, D., Mahajani, S., Tembe, P., Raut, A. 2013; 7 (1): 565–70