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 Home / About Us > Dr Maia Kokoeva

Contact info

Dr Maia Kokoeva
McGill University/MUHC Research Institute
1001, Décarie Blvd - Room E02.7218
Montreal, QC H4A 3J1

Tel: 1-514-934-1934, ext. 35360
E-mail: maia.kokoeva@mcgill.ca

 

Research keywords

  • Obesity
  • Diabetes
  • Hypothalamus
  • Adult neurogenesis
  • Neural plasticity
  • Neuroendocrinology
  • Genetic mouse models

 

Maia Kokoeva, PhD
Associate Professor of Medicine


Biographical Sketch

Dr Maia Kokoeva completed her undergraduate studies at the Department of Biology, Lomonosov Moscow State University and obtained her PhD degree from the Russian Academy of Sciences, Moscow. During her first postdoctoral fellowship at the Max Planck Institute for Biochemistry in Martinsried/Munich, Germany, under the supervision of Dr Dieter Oesterhelt, she investigated sensory signal transduction in the archaeon Halobacterium salinarum. By employing molecular genetic techniques in conjunction with behavioral analysis, she uncovered the signaling pathways that mediate the chemotactic responses to a variety of chemical attractants including several amino acids. She then joined the laboratory of Dr Jeffrey Flier at Harvard Medical School to continue her postdoctoral training with a focus on central regulation of energy balance in the mammals. Dr Kokoeva was intrigued by the observation that obese rodents and humans treated with the neuropeptide ciliary neurotrophic factor (CNTF) show a reduction in body weight that is sustained well beyond termination of treatment, a phenomenon not seen with any other weight lowering drug. In an attempt to elucidate the mechanistic basis for this effect, she discovered that CNTF potently stimulates neurogenesis in adult hypothalamic structures that are important for the regulation of energy balance. These findings indicate that neuronal circuits in the adult hypothalamus are not hard-wired and that plastic changes can have a long-lasting impact on a brain circuitry. Dr Kokoeva was appointed Assistant Professor at the Department of Medicine of McGill University in summer 2008.

Click here for pdf CV


Selected Scientific Contributions

1- Kokoeva MV, Yin H, Flier JS. Evidence for constitutive neural cell proliferation in the adult murine hypothalamus. J Comp Neurol 505:209-220, 2007.

2- Shi H, Kokoeva MV, Inouye K, Tzameli I, Yin H, Flier JS. Toll like receptor 4: A link between innate immunity and fatty acid-induced insulin resistance. J Clin Invest 116:3015-25, 2006.

  This paper was the subject of "News and Views" and "Preview" articles:

  • Tschop M and Thomas M. Fat fuels insulin resistance through Toll-like receptors. Nat Med 12:1359-1361, 2006.
  • Kim JK. Fat uses a TOLL-road to connect inflammation and diabetes. Cell Metab 4:417-419, 2006.

3- Kokoeva MV, Yin H, Flier JS. Neurogenesis in the hypothalamus of adult mice: potential role in energy balance. Science 310:679-83, 2005.

  This paper was the subject of a "News and Views" article:

  • Seeley RJ. More neurons, less weight. Nat Med 11:1276-1278, 2005.

Click here for PubMed listing


Research Interests

While much is known about the molecular basis of hypothalamic control in mammalian energy homeostasis, neural circuit plasticity including changes in neural cell numbers has only recently been implicated in body weight regulation. We want to decipher the mechanistic underpinnings of long-term changes in body weight set points by exploring plastic changes in the brain circuits that control feeding.

We have previously shown that exogenous induction of hypothalamic cell proliferation is associated with weight loss. We also have demonstrated that cells proliferate on an ongoing basis in the adult hypothalamus, even in the absence of external cues such as growth factor administration. We are currently investigating the role of these constitutively born cells in energy homeostasis by employing in vivo cell ablation approaches in conjunction with electrophysiological and ultrastructural studies.

The long-term goal of my lab is to mechanistically understand why some humans can maintain their body weight strikingly constant over most of their adult lives while others are confronted with gradual or abrupt increases in fat mass. Our studies may thus provide new insight in the etiology of obesity and ultimately help to develop new strategies for the prevention and treatment of obesity-related diseases.

   
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