School of Biomedical Sciences
The Chinese University of Hong Kong 香港中文大學

KE Ya Associate Professor

B.Med., Ph.D.

Telephone:  3943 6780

Email:  This email address is being protected from spambots. You need JavaScript enabled to view it.


 305A, Lo Kwee-Seong Integrated Biomedical Sciences Building, Area 39, CUHK






Prof. KE Ya (柯亞) is currently Associate Professor of the School of Biomedical Sciences, the Chinese University of Hong Kong. She was trained in medicine and received further training in biomedical sciences and has made significant contributions in understanding the etiology and pathogenic processes underlying neurodegenerative diseases. Currently, her main research interest is to decipher the neural circuits and mechanisms underlying animal and human behaviors, both innate and learned. Their malfunctions in different brain disorders are also investigated. To meet these challenges, a multi-disciplinary approach employing different neuroscience research tools like molecular biology, virus-based circuit mapping, opto/chemo-genetics, in vivo electrophysiological recording, brain imaging and novel behavioral paradigms is adopted.

  1. Network basis of cognitive functions. Cognitive functions underlie our ability to perceive, learn, memorize and also make decision. The brain network systems and their connectivity in mediating important cognitive functions including learning and memory, strategy-switching, multi-tasking and others are being investigated.
  2. Emotion and related innate behaviors. Disturbance in emotion as happens in stress, anxiety and depression could trigger various normal and abnormal behavioral responses. I am interested in the neural circuits that regulate emotion and related innate responses, such as repetitive behaviors and changes in feeding and appetite.
  3. Circuit aberrations and treatments in neurodegenerative diseases. Motor, cognitive and emotional deficits are common in neurodegenerative diseases like Alzheimer’s diseases and Parkinson’s disease. Aberrations in relevant neural circuits and novel treatments for these symptoms are explored.
  1. Mu, M.D., Geng, H.Y., Rong, K.L., Peng, R.C., Wang, S.T., Geng, L.T., Qian, Z.M., Yung, W.H., & Ke, Y.* (2020). A limbic circuitry involved in emotional stress-induced grooming. Nature Communications, 11(1), 2261(Editorial highlight)
  2. Qian, Z.M. & Ke, Y.* (2019). Hepcidin and its therapeutic potential in neurodegenerative disorders. Medicinal Research Reviews, 94(5):1672-1684.
  3. Li, C., Chan, D.C.W., Yang, X., Ke, Y.* & Yung, W.H.*. (2019). Prediction of Forelimb Reach Results From Motor Cortex Activities Based on Calcium Imaging and Deep Learning. Frontier Cellular Neuroscience, 12;13:88.
  4. Cui, Q.L., Li, Q., Geng, H.Y., Chen, L., Ip, N.Y., Ke, Y.* & Yung, W.H.* (2018). Dopamine receptors mediate strategy abandoning via modulation of a specific prelimbic cortex-nucleus accumbens pathway in mice. Proceedings of the National Academy of Science, USA. 115(21):E4890-E4899.
  5. Zhou, Y.F., Wu, X.M., Zhou, G., Mu, M.D., Zhang, F.L., Li, F.M., Qian, C., Du, F., Yung, W.H., Qian, Z.M., & Ke, Y.* (2018). Cystathionine b-synthase is required for body iron homeostasis. Hepatology, 67(1), 21-35. (Editorial highlight)
  6. Zhang, M.W., Zhao, P., Yung, W.H., Sheng, Y., Ke, Y.* & Qian, Z.M. (2018). Tissue iron is negatively correlated with TERC or TERT mRNA expression: A heterochronic parabiosis study in mice. Aging, (Albany NY). 10(12):3834-3850.
  7. Li, Q., Ko, H., Qian, Z.M., Yan, L.Y.C., Chan, D.C.W., Arbuthnott, G., Ke, Y.*, & Yung, W.H.* (2017). Refinement of learned skilled movement representation in motor cortex deep output layer. Nature Communications, 8, 15834.
  8. Wu, X.M., Qian, C., Zhou, Y.F., Yan, Y.C., Luo, Q.Q., Yung, W.H., Zhang, F.L., Jiang, L.R., Qian, Z.M., & Ke, Y.* (2017). Bi-directionally protective communication between neurons and astrocytes under ischemia. Redox Biology, 20(13), 20-31.
  9. Lu, L.N., Qian, Z.M., Wu, K.C., Yung, W.H., & Ke, Y.*. (2017). Expression of iron transporters and pathological hallmarks of parkinson's and alzheimer's diseases in the brain of young, adult, and aged rats. Molecular Neurobiology, 54(7), 5213-5224.
  10. Gong, J., Du, F., Qian, Z.M., Luo, Q.Q., Sheng, Y., Yung, W.H., Xu, Y.X., & Ke, Y.* (2016). Pre-treatment of rats with ad-hepcidin prevents iron-induced oxidative stress in the brain. Free Radical Biology Medcine, 90, 126-32.
  11. Xu, L.H., Xie, H., Shi, Z.H., Du, L.D., Wing, Y.K, Li, A.M., Ke, Y.*, & Yung, W.H.* (2015). Critical Role of Endoplasmic Reticulum Stress in Chronic Intermittent Hypoxia-Induced Deficits in Synaptic Plasticity and Long-Term Memory. Antioxidants & Redox Signaling, 23(9), 695-710.
  12. Du, F., Qian, Z.M., Luo, Q., Yung, W.H., & Ke, Y.* (2015). Hepcidin suppresses brain iron accumulation by downregulating iron transport proteins in iron-overloaded rats. Molecular Neurobiology, 52(1), 101-14.
  13. Huang, X.T., Qian, Z.M., He, X., Gong, Q., Wu, K.C., Jiang, L.R., Lu, L.N., Zhu, Z.J., Zhang, H.Y., Yung, W.H., & Ke, Y.* (2014). Reducing iron in the brain: a novel pharmacological mechanism of Huperzine A in the treatment of Alzheimer's disease. Neurobiology of Aging, 35(5), 1045-54.
  14. Li, Q., Qian, Z.M., Arbuthnott, G.W., Ke, Y.*, & Yung, W.H.* (2013). Cortical Effects of Deep Brain Stimulation: Implications for Pathogenesis and Treatment of Parkinson's Disease. JAMA Neurology, 71, 100-103 (Editorial highlight)
  15. Li, Q., Ke, Y.*, Chan, D.C.W., Qian, Z.M., Yung, K.K.L., Ko, H., Arbuthnott, G.W., & Yung, W.H.* (2012). Therapeutic deep brain stimulation in parkinsonian rats directly influences motor cortex. Neuron, 76, 1030-1041
  16. Wu, X.M., Qian, Z.M., Zhu, L., Du, F., Yung, W.H., Gong, Q., & Ke, Y.* (2011). Neuroprotective effect of ligustilide against ischemia-reperfusion injury via up-regulation of erythropoietin and down-regulation of RTP801. British Journal of Pharmacology, 164(2), 332-43.
  17. Du, F, Qian, Q., Qian, Z.M., Wu, X.M., Xie, H., Yung, W.H., & Ke, Y.* (2011). Hepcidin directly inhibits transferrin receptor 1 expression in astrocytes via a cyclic AMP-protein kinase a pathway. GLIA, 59(6), 936-45.
  18. Zhao, L., Qian, Z.M., Zhang, C., Yung, W.H., Du, F., & Ke, Y.* (2008). Amyloid beta-peptide 31-35-induced neuronal apoptosis is mediated by caspase-dependent pathways via cAMP-dependent protein kinase A activation. Aging Cell, 7(1), 47-57.
  19. Ke, Y., & Qian, Z.M. (2007). Brain iron metabolism: neurobiology and neurochemistry. Progress in Neurobiology, 83(3), 149-173.
  20. Ke, Y., & Qian, Z.M. (2003). Iron misregulation in the brain: a primary cause of neurodegenerative disorders. Lancet Neurology, 2(4), 246-253.

    *  Corresponding / Co-corresponding author