Curriculum Vitae
Cheng-Xin Gong, M.D.
CHENG-XIN GONG, M.D.
Head, Laboratory of Brain Metabolism
New York State Institute for Basic Research in Developmental Disabilities
1050 Forest Hill Road, Staten Island, New York 10314
Tel: 718-494-5248 (Office)/5390 (Lab); Fax: 718-494-1080
E-mails: cxgong@mail.csi.cuny.edu, cxgong@verizon.net
Adjunct Professor, Graduate Center
The City University of New York, New York, U.S.A.
EDUCATION
1978 - 1983
1985 - 1988
1991 - 1995
Medical student, Xianning Medical College, Hubei, China
Major: Medical science
Postgraduate student, Tongji Medical University, Wuhan, China
Major: Biochemistry
Postdoctoral fellow, Laboratory of Chemical Neuropathology (Dr. Khalid Iqbal's
Lab), New York State Institute for Basic Research in Developmental Disabilities,
Staten Island, New York
Major: Molecular mechanisms of Alzheimer’s disease
EMPLOYMENT HISTORY
1983 - 1985
1988 - 1991
1991 - 1998
Junior Teacher, Dept. of Biochemistry, Xianning Medical College, Hubei, China
Lecturer, Dept. of Biochemistry, Xianning Medical College
Postdoctoral Fellow and then Research Scientist I~II, Chemical Neuropathology
Laboratory (Dr. Khalid Iqbal’s lab), New York State Institute for Basic Research
in Developmental Disabilities, Staten Island, New York
1998 - 2000 Research Scientist IV, Department of Neurochemistry, New York State Institute
for Basic Research in Developmental Disabilities, Staten Island, New York
2000 - present Head of Laboratory of Brain Metabolism, New York State Institute for Basic
Research in Developmental Disabilities, New York
2007 - present Research Scientist V, Department of Neurochemistry, New York State Institute
for Basic Research in Developmental Disabilities, Staten Island, New York
OTHER PROFESSIONAL ACTIVITIES
Visiting Professor
Xianning Medical College, China (since 1996)
Nantong Medical College, Nantong, China (since 2004)
Wuhan University School of Medicine, Wuhan, China (since 2004)
Adjunct Professor
Tongji Medical College of Huazhong University of Science and
Technology, Wuhan, China (since 1998)
Graduate Center of the City University of New York, New York (since
2001)
Grant Reviewer
National Institutes of Health (NIH), USA
Alzheimer’s Association, USA
Philip Morris External Research Program, USA
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Curriculum Vitae
Cheng-Xin Gong, M.D.
Alzheimer's Research Trust, UK
The La Marato de Foundation, Spain
The Indiana Alzheimer Disease Center, USA
The PSC-CUNY Research Award Program of the City University of New
York, USA.
NIH Study Section
Member of Cell Death and Injury in Chronic Neurodegeneration (CDIN)
and Brain Disorders and Clinical Neurosciences Special Panel (ZRG1
BDCN-N) (2005 – 2008)
Peer Reviewer
For more than 20 academic journals in the fields of neuroscience, biology
and biochemistry (since 2000)
Editorial Board
American Journal of Alzheimer’s Disease and Other Dementias (since
2005)
Journal of Alzheimer’s Disease (Associate Editor, since 2005)
Neurochemical Research (since 2006)
International Journal of Biological Chemistry (since 2006)
Trends in Medical Research (since 2006)
Journal of Medical Sciences (since 2006)
Journal of Medical Molecular Biology (since 2006)
Medjaden (Associate Editor-in-Chief, since 2006)
Molecular Neurodegeneration (Associate Editor, since 2008)
Journal of Molecular Neuroscience (since 2009)
PLoS ONE (since 2009)
Advisory Board
International Scientific Advisory Board of the first International
conference on Alzheimer's Disease and Related Neurodegenerative
Disorders, Wuhan, China (2001)
Conference Chair
Co-Chair, Oral Session of the 10th International Conference on
Alzheimer's Disease and Related Disorders, Madrid, Spain (2006)
Chair, Neurodegenerative Drug Discovery and Development Session, the
6th Annual Congress of International Drug Discovery Science and
Technology, Beijing, China (2008)
Modulator, Mini-Symposium on Future therapeutics of Alzheimer’s
Disease and related Neurodegenerative Disorders, NYS Institute for
Basic Research in Developmental Disabilities, NY (2008)
PROFESSIONAL SOCIETIES
Member, American Association for the Advancement of Science (AAAS)
Member, International Society for Neurochemistry (ISN)
Member, Society for Neuroscience (SfN), USA
Member, Society for Chinese Neuroscientist in North America
Member, International Society to Advance Alzheimer Research and Treatment (ISTAART)
RESEARCH GRANTS (Principal investigator/program director only)
1. RO3 AG14875:
2
Curriculum Vitae
Cheng-Xin Gong, M.D.
a) Title: Phosphatase inhibition and tau phosphorylation
b) Principal investigator: Cheng-Xin Gong
c) Duration: 09/30/97 - 9/30/99
d) Amount: $87,000
e) Funding Agency: NIH/NIA
2. RO1 AG16760:
a) Title: Tau glycosylation in Alzheimer’s disease
b) Principal investigator: Cheng-Xin Gong
c) Duration: 05/01/99 - 04/30/04
d) Amount: $590,000 (direct costs)
e) Funding Agency: NIH/NIA
3. 1 F05 NS42131:
a) Title: O-GlcNAcylation of tau in Alzheimer’s disease
b) Principal investigator/mentor: Cheng-Xin Gong
c) Duration: 09/01/01 - 08/31/02
d) Amount: $40,196
e) Funding Agency: WHO/NIND
4. The Li Foundation Fellowship:
a) Title: Pathogenic mechanism of Alzheimer’s disease
b) Principal investigator: Cheng-Xin Gong
c) Duration: 08/20/01 - 08/20/07
d) Amount: $210,000
e) Funding Agency: The Li Foundation, New York
5. The Li Foundation Travel Grant:
a) Title: International Collaboration for Studies on Pathogenic mechanism of Alzheimer’s disease
b) Principal investigator: Cheng-Xin Gong
c) Duration: 04/01/03 - 03/30/06
d) Amount: $13,500
e) Funding Agency: The Li Foundation, Inc., New York
6. NIRG-03-4721:
a) Title: Role of protein phosphatase 5 in tau phosphorylation
b) Program director: Cheng-Xin Gong (Co-P.I.)
c) Duration: 08/01/03 - 07/31/05
d) Funding Agency: Alzheimer’s Association, USA
e) Amount: $100,000
7. IIRG-05-13095:
a) Title: O-GlcNAcylation and phosphorylation of tau protein
b) Program director: Cheng-Xin Gong
c) Duration: 09/01/05 - 08/31/08
d) Funding Agency: Alzheimer’s Association, USA
e) Amount: $240,000
8. R01 AG027429-01:
a) Title: O-GlcNAcylation of tau: a link between glucose metabolism and neurodegeneration
b) Principal investigator: Cheng-Xin Gong
c) Duration: 03/01/06 - 02/28/11
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Curriculum Vitae
Cheng-Xin Gong, M.D.
d) Funding Agency: NIH/NIA
e) Amount: $1,673,500
9. R21 R21AG031969:
a) Title: Preclinical testing of an O-GlcNAcase inhibitor to block neurodegeneration for AD
b) Principal investigator: Cheng-Xin Gong (Co-PI)
c) Duration: 12/01/08 - 11/30/10
d) Funding Agency: NIH/NIA
e) Amount: $356,000
INVITED SEMINARS/LECTURES
1. Mechanism of Alzheimer’s neurofibrillary degeneration, invited by Tongji Medical University, Wuhan,
China, June 16, 1996
2. Protein phosphatases and Alzheimer’s neurofibrillary degeneration, invited by Tongji Medical University,
Wuhan, China, invited by Hubei Chapter of Chinese Medical Association, June 10, 1998
3. Protein phosphatases and Alzheimer's neurofibrillary degeneration, invited by Tongji Medical University
and Society of Pathophysiology of Hubei, Wuhan, China, March 23, 2000.
4. Role of protein phosphatases in Alzheimer's neurofibrillary degeneration, invited by the Institute of
Biophysics, Academia Sinica, Beijing, China, October 18, 2001.
5. Tau Phosphatases and Neurofibrillary Degeneration of Alzheimer Disease, invited by the First International
Conference on Alzheimer's Disease and Related Neurodegenerative Disorders, Wuhan, October 22-25,
2001.
6. Alzheimer's disease: advance in basic research, diagnosis, and treatment, invited by Wuhan Medical
Association, Wuhan, China, November 18, 2002.
7. Neurofibrillary degeneration of Alzheimer's disease, invited by the Center of Developmental Neuroscience,
College of Staten Island of the City University of New York, New York, March 6, 2003.
8. Post-translational modifications of tau protein in Alzheimer’s disease, invited by the 1st International
Conference of Brain Aging, Bucharest, November 2003.
9. A novel protein phosphatase (PP5) and microtubule-associated protein tau, invited by the Institute of
Biochemistry and Cell Biology, Chinese Academy of Science, Shanghai, and Nantong Medical College,
Nantong, China, March, 2004.
10. Glycosylation of tau protein in Alzheimer's disease, invited by the 4th Academic Symposium on dementia
and Related Disorders, Guanzhou, China, May 12-16, 2004.
11. Impaired glucose uptake/metabolism contributes to hyperphosphorylation of tau via reduction of OGlcNAcylation: a novel mechanism involved in Alzheimer disease, invited by the 9th International
Conference on Alzheimer’s Disease and Related Disorders, Philadelphia, July 17-22, 2004.
12. Neurofibrillary degeneration and psychotic symptoms of Alzheimer's disease, invited by Center of
Developmental Neuroscience, College of Staten Island of the City University of New York, New York,
October 14, 2004.
13. A new mechanism of neurofibrillary degeneration in Alzheimer disease: dysregulation of tau OGlcNAcylation, invited by Institute of Pathology, Case Western Reserve University, Cleveland, Ohio, April
11, 2005.
14. Deregulation of O-GlcNAcylation of Tau Protein: A New Mechanism of Neurodegeneration, invited by the
Institute of Biochemistry and Cell Biology, Chinese Academy of Science, Shanghai, China, July 15, 2005.
15. Alzheimer’s Disease: Advances in Basic Research, Diagnosis, and Treatments, invited lecture by the
People’s Hospital of Chibi City, Chibi, China, July 19, 2005.
17. Neurofibrillary degeneration of Alzheimer's disease, invited by the Center of Developmental Neuroscience,
College of Staten Island of the City University of New York, New York, September 29, 2005.
18. Targeting Neurodegeneration of Alzheimer Disease — A Scientific Approach Understanding Disease
Mechanism, invited by Beijing University of Traditional Chinese Medicine, Beijing, China, November 24,
2005.
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Curriculum Vitae
Cheng-Xin Gong, M.D.
19. Mechanisms of Neurofibrillary Degeneration in Alzheimer Disease — How to Study the Basic Disease
Mechanism, invited by the Capital University of Medical Sciences, Beijing, China, November 28, 2005.
20. Advances in Neurofibrillary Degeneration of Alzheimer Disease, invited by the Neuroscience Research
Institute of Beijing University, Beijing, China, November 29, 2005.
21. Neurofibrillary Degeneration of Alzheimer Disease: Role of Posttranslational Modifications of Tau, invited
by the Fourth International Neuroscience Symposium, Kunming-Lijiang, China, July 3-8, 2006.
22. O-Glycosylation Regulates Phosphorylation of Tau: A Novel Mechanism Leading to Neurofibrillary
Degeneration in Alzheimer Disease, invited symposium by the 10th International Conference on
Alzheimer's Disease and Related Disorders, Madrid, Spain, July 15-20, 2006.
23. Brain Glucose Metabolism and Neurofibrillary Degeneration – Role of O-Glycosylation and
Phosphorylation of Tau Protein, invited by New York University, November 30, 2006.
24. Doing Biomedical Research: Walking through Studies on Alzheimer’s Disease, invited by Tongji Medical
College of the Huazhong University of Science and Technology, Wuhan, China, May 10, 2007.
25. Alzheimer's disease, invited by the Center of Developmental Neuroscience, College of Staten Island of the
City University of New York, New York, October 4, 2007.
26. Neurofibrillary Degeneration of Alzheimer Disease, invited by College of Staten Island of the City
University of New York, New York, September 25, 2008.
27. Hyperphosphorylation of Tau: A Promising Therapeutic Target for Alzheimer's Disease, invited by the 6th
Annual Congress of International Drug Discovery Science and Technology, Beijing, China, October 21,
2008.
28. Doing Biomedical Research: Walking through Studies on Alzheimer’s Disease, invited by Beijing
University of Traditional Chinese Medicine, Beijing, China, October 22, 2008.
29. Phosphorylation and O-GlcNAcylation of Tau: A Key Player of Neurofibrillary Degeneration, invited by
Tsinghua University, Beijing, China, October 23, 2008.
PUBLICATIONS (1993 – present only):
(A) Original Peer-Reviewed Research Articles:
1. Gong, C.-X., Singh, T. J., Grundke-Iqbal, I. and Iqbal, K. Phosphoprotein phosphatase activities in
Alzheimer disease brain. J Neurochem 1993; 61(3):921-927
2. Gong, C.-X., Singh, T. J., Grundke-Iqbal, I. and Iqbal, K. Alzheimer disease abnormally phosphorylated tau
is dephosphorylated by brain protein phosphatase 2B. J Neurochem 1994; 62:803-806
3. Gong, C.-X., Grundke-Iqbal I., Damuni, Z. and Iqbal K. Dephosphorylation of microtubule-associated
protein tau by protein phosphatase-1 and -2C and its implication in Alzheimer disease. FEBS Lett. 1994;
341:94-98
4. Gong, C.-X., Grundke-Iqbal, I. and Iqbal, K. Dephosphorylation of Alzheimer disease abnormally
hyperphosphorylated tau by protein phosphatase 2A. Neuroscience 1994; 61:765-772
5. Gong, C.-X., Shaikh, S., Wang, J.-Z., Zaidi, T., Grundke-Iqbal, I., and Iqbal, K. Protein phosphatase
activity towards abnormally phosphorylated tau: decrease in Alzheimer disease brain. J. Neurochem. 1995;
65:732-738
6. Wang, J.-Z., Gong, C.-X., Zaidi, T., Grundke-Iqbal, I., and Iqbal, K. Dephosphorylation of Alzheimer
paired helical filaments by protein phosphatase-2A and -2B. J. Biol. Chem. 1995; 270(9):4854-4860
7. Gong, C.-X., Shaikh, S., Grundke-Iqbal, I., and Iqbal, K. Inhibition of protein phosphatase-2B (calcineurin)
activity towards Alzheimer abnormally phosphorylated tau by neuroleptics. Brain Res 1996; 741:95-102
8. Pei, J.-J., Gong, C.-X., Wu, Q.-L., Cowburn, R. F., Winblad, B., Iqbal, K., and Grundke-Iqbal, I.
Subcellular distribution of protein phosphatases and abnormally hyperphosphorylated tau in the temporal
cortex from Alzheimer disease and control. J Neurol Transmission 1998; 105:69-83.
9. Wang, J.-Z., Gong, C.-X., Grandke-Iqbal, I., and Iqbal, K. Dephosphorylation of neurofibrillary tangles in
Alzheimer brain. J. Chin Neurol 1998; 31(3):146-148
10. Wang, J.-Z., Gong, C.-X., Iqbal, K., and Grandke-Iqbal, I. Abnormal posttranslational modifications of
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Curriculum Vitae
Cheng-Xin Gong, M.D.
Alzheimer microtubule-associated protein tau. Clin Neurosci 1998; 6(1):1-5.
11. Wang, J.-Z., Gong, C.-X., Grandke-Iqbal, I., and Iqbal, K. Deglycosylation of neurofibrillary tangles in
Alzheimer disease. Chin J Neurosci 1998; 14(2):63-67.
12. Wang, J.Z., Gong, C.X., Wang, Q. Relationship of Alzheimer tau modification and the biological activity.
Prog Bichem Biophys 1999; 26(2):11-14.
13. Wang, J.Z., Gong, C.X., Wang, Q. Effect of protein phosphatase on Alzheimer tangles. Acta Bichem
Biophys 1999; 15(1):123-129
14. Cheng, L.Y., Wang, J.-Z., Gong, C.-X., Pei, J.-J., Zaidi, T., Grandke-Iqbal, I., and Iqbal, K. Multiple forms
of phosphatase from human brain: isolation and partial characterization of affi-gel blue binding
phosphatases. Neurochem Res 2000; 25(1):107-120
15. Gong, C.-X., Wegiel, J., Lidsky, T., Zuck, L., Avila, J., Wisniewski, H.M., Grandke-Iqbal, I., and Iqbal, K.
Regulation of phosphorylation of neuronal microtubule-associated proteins MAP1b and MAP2 by protein
phosphatase-2A and -2B in rat brain. Brain Res 2000; 853:299-309.
16. Gong, C.-X., Lidsky, T., Wegiel, J., Wisniewski, H.M., Grandke-Iqbal, I., and Iqbal, K. Phosphorylation of
Microtubule-associated Protein Tau Is Regulated by Protein Phosphatase 2A: Implication for
Neurofibrillary Degeneration in Alzheimer Disease. J Biol Chem 2000; 275(8):5535-5544.
17. Bennecib, M., Gong, C.-X., Grandke-Iqbal, I., and Iqbal, K. Role of protein phosphatase-2A and -1 in the
regulation of GSK-3, cdk5 and cdc2, and the phosphorylation of tau in rat forebrain. FEBS Lett 2000;
485:87-93.
18. Bennecib, M., Gong, C.-X., Wegiel J., Lee, M.L., Grandke-Iqbal, I., and Iqbal, K. Inhibition od protein
phosphatases and regulation of tau phosphorylation in rat brain. Alzheimer's reports 2000; 3:295-304
19. Gong, C.-X., Lidsky, T., Wegiel, J., Grandke-Iqbal, I., and Iqbal, K. Metabolically active rat brain slices as
a model to study the regulation of protein phosphorylation in mammalian brain. Brain Res. Protocols 2001;
6:134-140.
20. Bennecib, M., Gong, C.-X., Grandke-Iqbal, I., and Iqbal, K. Inhibition of PP-2A upregulates CaMKII in rat
forebrain and induces hyperphosphorylation of tau at Ser 262/356. FEBS Lett 2001; 490:15-22.
21. Cheng, L.Y., Wang, J.-Z., Gong, C.-X., Pei, J.-J., Zaidi, T., Grandke-Iqbal, I., and Iqbal, K. Multiple forms
of phosphatase from human brain: isolation and partial characterization of affi-gel blue nonbinding
phosphatase activities. Neurochem Res 2001; 26(4): 425-438.
22. Liu, F., Zaidi, T., Grandke-Iqbal, I., Iqbal, K., Merkle, R.K., and Gong, C.-X. Role of Glycosylation in
hyperphosphorylation of tau in Alzheimer's Disease. FEBS Lett. 2002; 512:101-106.
23. Pei, J.J., Braak, H., Gong, C.-X., Grandke-Iqbal, I., Iqbal, K., Winblad, B., and Cowburn, R.F. Upregulation of cell division cycle (cdc) 2 kinase in neurons with early stage Alzheimer’s disease
neurofibrillary degeneration. Acta Neuropathol (Berl) 2002; 104:369-376.
24. Liu, F., Zaidi, T., Grandke-Iqbal, I., Iqbal, K., and Gong, C.-X. Aberrant glycosylation modulates
phosphorylation of tau by protein kinase A and dephosphorylation of tau by protein phosphatase 2A and 5.
Neuroscience 2002; 115:829-937.
25. Liu, F., Grandke-Iqbal, I., Iqbal, K., and Gong, C.-X. Involvement of aberrant glycosylation in
phosphorylation of tau by cdk5 and GSK-3. FEBS Lett. 2002; 530:209-214.
26. Gong, C.-X., Wang, J.-Z., Grandke-Iqbal, I., and Iqbal, K. Inhibition of protein phosphatase 2A induces
phosphorylation and accumulation of neurofilaments in metabolically active rat brain slices. Neurosci Lett
2003; 340:107-110.
27. Qian, W., Liu, F., Gong, C.-X., Jin, S. The expression and purification of recombinant O-GlcNAc
transferase in insect cells. Acta Acad Med Nantong 2003; 23:16-19.
28. Qian, W., Liu, F., Jin, S., Gong, C.-X. Effect of O-GlcNAcylation on phosphorylation of tau. Prog Biochem
Biophys 2003; 30:623-628.
29. Pei, J.-J., Gong, C.-X., An, W.-L., Winblad, B., Cowburn, R.F., Grandke-Iqbal, I., and Iqbal, K. Okadaicacid-induced inhibition of protein phosphatase 2A produces activation of mitogen-activated protein kinase
ERK1/2, MEK1/2, and p70 S6, similar to that in Alzheimer’s disease. Am. J. Pathol. 2003; 163:854-858.
30. Gong, C.-X., Liu, F., Wu, G., Rossie, S., Wegiel, J., Li, L., Grundke-Iqbal, I., and Iqbal, K.
Dephosphorylation of microtubule-associated protein tau by protein phosphatase 5. J. Neurochem. 2004;
88:298-310.
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Curriculum Vitae
Cheng-Xin Gong, M.D.
31. Liu, F., Iqbal, K., Grundke-Iqbal, I., Hart, G.W., and Gong, C.-X. O-GlcNAcylation regulates
phosphorylation of tau: A mechanism involved in Alzheimer's disease. Proc Natl Acad Sci USA. 2004;
101:10804-10809.
32. Tian Q, Lin ZQ, Wang XC, Chen J, Wang Q, Gong C-X, Wang JZ. Injection of okadaic acid into the
meynert nucleus basalis of rat brain induces decreased acetylcholine level and spatial memory deficit.
Neuroscience. 2004; 126(2):277-284.
33. Haque N, Gong CX, Sengupta A, Iqbal K, Grundke-Iqbal I. Regulation of microtubule-associated proteins,
protein kinases and protein phosphatases during differentiation of SY5Y cells. Brain Res Mol Brain Res.
2004; 129(1-2):163-170.
34. Liu, SJ, Zhang, JY, Li, HL, Fang, ZY, Wang Q, Deng, HM, Gong, CX, Grundke-Iqbal, I, Iqbal, K, Wang,
JZ. Tau becomes a more favorable substrate for GSK-3 when it is prephosphorylated by PKA in rat brain. J.
Biol. Chem. 2004; 279:50078-50088.
35. Huang, Y., Tanimukai, H., Liu, F., Iqbal, K., Grandke-Iqbal, I., and Gong, C.-X. Elevation of the level and
activity of acid ceramidase in Alzheimer's disease brain. Eur. J. Neurosci. 2004; 20:3489-3497. (This paper
was highlighted by Nature Review Neuroscience 2005; 6:94)
36. Wang, L-Y, Diao, L-M, Tian, Q, Wang, J-Z, Gong, C-X. Protein phosphatase 2A regulate phosphorylation
of microtubule-associated protein 1b. Prog Biochem Biophys 2004; 31:986-990.
37. Qian, W., Liu, F., Gong, C.-X., Jin, S. Expression of recombinant O-GlcNAc transferase in cultured
prokaryotic and eukaryotic cells and its purification. Acta Acad Med Nantong 2004; 24:1-4.
38. Liu, F., Iqbal, K., Grundke-Iqbal, I., Rossie, S., Gong, C.-X. Dephosphorylation of tau by protein
phosphatase 5: Impairment in Alzheimer disease. J. Biol. Chem. 2005; 280:1790-1796.
39. Sun, L., Wang, X., Liu, S., Wang, Q., Wang, J., Bennecib, M., Gong, C.-X., Sengupta, A., Grundke-Iqbal,
I., Iqbal, K. Bilateral injection of isoproterenol into hippocampus induces Alzheimer-like
hyperphosphorylation of tau and spatial memory deficit in rat. FEBS Lett. 2005; 579:251-258.
40. Huang, Y., Liu, F., Grandke-Iqbal, I., Iqbal, K., and Gong, C.-X. NFkappaB precursor, p105, and NFkappaB inhibitor, IkappaBgamma, are both elevated in Alzheimer disease brain. Neurosci. Lett. 2005;
373:115-118.
41. Yin, D.-M., Shi, J.-H., Gu, X.-L., Shen, Q., Gong, C.-X., and Liu, F. Rapid dephosphorylation of
microtubule-associated protein tau during postmortem period. Prog Biochem Biophys 2005; 32:1150-1155.
42. Liu, F., Grundke-Iqbal, I., Iqbal, K., Gong, C.-X. Contributions of various protein phosphatases in the
regulation of phosphorylation of tau protein. Eur. J. Neurosci. 2005; 22:1942-1950.
43. Liu, F., Grundke-Iqbal, I., Iqbal, K., Oda, Y., Tomizawa, K., Gong, C.-X. Truncation and activation of
calcineurin A by calpain l in Alzheimer disease brain. J. Biol. Chem. 2005; 280:37755-37762.
44. Yang, Y., Hu, S.-H., Zhang, J.-H., Zhang, M.-X., Gong, C.-X. Alzheimer-like hyperphosphorylation of tau
in brains of rats with obesity and type 2 diabetes. Prog. Biochem. Biophys. 2006; 33:458-464.
45. Li, X., Lu, F., Wang, J.-Z., Gong, C.-X. Concurrent alteration of O-GlcNAcylation and phosphorylation of
tau in mouse brains during fasting. Eur. J. Neurosci. 2006; 23:2078-2086.
46. Liu, F., Liang, Z., Shi, J., Yin, D., El-Akkad, E., Grundke-Iqbal, I., Iqbal, K., Gong, C.-X. PKA modulates
GSK-3- and cdk5-catalyzed phosphorylation of tau in site- and kinase-specific manners. FEBS Lett. 2006;
580:6269-6274.
47. Yang, Y., Hu, S.-H., Zhang, J.-H., Zhang, M.-X., Gong, C.-X. Alzheimer-like hyperphosphorylation
induced by dysregulated insulin signaling transduction and impaired glucose metabolism in type 1 diabetes
millitus. Chn. J. Biochem. Mol. Biol. 2006; 22:902-908.
48. Liang Z, Liu F, Grundke-Iqbal I, Iqbal K, Gong CX. Down-regulation of cAMP-dependent protein kinase
by over-activated calpain in Alzheimer disease brain. J Neurochem. 2007; 103(6):2462-70.
49. Hu, S.-H., Yang, Y., Zhang, J.-H., Zhang, M.-X., Gong, C.-X. Rosiglitazone ameliorate Alzheimer-like
hyperphosphorylation of tau protein in the hippocampus of rats with insulin resistance. Prog. Biochem.
Biophys. 2007; 34:533-537.
50. Liu F, Li B, Tung EJ, Grundke-Iqbal I, Iqbal K, Gong CX. Site-specific effects of tau phosphorylation on
its microtubule assembly activity and self-aggregation. Eur J Neurosci. 2007; 26(12):3429-36.
51. Deng, Y., Li, B., Liu, F., Iqbal, K., Grundke-Iqbal, I., Brandt, R., Gong, C.-X. Regulation between OGlcNAcylation and phosphorylation of neurofilament-M and their dysregulation in Alzheimer disease.
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Curriculum Vitae
Cheng-Xin Gong, M.D.
FASEB J. 2008; 22(1):138-45.
52. Liu Y, Liu F, Iqbal K, Grundke-Iqbal I, Gong CX. Decreased glucose transporters correlate to abnormal
hyperphosphorylation of tau in Alzheimer disease. FEBS Lett. 2008; 582(2):359-64.
53. Liang Z, Liu F, Iqbal K, Grundke-Iqbal I, Wegiel J, Gong CX. Decrease of protein phosphatase 2A and its
association with accumulation and hyperphosphorylation of tau in Down syndrome. J Alzheimer’s Dis.
2008; 13(3):295-302.
54. Liu F, Liang Z, Wegiel J, Hwang YW, Iqbal K, Grundke-Iqbal I, Ramakrishna N, Gong CX.
Overexpression of Dyrk1A contributes to neurofibrillary degeneration in Down syndrome. FASEB J. 2008;
22(9):3224-33. PMID: 18509201
55. Wegiel J, Dowjat K, Kaczmarski W, Kuchna I, Nowicki K, Frackowiak J, Mazur Kolecka B, Wegiel J,
Silverman WP, Reisberg B, Deleon M, Wisniewski T, Gong CX, Liu F, Adayev T, Chen-Hwang MC,
Hwang YW. The role of overexpressed DYRK1A protein in the early onset of neurofibrillary degeneration
in Down syndrome. Acta Neuropathol. 2008; 116(4):391-407. PMID: 18696092
56. Shi J, Zhang T, Zhou C, Chohan MO, Gu X, Wegiel J, Zhou J, Hwang YW, Iqbal K, Grundke-Iqbal I,
Gong CX, Liu F. Increased dosage of Dyrk1A alters ASF-regulated alternative splicing of tau in Down
syndrome. J Biol Chem. 2008; 283(42):28660-9. PMID: 18658135
57. He X, Huang Y, Li B, Gong CX, Schuchman EH. Deregulation of sphingolipid metabolism in Alzheimer's
disease. Neurobiol Aging. 2008; Jun 9. [Epub ahead of print] PMID: 18547682
58. Yu Y, Run X, Liang Z, Li Y, Liu F, Liu Y, Iqbal K, Grundke-Iqbal I, Gong CX. Developmental regulation
of tau phosphorylation, tau kinases, and tau phosphatases. J. Neurochem. 2009; In press.
59. Liang Z, Liu F, Iqbal K, Grundke-Iqbal I, Gong CX. Dysregulation of Tau Phosphorylation in Mouse Brain
during Excitotoxic Damage. J. Alzheimer’s Dis. 2009; In press.
60. Run X, Liang Z, Zhang L, Iqbal K, Grundke-Iqbal I, Gong CX. Anesthesia induces phosphorylation of tau.
J. Alzheimer’s Dis. 2009; In press.
(B) Review Articles:
1. Iqbal, K., Alonso, A., Gong, C.-X., Khatoon, S., Kudo, T., Singh, T. and Grundke-Iqbal, I. Molecular
pathology of Alzheimer neurofibrillary degeneration. Acta Neurobiol Exp 1993; 53:325-335
2. Iqbal, K., Alonso, A. C., Gong, C.-X., Khatoon, S., Singh, T.J. and Grundke-Iqbal, I. Mechanism of
Neurofibrillary Degeneration in Alzheimer's Disease. Mol. Neurobiol. 1994: 9: 119-123
3. Iqbal, K., Alonso, A. C., Gong, C.-X., Haque, N., Khatoon, S., Pei, J. J., Sing, T., Tanaka, T., Wang, J. and
Grundke-Iqbal, I. Cytoskeletal changes in Alzheimer disease. Ann. Psychiat. 1994; 4:123-135
4. Iqbal, K., Alonso, A. del C., Gong, C.-X., Khatoon, S., Pei, J.-J., Wang, J.-Z., and Grundke-Iqbal, I.
Mechanisms of neurofibrillary degeneration and the formation of neurofibrillary tangles. J Neurol
Transmission 1998; S53:169-180.
5. Gong, C.-X., Wu, Q. Web sites on the research, diagnosis and management of Alzheimer’s Disease. News
Lett Senile Dementia 1999; 1(2):12-14.
6. Iqbal, K., Alonso, A. del C., Gondal, J. A., Gong, C.-X., Haque, N., Khatoon, S., Sengupta, A., Wang, J.Z., and Grundke-Iqbal, I. Mechanisms of neurofibrillary degeneration and pharmacologic therapeutic
approach. J Neural Transmission 2000; 59:213-222.
7. Iqbal, K., Alonso, A. del C., El-Akkad, E., Gong, C.-X., Haque, N., Khatoon, S., Pei, J.J., Tsujio, I., Wang,
J., and Grundke-Iqbal, I. Significance and mechanism of Alzheimer neurofibrillary degeneration and
therapeutic targets to inhibit the lesion. J. Mol. Neurosc. 2002; 19:95-99.
8. Iqbal, K., Alonso, A. del C., El-Akkad, E., Gong, C.-X., Haque, N., Khatoon, S., Tsujio, I., and GrundkeIqbal, I. Pharmacological targets to inhibit Alzheimer neurofibrillary degeneration. J. Neural Transm. 2002;
62:309-319.
9. Iqbal, K., Alonso, A. del C., El-Akkad, E., Gong, C.-X., et al. Alzheimer neurofibrillary degeneration:
therapeutic targets and high-throughput assays. J. Mol. Neurosc. 2003; 20:425-429.
10. Iqbal, K., Alonso, A. del C., Chen, S., Chohan, M.O., El-Akkad, E., Gong, C.-X., Khatoon, S., Li, B., Liu,
F., Rahman, A., Tanimukai, H., and Grundke-Iqbal, I. Tau pathology in Alzheimer disease and other
tauopathies. Biochim. Biophys. Acta. 2005; 1739:198-210.
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Curriculum Vitae
Cheng-Xin Gong, M.D.
11. Gong, C.-X., Liu F., Grundke-Iqbal, I., Iqbal, K. Post-translational modifications of tau protein in
Alzheimer’s disease. J. Neural Transm. 2005; 112:813-838.
12. Gong, C.-X., Liu F., Grundke-Iqbal, I., Iqbal, K. Hypothesis: Impaired brain glucose metabolism leads to
Alzheimer neurofibrillary degeneration through a decrease in tau O-GlcNAcylation. J. Alzheimer’s Dis.
2006; 9:1-12.
13. Gong, C.-X., Wang, J.-Z. Role of Tau Protein in Neurofibrillary Degeneration of Alzheimer Disease. J.
Med Mol Biol 2006;3:163-169.
14. Liu F., Liang, Z., Gong, C.-X. Hyperphosphorylation of tau and protein phosphatases in Alzheimer disease.
Panminerva Med. 2006; 48:97-108.
15. Gong, C.-X., Liu F., Grundke-Iqbal, I., Iqbal, K. Dysregulation of protein phosphorylation/
dephosphorylation in Alzheimer disease: a potential therapeutic target. J. Biomed. Biotech. 2006; DOI
10.1155/JBB/2006/31825.
16. Liu F., Gong, C.-X. Tau exon 10 alternative splicing and tauopathies. Mol. Neurodegeneration. 2008;
10;3:8. PMID: 18616804
17. Gong, C.-X., Iqbal, K. Hyperphosphorylation of Microtubule-Associated Protein Tau: A Promising
Therapeutic Target for Alzheimer Disease. Curr. Medicin. Chem. 2008; 15:2321-8. PMID: 18855662
(C) Book Chapters:
1. Iqbal, K., Alonso, A.C., Gong, C.-X., Haque, N., Khatoon, S., Pei, J. J., Singh, T.S., Tanaka, T., Wang, J.Z., and Grundke-Iqbal, I. Alzheimer neurofibrillary degeneration: importance, mechanism and therapeutic
approaches. In Iqbal, K. et al (editor): Research Advances in Alzheimer's Disease and Related Disorders.
John Wiley & Sons Ltd, Chichester, p514-522, 1995
2. Iqbal, K., Alonso del C., Gong, C.-X., Haque, N., Khatoon, S., Pei, J.J., Singh, T., Tanaka, T., Wang, J.-Z.,
and Grundke-Iqbal, I. Role of neurofibrillary degeneration in Alzheimer disease. In: Aging of the Brain and
Alzheimer Disease, Vol. 1, edited by Z.C. Zheng, P.R.China, p.149-156, 1995
3. Iqbal, K., Alonso, A. del C., Gong, C.-X., Haque, N., Khatoon, S., Kudo, T., Pei, J.-J., Singh, T. J., Tanaka,
T., Wang, J.-Z., and Grundke-Iqbal, I. Alzheimer neurofibrillary degeneration: a feasible and key target for
therapeutics. In Becker, R. et al (ed): Alzheimer Disease: From Molecular Biology to Therapy. Birkhauser
Boston, Inc., pp.31-36, 1996
4. Iqbal, K., Alonso, A. del C., Gong, C.-X., Khatoon, S., Pei, J.-J., Wang, J.-Z., and Grundke-Iqbal, I. Tau
phosphatases. In Kosik, K. And Avila, J. (Ed): Brain Microtubule Associated Proteins: Modifications and
Disease, New York, pp. 95-111, 1997
5. Iqbal, K., Alonso, A. del C., Gondal, J. A., Gong, C.-X., Haque, N., Khatoon, S., Sengupta, A., and
Grundke-Iqbal, I. Inhibition of neurofibrillary degeneration: a rational and promising therapeutic target. In
Iqbal, K. et al (editor): Alzheimer's Disease and Related Disorders: Etiology, Pathogenesis and
Therapeutics. John Wiley & Sons Ltd, Chichester, 1999; pp 269-280.
6. Iqbal, K., Alonso, A. del C., El-Akkad, E., Gong, C.-X., et al. Alzheimer neurofibrillary degeneration:
significance and therapeutic targets. In K. Iqbal and B. Winblad (Ed): Alzheimer’s Disease and Related
Disorders: Research Advance. “Ana Aslan” International Academy of Aging, Bucharest, 2003, pp275-290.
7. Iqbal, K., Alonso, A. del C., El-Akkad, E., Gong, C.-X., et al. Pivotal roles of neurofibrillary degeneration
in Alzheimer disease and therapeutic targets. In Moecular Neurobiology of Alzheimer Disease and Related
Disorders (Eds: Takeda, M., Tanaka, T., and Cacabelos, R.), Basel, Karger, 2004, pp42-51.
8. Wang, JZ, Liu, SJ, Wang, X-C, Tian, Q, Zhou, X-W, Liu, R, Zhang, JY, Yang, Y, Wang Q, Gong, CX,
Grundke-Iqbal, I, Iqbal, K, Regulation of tau phosphorylation by protein kinase A and glucose synthase
kinase-3 in rat. Research Advance in Alzheimer Disease and Related Dementia (Eds: K. Iqbal and B.
Winblad), Alzheimer’s Association. 2004, pp. 114-126.
9. Iqbal, K., Alonso, A. del C., El-Akkad, E., Gong, C.-X., Haque, N., Khatoon, S., Tanimukai, H., Tsujio, I.,
and Grundke-Iqbal, I. Neurofibrillary degeneration: A promising target for the treatment of Alzheimer
disease and other tauopathies. In: Hanin, I., Fisher, A., and Cacabelos, R. (eds): Progress in Alzheimer’s
Disease and Parkison’s Disease. Parthenon Publishing Group, Lancaster, UK, 2005.
10. Gong, C.-X., Liu F., Grundke-Iqbal, I., Iqbal, K. O-glycosylation regulates hyperphosphorylation of tau: a
9
Curriculum Vitae
Cheng-Xin Gong, M.D.
novel mechanism leading to neurofibrillary degeneration in Alzheimer disease. In Iqbal, K. et el (eds):
Alzheimer’s Disease: New Advances. Medimond International Proceedings, Madrid, 2007, pp 253-261.
11. Iqbal, K., Alonso, A. del C., Chohan, M.O., El-Akkad, E., Gong, C.-X., et al. Molecular basis of tau protein
pathology: role of abnormal hyperphosphorylation. In Dawbarn, D. and Allen, S.J. (eds): Neurobiology of
Alzheimer’s disease, 3rd Edition. Oxfort University Press, New York, 2007, pp. 111-131.
12. Gong, C.-X. NF-κB in brain diseases. In: Blass, J. (ed): Handbook of neurochemistry and Molecular
Neurobiology / Disease Mechanisms. Kluwer Academic/Plenm Publishing, New York, 2009 (in press).
Major Research Achievements
Dr. Gong, Head of Laboratory of Brain Metabolism
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Curriculum Vitae
Cheng-Xin Gong, M.D.
The overall goal of Dr. Gong’s research lab is to understand the molecular mechanism of
neurodegeneration in various brain diseases and ultimately to develop therapeutic strategies to
treat diseases with neurodegeneration.
Dr. Gong has made significant contributions and received wide recognition in the field of
neurofibrillary degeneration. He was the first in the world to discover that protein phosphatase 2A is
down-regulated in Alzheimer’s disease (AD) brain and this deregulation partially underlies the
abnormal hyperphosphorylation of tau and neurofibrillary degeneration of AD. This discovery has
been confirmed by several other laboratories and has become the basis for many scientists to
further investigate the molecular mechanism of neurofibrillary degeneration and for some
pharmaceutical companies to develop therapies for neurofibrillary degeneration. He was also the first
to discover a novel modification, named O-GlcNAcylation, of human brain tau protein and found
that tau O-GlcNAcylation regulates tau phosphorylation and its deregulation may play an important
role in neurodegeneration of AD (PNAS 2004, 101:10804-10809). On the basis of this finding, He
recently proposed a new hypothesis explaining the mechanism by which impaired brain glucose
uptake/mechanism contributes to neurodegeneration (J Alz Dis; 2006, 9:1-12). Very recently, Dr.
Gong’s lab found the important role of Dyrk1A (dual-specificity tyrosine phosphorylation-regulated
kinase), a ser/thr protein kinase that is over-expressed in the brain of individuals with Down
syndrome (DS) due to trisomy 21, in the neurofibrillary degeneration of DS (FASEB J. 2008,
22:3224-3233; J. Biol. Chem. 2008, 283:28660-28669). These findings revealed a new mechanism
leading to neurofibrillary degeneration and may provide novel strategy to prevent and treat
neurofibrillary degeneration in DS.
Major research Impacts
New York State Institute for Basic research in Developmental Disabilities
1. The institute was among the first to discover the APP gene, which encodes the precursor
protein of amyloid β peptide, and to identify tau as the protein component of neurofibrillary
tangles. These two discoveries in 1980’are the foundation of modern research on Alzheimer’s
disease. The institute was among the four leading institutions in the world for Alzheimer’s
disease research.
2. The institute’s first director, Dr. G. Jervis, discovered the genetic deficit that leads to
phenylketonuria (PKU), a cause of severe mental retardation. This finding led to the
development of a special diet that prevents mental retardation in the affected children and of
the newborn screening programs for PKU that are now used universally.
3. The institute developed, for the first time, screening tests for fragile X syndrome, the most
common inherited cause of mental retardation.
4. The institute was the first to demonstrate the association between fragile X and autism.
5. The institute discovered that taurine, a compound present in human milk, is essential for
normal brain development. Because of this discovery, all US government-approved infant
formulas are required to have taurine.
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