With shifting demographics and an increasingly ageing global population, the prevalence and associated burden of diseases of old age, especially neurodegenerative diseases, is expected to increase dramatically over the next three decades. Therapies to prevent neurodegenerative diseases remain lacking and existing treatments are largely palliative. Our laboratory focuses on understanding how discrete genetic factors contribute to the development of neurodegenerative diseases.
A major focus of our lab is Huntington disease (HD), a monogenic and highly penetrant progressive dementia. HD provides an opportunity to gain insights into fundamental mechanisms involved in neurodegeneration. Our aim is to define key disease processes and to develop novel approaches for therapeutic intervention.
A major challenge in the study of neurodegenerative diseases has been the inaccessibility of the affected tissue, namely the brain. Two major technological breakthroughs are beginning to overcome this challenge. The first advance is the development of genetic and pharmacological approaches to direct the differentiation of human pluripotent stem cells into neuronal types of interest. The second major advance is ability to precisely edit specific loci in the genome using programmable sequence-specific nucleases. We have leveraged these tools to develop isogenic stem cell-based models of neurodegenerative disease in human neurons. This will allow us to better understand the precise contribution of specific genetic factors to disease processes in a physiologically relevant human context.
Transgenic animal models of NDDs enable the longitudinal study of cell-autonomous and non-cell-autonomous disease processes in the context of the whole organism, allowing the characterization of disease phenotypes on the behavioural, neuroanatomical, cellular, and biochemical levels. We combine deep phenotyping of animal models of NDDs with genetic and pharmacological interventions to define disease mechanisms and evaluate their potential as targets for therapy.
Mahmoud Pouladi obtained his BSc in Molecular Biology and MSc in Medical Sciences from McMaster University (Hamilton, Canada). He completed his PhD studies in the Department of Medical Genetics under the mentorship of Dr. Michael Hayden at the University of British Columbia (Vancouver, Canada). His research has focused on the development and use of animal models of Huntington disease to reveal disease processes and to evaluate candidate therapeutics as potential treatments for Huntington disease.
Mahmoud Pouladi has been the recipient of a number of awards and distinctions including the University of British Columbia’s CFRI Award for Outstanding Achievement by a Doctoral Candidate, the Canadian Institutes of Health Research Brain Star Award, and the British Columbia Innovation Council’s Ripples of Hope Award in Biotechnology & Entrepreneurship.
Lab website: http://www.pouladilab.org
Xiaohong earned her Bachelor’s Degree in Clinical Medicine in 2008, and Ph.D. in Histology and Embryology in 2013, both from Harbin Medical University, China. She was a visiting Ph.D. student in GlaxoSmithKline R&D China from August 2009 to May 2013. In GSK, her research mainly focused on neurodegenerative disease (Alzheimer’s disease and Parkinson’s disease) modeling and drug screening using hESC/hiPSC-derived neuronal cells. In June 2013, she joined in TLGM as a Research Fellow. Currently, her main project focuses on using hiPSCs and genome engineering to validate a potential therapeutic target in Huntington disease.
In 2013, Marta joined the Translational Laboratory in Genetic Medicine as a Research Fellow where she is currently studying the neuropathology of Huntington’s disease as well as evaluating the therapeutic potential of several drugs for the treatment of this neurodegenerative disorder.
Kagistia graduated from Utrecht University in 2009 with a Master’s degree in Cancer Genomics and Developmental Biology, and she continued her doctorate study at the National University of Singapore, Department of Paediatrics in 2010. She carried out her PhD research at the Genome Institute of Singapore and her study focused on characterizing functional impacts of chromosomal rearrangements in idiopathic Neurodevelopmental Disorders.
In 2014, Kagistia joined TLGM and her current research project in Pouladi’s lab is to study the impact of CAG repeat length of Huntingtin on biological and molecular processes and its relevance to the pathogenesis of Huntington disease.
Jinqiu graduated from National University of Singapore with a Ph.D. degree in Molecular Biology in 2004. She joined Genome Institute of Singapore focusing on studying the mechanism of pluripotency of human embryonic stem cells. She then established disease models by genomic modification of human ES cells or by reprogramming patient fibroblast cells to induced pluripotent stem cells (iPSCs). These models include Hutchinson Gilford Progeria Syndrome, familial dilated cardiomyopathy and others. Now she is interested in developing non-human primate (NHP) models of human Huntington’s disease and establishing forward genetic screens in neural cells derived from iPSCs of Huntington disease.
Ruizhu graduated from Cornell University with a Bachelor’s degree in Biology in 2007. Thereafter, she worked as a research assistant at the Singapore Immunology Network before embarking on her doctoral studies at Stanford University. She did her dissertation on the development of intestinal dendritic cells under the supervision of Dr. Eugene Butcher and obtained her PhD degree in Immunology in 2014. She joined TLGM as a Research Fellow in 2015 to study the role of microglia in Huntington Disease.
Harwin received his B.S. in Molecular Biology from the University of Wisconsin-Madison in 2008. As an undergraduate, Harwin worked at the laboratory of Dr. Jing Zhang where he studied the role of oncogenic K-ras mutations in leukemia and myeloma. Harwin then spent a year as a research assistant in the Institute of Medical Biology in the laboratory of Dr. Lim Sai Kiang. In 2009, Harwin left for Stanford University to start his doctoral studies, where he used zebrafish to understand the genetic controls of oligodendrocyte development and central nervous system myelination under the guidance of Dr. William Talbot. Harwin joined TLGM in 2015 as a Research Fellow to establish novel animal models for Huntington Disease.
Costanza graduated from the University of Pavia in 2011 with a Master degree in Medical and Pharmaceutical Biotechnologies, she joined the Laboratory of Stem Cell Biology and Pharmacology of Neurodegenerative Diseases in Milan where she worked on a project on Huntington disease. In 2015 she started her PhD studies at TLGM and her investigation will be focused on white matter atrophy in a mouse model of Huntington disease.
Amin completed his M.D. degree with first class honors at Isfahan University of Medical Sciences. In addition, he achieved a gold medal (as the first individual rank) in the National Medical Students' Academic Olympiad in the field of Scientific Reasoning in Basic Science. He trained as a medical research assistant in several research institutes such as the Stem Cell Department of Royan Institute where he worked on translational research projects towards his goal of becoming a Clinician-Scientist. In August 2015, He received the Singapore International Graduate Award (SINGA scholarship) and was admitted into the PhD program at the Yong Loo Lin School of Medicine, National University of Singapore. He joined the Pouladi lab at TLGM, where he will employ human stem cell-derived neural cells to model genetic forms of dementia, and in particular HD.
Bernice is a Senior Research Officer in the Neurodegenerative diseases group (Pouladi Lab). She obtained her BSc (Hons) in Molecular Biology and Biomedical Sciences in 2006 and her MSc in Bioinformatics shortly after. She has a decade of research experience from her time in TLGM, Harvard University (School of Public Health) and Genome Institute of Singapore. Her interest is in functional genomics.
Tan Liang Juin (Amberlyn) previously worked as a laboratory technologist in an animal breeding facility at the National University of Singapore (CARE). She then completed her undergraduate studies at Murdoch University and obtained her bachelor degree in Science in 2013. She then joined TLGM as a Research Officer and is in charge of managing and maintaining the animal colony of TLGM. She also assists in drug trials using mouse models to find approaches to therapy for Huntington’s disease.
Chen MZ, Moily NS, Bridgford J, Wood RJ, Radwan M, Bridgford J, Smith TA, Song Z, Tang BZ, Tilley L, Xu X, Reid GE, Pouladi MA, Hong Y, Hatters DM. A thiol probe for measuring unfolded protein load and proteostasis in cells. Nature Communications. 2017. In Press.
Takata K, Kozaki T, Lee CZW, Thion MS, Otsuka M, Lim S, Utami KH, Fidan K, Park DS, Malleret B, Chakarov S, See P, Low D, Low G, Garcia-Miralles M, Zeng R, Zhang J, et al. Garel S, Pouladi MA, Ginhoux F. Induced-Pluripotent-Stem-Cell-Derived Primitive Macrophages Provide a Platform for Modeling Tissue-Resident Macrophage Differentiation and Function. Immunity. 2017 Jul 18;47(1):183-198.e6. doi: 10.1016/j.immuni.2017.06.017.
Xu X, Tay YL, Huang Y, Yoon SI, Sim B, Ooi J, Utami KH, Ziaei A, Ng B, Radulescu C, Ng A, Low D, Loh M, Venkatesh B, Ginhoux F, Augustine GJ, Pouladi MA. Reversal of phenotypic abnormalities by CRISPR/Cas9-mediated gene correction in Huntington disease patient-derived induced pluripotent stem cells. Stem Cell Reports 2017 Mar 14;8(3):619-633. doi: 10.1016/j.stemcr.2017.01.022.
Southwell AL, Skotte NH, Villanueva EB, Østergaard ME, Gu X, Kordasiewicz HB, Kay C, Cheung D, Xie Y, Waltl S, Dal Cengio L, Doty CN, Petoukhov E, Findlay-Black H, Iworima D, Slama R, Ooi J, Pouladi MA, Yang XW, Swayze EE, Seth PP, Hayden MR. A novel humanized mouse model of Huntington disease for preclinical development of therapeutics targeting mutant huntingtin alleles. Human Molecular Genetics. 2017 Jan 18. pii: ddx021. doi: 10.1093/hmg/ddx021.
Julien SG, Kim SY, Brunmeir R, Sinnakannu JR, Ge X, Li H, Ma W, Yaligar J, Prakash B, Velan SS, Röder PV, Zhang Q, Sim CK, Wu J, Garcia-Miralles M, Pouladi MA, Xie W, McFarlane C, Han W, Xu F. Narciclasine attenuates diet-induced obesity by promoting oxidative metabolism in skeletal muscle. PLoS Biology. 2017 Feb 16;15(2):e1002597. doi: 10.1371/journal.pbio.1002597.
Garcia-Miralles M, Hong X, Tan LJ, Caron NS, Huang Y, To XV, Lin RY, Franciosi S, Papapetropoulos S, Hayardeny L, Hayden MR, Chuang KH, Pouladi MA. Laquinimod rescues striatal, cortical and white matter pathology and results in modest behavioural improvements in the YAC128 model of Huntington disease. Scientific Reports. 2016 Aug 16;6:31652. doi: 10.1038/srep31652.
Itahana Y, Zhang J, Göke J, Vardy LA, Han R, Iwamoto K, Cukuroglu E, Robson P, Pouladi MA, Colman A, Itahana K. Histone modifications and p53 binding poise the p21 promoter for activation in human embryonic stem cells. Scientific Reports. 2016 Jun 27;6:28112. doi: 10.1038/srep28112.
Maillet A, Tan K, Chai X, Sadananda SN, Mehta A, Ooi J, Hayden MR, Pouladi MA, Ghosh S, Shim W, Brunham LR. Modeling doxorubicin-induced cardiotoxicity in human pluripotent stem cell derived-cardiomyocytes. Scientific Reports. 2016. doi:10.1038/srep25333
Teo R, Hong X, Yu-Taeger L, Huang Y, Tan LJ, Xie Y, To XV, Guo L, Rajendran R, Novati A, Calaminus C, Riess O, Hayden MR, Nguyen HP, Chuang KH, Pouladi MA. Structural and molecular myelination deficits occur prior to neuronal loss in the YAC128 and BACHD models of Huntington disease. Human Molecular Genetics. 2016. doi: 10.1093/hmg/ddw122.
Garcia-Miralles M, Ooi J, Ferrari Bardile C, Tan LJ, George M, Drum CL, Lin RY, Hayden MR, Pouladi MA. Treatment with the MAO-A inhibitor clorgyline elevates monoamine neurotransmitter levels and improves affective phenotypes in a mouse model of Huntington disease. Experimental Neurology. 2016. doi:10.1016/j.expneurol.2016.01.019
Riechers SP, Butland S, Deng Y, Skotte N, Ehrnhoefer DE, Russ J, Laine J, Laroche M, Pouladi MA, Wanker E, Hayden MR, Graham RK. Interactome network analysis identifies multiple caspase-6 interactors involved in the pathogenesis of HD. Human Molecular Genetics. 2016. doi: 10.1093/hmg/ddw036.
Southwell AL, Franciosi S, Villanueva EB, Xie Y, Winter LA, Veeraraghavan J, Jonason A, Felczak B, Zhang W, Kovalik V, Waltl S, Hall G, Deng Y, Pouladi MA, Smith ES, Bowers WJ, Zauderer M, Hayden MR. Anti-semaphorin 4D immunotherapy ameliorates neuropathology and some cognitive impairment in the YAC128 mouse model of Huntington disease. Neurobiology of Disease. 2015. doi:10.1016/j.nbd.2015.01.002
Wong BKY, Ehrnhoefer DE, Graham RK, Martin DD, Ladha S, Uribe V, Stanek LM, Franciosi S, Qiu X, Deng Y, Kovalik V, Zhang W, Pouladi MA, Shihabuddin LS, Hayden MR. Partial rescue of some features of Huntington Disease in the genetic absence of caspase-6 in YAC128 mice. Neurobiology of Disease. 2015. doi: 10.1016/j.nbd.2014.12.030
Philips T, Rothstein JD, Pouladi MA. Preclinical models needed in translation? A Pro/Con debate. Movement Disorders Journal. 2014. 29: 1391-1396.
Pouladi MA, Morton AJ, Hayden MR. Choosing an Animal Model for the Study of Huntington Disease. Nature Reviews Neuroscience. 2013. 14: 708–721.
Marco S, Giralt A, Petrovic MM, Pouladi MA, Martínez-Turrillas R, Martínez-Hernández J, Kaltenbach LS, Torres-Peraza J, Graham RK, Watanabe M, Luján R, Nakanishi N, Lipton SA, Lo DC, Hayden MR, Alberch J, Wesseling JF, Pérez-Otaño I. Suppressing aberrant GluN3A expression rescues NMDA receptor dysfunction, synapse loss and motor and cognitive decline in Huntington’s disease models. Nature Medicine. 2013. 19: 1030-8.
Graham RK, Deng Y, Pouladi MA, Vaid K, Ehrnhoefer DE, Southwell AL, Bissada N, Franciosi S, Hayden MR. Caspase-6-resistant mutant huntingtin does not rescue the toxic effects of caspase-cleavable mutant huntingtin in vivo. Journal of Huntington’s disease. 2012. doi:10.3233/JHD-120038.
Southwell AL, Warby SC, Carroll JB, Doty CN, Skotte NH, Zhang WN, Villanueva EB, Kovalik V, Xie Y, Pouladi MA, Collins JA, Yang W, Franciosi S, Hayden MR. A fully humanized transgenic mouse model of Huntington disease. Human Molecular Genetics. 22: 18-34.
Pouladi MA, Brillaud E, Xie Y, Conforti P, Graham RK, Ehrnhoefer DE, Franciosi S, Zhang W, Zapala M, Poucheret P, Compte E, Maurel J-C, Zuccato C, Cattaneo E, Neri C, Hayden MR. NP03, a novel low-dose lithium formulation, is neuroprotective in the YAC128 mouse model of Huntington disease. Neurobiology of Disease. 2012. 48: 282-289.
Pouladi MA, Stanek LM, Xie Y, Franciosi S, Deng Y, Butland S, Warby S, Zhang W, Cheng SH, Shihabuddin LS, Hayden MR. Marked differences in neurochemistry and aggregates despite similar behavioural and neuropathological features of Huntington disease in the full-length BACHD and YAC128 mice. Human Molecular Genetics. 2012. 21: 2219-2232.
Huang Y, Pouladi MA. Heritability of pain sensitivity and opioid analgesia. Clin Genet. 2012. 82: 376-7.
Teo R, Pouladi MA. PS: Pain and sodium channels. Clin Genet. 2012. 82: 374-6.
Pouladi MA. Painful gains: missense mutations in SCN9A and idiopathic small nerve fibre neuropathy. Clin Genet. 2012. 82: 374.
Uribe V, Wong BKY, Graham RK, Cusack CL, Skotte NH, Pouladi MA, Xie Y, Deng Y, Ehrnhoefer DE, Franciosi S, Bissada N, Spreeuw A, Zhang W, Vaid K, Deshmukh M, Howland D, Hayden MR. Rescue from excitotoxicity and axonal degeneration accompanied by age-dependent behavioral and neuroanatomical alterations in caspase-6-deficient mice. Human Molecular Genetics. 2012. 21: 1954-67.
Song W, Chen J, Petrilli A, Liot G, Klinglmayr E, Zhou Y, Poquiz P, Tjong J, Pouladi MA, Hayden MR, Masliah E, Ellisman M, Rouiller I, Schwarzenbacher R, Bossy B, Perkins G, Bossy-Wetzel E. Mutant huntingtin binds the mitochondrial fission GTPase dynamin-related protein-1 and increases its enzymatic activity.Nature Medicine. 2011. 17 (3): 377-382.
Simpson JM, Gil-Mohapel JM, Pouladi MA, Ghilan M, Xie Y, Hayden MR, Christie BR. Altered adult hippocampal neurogenesis in the YAC128 transgenic mouse model of Huntington disease.Neurobiol Dis. 2011. 41: 249-60.
Graham RK, Deng Y, Carroll J, Vaid K, Cowan C, Pouladi MA, Metzler M, Bissada N, Wang L, Faull RL, Gray M, Yang XW, Raymond LA, Hayden MR. Cleavage at the 586 amino acid caspase-6 site in mutant huntingtin influences caspase-6 activation in vivo. J Neurosci. 2010. 30: 15019-15029.
Valenza M, Leoni V, Karasinska JM, Petricca L, Fan J, Carroll J, Pouladi MA, Fossale E, Nguyen HP, Riess O, MacDonald M, Wellington C, DiDonato S, Hayden M, Cattaneo E. Cholesterol defect is marked across multiple rodent models of Huntington's disease and is manifest in astrocytes.J Neurosci. 2010. 30: 10844-10850.
Milnerwood AJ, Gladding CM, Pouladi MA, Kaufman AM, Hines RM, Boyd JD, Ko RW, Vasuta OC, Graham RK, Hayden MR, Murphy TH, Raymond LA. Early Increase in Extrasynaptic NMDA Receptor Signaling and Expression Contributes to Phenotype Onset in Huntington’s Disease Mice. Neuron. 2010. 65: 178–190.
Pouladi MA, Xie Y, Skotte NH, Ehrnhoefer DE, Graham RK, Kim JE, Bissada N, Yang XW, Paganetti P, Friedlander RM, Leavitt BR, Hayden MR. Full-length huntingtin levels modulate body weight by influencing insulin-like growth factor 1 expression. Human Molecular Genetics. 2010. 19: 1528-1538.
Becanovic K, Pouladi MA, Lim RS, Kuhn A, Pavlidis P, Luthi-Carter R, Hayden MR, Leavitt BR. Transcriptional changes in HD identified using genome-wide expression profiling and cross platform analysis.Hum Mol Genet. 2010. 19: 1438–1452.
Okamoto S*, Pouladi MA*, Talantova M*, Yao D, Xia P, Ehrnhoefer DE, Zaidi R, Clemente A, Kaul M, Graham RK, Zhang D, Vincent Chen HS, Tong G, Hayden MR, Lipton SA. Balance between synaptic versus extrasynaptic NMDA receptor activity influences inclusions and neurotoxicity of mutant huntingin. Nature Medicine. 2009. 15: 1407–1413. (* equal contribution)
Pouladi MA, Graham RK, Karasinska JM, Xie Y, Santos RD, Petersén A, Hayden MR. Prevention of depressive behaviour in the YAC128 mouse model of Huntington disease by mutation at residue 586 of huntingtin. Brain. 2009. 132: 919-32.
Graham RK, Pouladi MA, Joshi P, Lu G, Deng Y, Wu NP, Figueroa BE, Metzler M, André VM, Slow EJ, Raymond L, Friedlander R, Levine MS, Leavitt BR, Hayden MR. Differential susceptibility to excitotoxic stress in YAC128 mouse models of HD between initiation and progression of disease. J Neurosci. 2009. 29: 2193-204.
MacDonald ML, van Eck M, Hildebrand RB, Wong BW, Bissada N, Ruddle P, Kontush A, Hussein H, Pouladi MA, Chapman MJ, Fievet C, van Berkel TJ, Staels B, McManus BM, Hayden MR. Despite Antiatherogenic Metabolic Characteristics, SCD1-Deficient Mice Have Increased Inflammation and Atherosclerosis. Arterioscler Thromb Vasc Biol. 2009. 29: 341-7.
Björkqvist M, Wild EJ, Thiele J, Silvestroni A, Andre R, Lahiri N, Raibon E, Lee RV, Benn CL, Soulet D, Magnusson A, Woodman B, Landles C, Pouladi MA, Hayden MR, Khalili-Shirazi A, Lowdell MW, Brundin P, Bates GP, Leavitt BR, Möller T, Tabrizi SJ. A novel pathogenic pathway of immune activation detectable before clinical onset in Huntington’s disease. J Exp Med. 2008. 205: 1869-77.
Kuhn A, Goldstein DR, Hodges A, Strand AD, Sengstag T, Kooperberg C, Becanovic K, Pouladi MA, Sathasivam K, Cha JH, Hannan AJ, Hayden MR, Leavitt BR, Dunnett SB, Ferrante RJ, Albin R, Shelbourne P, Delorenzi M, Augood SJ, Faull RL, Olson JM, Bates GP, Jones L, Luthi-Carter R. Mutant huntingtin's effects on striatal gene expression in mice recapitulate changes observed in human Huntington's disease brain and do not differ with mutant huntingtin length or wild-type huntingtin dosage. Human Molecular Genetics. 2007. 16: 1845-61.
Robbins CS*, Pouladi MA*, Fattouh R, Dawe DE, Vujicic N, Richards CD, Jordana M, Inman MD, Stampfli MR. Mainstream cigarette smoke exposure attenuates airway immune inflammatory responses to surrogate and common environmental allergens in mice, despite evidence of increased systemic sensitization. J Immunol. 2005. 175: 2834-42. (* equal contribution)
Fattouh R, Pouladi MA, Alvarez D, Johnson JR, Walker TD, Goncharova S, Inman MD, Jordana M. House Dust Mite Facilitates Ovalbumin-specific Allergic Sensitization and Airways Inflammation. Am J Respir Crit Care Med. 2005. 172: 314-21.
Drannik AG, Pouladi MA, Robbins CS, Goncharova SI, Kianpour S, Stämpfli MR. Impact of Cigarette Smoke on Clearance and Inflammation following Pseudomonas aeruginosa Infection. Am J Respir Crit Care Med. 2004. 170: 1167.
Swirski FK, Gajewska BU, Robbins CS, D'Sa A, Johnson JR, Pouladi MA, Inman MD, Stämpfli MR. Concomitant airway expression of granulocyte-macrophage colony-stimulating factor and decorin, a natural inhibitor of transforming growth factor-beta, breaks established inhalation tolerance. Eur J Immunol. 2004. 34: 2375.
Robbins CS, Dawe DE, Goncharova SI, Pouladi MA, Drannik AG, Swirski FK, Cox G, Stämpfli MR. Cigarette smoke decreases pulmonary dendritic cells and impacts antiviral immune responsiveness. Am J Respir Cell Mol Biol. 2004. 30: 202.
Pouladi MA, Robbins CS, Swirski FK, Cundall M, McKenzie AN, Jordana M, Shapiro SD, Stämpfli MR. Interleukin-13-dependent expression of matrix metalloproteinase-12 is required for the development of airway eosinophilia in mice. Am J Respir Cell Mol Biol. 2004. 30: 84.
Coppolino MG, Dierckman R, Loijens J, Collins RF, Pouladi MA, Jongstra-Bilen J, Schreiber AD, Trimble WS, Anderson R, Grinstein S. Inhibition of phosphatidylinositol-4-phosphate 5-kinase Ialpha impairs localized actin remodeling and suppresses phagocytosis. J Biol Chem. 2002. 277: 43849.
Pouladi MA, and Hayden MR. "Introduction to Huntington’s Disease" in Huntington’s Dementia, 2007, first ed.
Pouladi MA, Bezprozvanny I, Raymond LA, Hayden MR. "Molecular Pathogenesis of Huntington’s Disease: The Role of Excitotoxicity" in Genetic Instabilities and Neurological Diseases, 2006, second ed, pp 251-260.
3. Hayden MR, Pouladi MA, Kremer B. "Basal Ganglia Disorders" in Emery & Rimoin’s Principles and Practice of Medical Genetics, 2006, fifth ed, pp 2703-2736.
We are always looking for bright, curious, and highly motivated individuals with a passion for science, especially neurodegenerative diseases and stem cell biology, to join our team. PhD students and post-doctoral fellows excited by our research, and looking to join a dynamic and multi-disciplinary team should submit a statement of interest, curriculum vitae, and the names of 2-3 referees willing to provide letters of reference directly to Dr. Mahmoud Pouladi (pouladi [at] tlgm.a-star.edu.sg).
A number of fellowship opportunities are available for promising candidates:
For PhD candidates:
• The Singapore International Graduate Award (SINGA) provides a unique opportunity to pursue your PhD in Singapore. Open to all International students. Terms of the fellowship and eligibility criteria are available at this website: http://www.a-star.edu.sg/singa-award/
For post-doctoral fellows (from EU countries):
• Marie Skłodowska-Curie Actions (MSCA) Global Fellowships: awarded for a period of up to 2-3 years. Details of the award and eligibility criteria are available here: http://ec.europa.eu/research/mariecurieactions/index_en.htm
• The Singapore International Pre-Graduate Award (SIPGA) supports short-term research attachments for international students at A*STAR. It provides a unique opportunity for top overseas students to experience the vibrant scientific environment at A*STAR. This award will normally be for students in the later years of a Bachelor or Master level program. Details of the SIPGA program are available at this website: http://www.a-star.edu.sg/SIPGA/
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