Lisa Chakrabarti

Contact

• workRoom A61 School of Veterinary Medicine and Science
  Sutton Bonington Campus
  Sutton Bonington
  Leicestershire
  LE12 5RD
  UK
• work0115 951 6650
• fax0115 951 6440
• Lisa.Chakrabarti@nottingham.ac.uk

Biography

Lisa Chakrabarti received a BSc (Hons) in Zoology from the University of Leeds. Following this she went on to work with Kay Davies on Muscular Dystrophy and Fragile X Syndrome. In 1997 she received a D.Phil in Biochemistry from the University of Oxford. Postdoctoral work took her to work with Leroy Hood in the Department of Biotechnology at the University of Washington in Seattle and then with John Collinge in the MRC Prion Unit at the University of London. In 2007 she was promoted to Assistant Professor in the Department of Laboratory Medicine at the University of Washington, Seattle where she carried out research on the molecular basis of neurodegeneration. In 2010 she was appointed Lecturer in Protein Biochemistry at the School of Veterinary Medicine and Science at the University of Nottingham.

Expertise Summary

Lisa Chakrabarti is a Lecturer in protein Biochemistry and involved in Neuroscience teaching. She is convenor for the Biochemistry integrated module.

Teaching Summary

My major areas of teaching are within Neuroscience and Biochemistry.

Research Summary

My current research interests focus upon understanding the molecular basis of neurodegeneration. The cost of managing neurodegenerative disease is currently calculated at EUR 72 billion annually.… read more

Recent Publications

• CHAKRABARTI L, SCAFIDI J, GALLO V and HAYDAR TF, 2011. Environmental Enrichment Rescues Postnatal Neurogenesis Defect In The Male And Female Ts65dn Mouse Model Of Down Syndrome. Developmental Neuroscience. 33(5), 428-41
• LATHROP, MELISSA J, CHAKRABARTI, LISA, ENG, JEREMIAH, HARKER RHODES, C, LUTZ, THOMAS, NIETO, AMELIA, DENNY LIGGITT, H, WARNER, SANDRA, FIELDS, JENNIFER, STÖGER, REINHARD and FIERING, STEVEN, 2010. Deletion of the Chd6 exon 12 affects motor coordination. Mammalian genome : official journal of the International Mammalian Genome Society. 21(3-4), 130-142
• CHAKRABARTI, LISA, ZAHRA, RABAAB, JACKSON, STEPHEN M, KAZEMI-ESFARJANI, PARSA, SOPHER, BRYCE L, MASON, AMANDA G, TONEFF, THOMAS, RYU, SOYOUNG, SHAFFER, SCOTT, KANSY, JANICE W, ENG, JEREMIAH and MERRIHEW,, 2010. Mitochondrial dysfunction in NnaD mutant flies and Purkinje cell degeneration mice reveals a role for Nna proteins in neuronal bioenergetics. Neuron. 66(6), 835-47
• CHAKRABARTI, LISA, ENG, JEREMIAH, IVANOV, NISHI, GARDEN, GWENN A and LA SPADA, ALBERT R, 2009. Autophagy activation and enhanced mitophagy characterize the Purkinje cells of pcd mice prior to neuronal death. Molecular brain. 2(1), 24

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Current Research

My current research interests focus upon understanding the molecular basis of neurodegeneration. The cost of managing neurodegenerative disease is currently calculated at EUR 72 billion annually. However, treatment for these disorders is limited, mostly consisting of perfunctory symptom control - often with undesirable side effects in both the short and long term. Risk of neurodegeneration for an individual increases with age, and the proportion of the European population aged over 65 is likely to rise to 25% by 2030 (from 16% today). Therefore, the incidence of these conditions, as well as the social and financial costs of treating them, is set to rise steeply in the coming years. Better strategies for prevention and treatment must be sought as a matter of urgency. Neurodegenerative diseases typically have a slow insidious onset and the course of disease is often lengthy.

We are using proteomics and genomics technologies, together with organotypic slice culture to analyse the changes that occur in neurons which eventually lead to their demise. We have identified the importance of the protein NNA1/ CCP1 for cerebellar health and how genetic changes can alter the expression or stability of the protein. We have also looked using ultrastructural methods and found that a process known as autophagy is occurring in a dramatically different way in affected neurons when compared with normal brain. Much of what we have found appears to also apply to the degenerating retina such as is found in the human disease Retinitis Pigmentosa. Our findings using a model of neurodegenerative disease have provided detail in areas such as the involvement of mitochondria in these disorders. In the case of neurodegeneration it is difficult to gain a clear insight into presymptomatic disease and early events. Post mortem brain and retina provide only a snapshot of a ravaged tissue with elevated markers of cell death and inflammation. I am interested in studying the cusp of development to maturity gained in the neuron, revealing the cause of the disease process rather than the result. The retina degenerates more slowly in the majority of retinal disease processes in humans. By gathering data at a pre/early symptomatic stage we gain advantage over a tissue already depleted of affected neurons. Our studies allow the possibility of moving towards therapies that can be applied before neuronal loss leads to symptomatic disease, a far preferable approach than to try and repair the damage once disease has run its course.

Past Research

Previously I have been interested in finding and characterising genes responsible for mental retardation, developmental delay and dementia. I have also used methods of genetic linkage analysis to locate susceptibility loci for complex disease such as prostate cancer, rhuematoid arthritis and diabetes.

• CHAKRABARTI L, SCAFIDI J, GALLO V and HAYDAR TF, 2011. Environmental Enrichment Rescues Postnatal Neurogenesis Defect In The Male And Female Ts65dn Mouse Model Of Down Syndrome. Developmental Neuroscience. 33(5), 428-41
• LATHROP, MELISSA J, CHAKRABARTI, LISA, ENG, JEREMIAH, HARKER RHODES, C, LUTZ, THOMAS, NIETO, AMELIA, DENNY LIGGITT, H, WARNER, SANDRA, FIELDS, JENNIFER, STÖGER, REINHARD and FIERING, STEVEN, 2010. Deletion of the Chd6 exon 12 affects motor coordination. Mammalian genome : official journal of the International Mammalian Genome Society. 21(3-4), 130-142
• CHAKRABARTI, LISA, ZAHRA, RABAAB, JACKSON, STEPHEN M, KAZEMI-ESFARJANI, PARSA, SOPHER, BRYCE L, MASON, AMANDA G, TONEFF, THOMAS, RYU, SOYOUNG, SHAFFER, SCOTT, KANSY, JANICE W, ENG, JEREMIAH and MERRIHEW,, 2010. Mitochondrial dysfunction in NnaD mutant flies and Purkinje cell degeneration mice reveals a role for Nna proteins in neuronal bioenergetics. Neuron. 66(6), 835-47
• CHAKRABARTI, LISA, ENG, JEREMIAH, IVANOV, NISHI, GARDEN, GWENN A and LA SPADA, ALBERT R, 2009. Autophagy activation and enhanced mitophagy characterize the Purkinje cells of pcd mice prior to neuronal death. Molecular brain. 2(1), 24
• CHAKRABARTI, LISA, ENG, JEREMIAH, MARTINEZ, REFUGIO A, JACKSON, STEPHEN, HUANG, JING, POSSIN, DANIEL E, SOPHER, BRYCE L and LA SPADA, ALBERT R, 2008. The zinc-binding domain of Nna1 is required to prevent retinal photoreceptor loss and cerebellar ataxia in Purkinje cell degeneration (pcd) mice. Vision research. 48(19), 1999-2005
• CHAKRABARTI, LISA, NEAL, JAMES T, MILES, MICHAEL, MARTINEZ, REFUGIO A, SMITH, ANNETTE C, SOPHER, BRYCE L and LA SPADA, ALBERT R, 2006. The Purkinje cell degeneration 5J mutation is a single amino acid insertion that destabilizes Nna1 protein. Mammalian genome : official journal of the International Mammalian Genome Society. 17(2), 103-10
• SKIBINSKI, GAIA, PARKINSON, NICHOLAS J, BROWN, JEREMY M, CHAKRABARTI, LISA, LLOYD, SARAH L, HUMMERICH, HOLGER, NIELSEN, JØRGEN E, HODGES, JOHN R, SPILLANTINI, MARIA GRAZIA, THUSGAARD, TOVE and BRAND, 2005. Mutations in the endosomal ESCRTIII-complex subunit CHMP2B in frontotemporal dementia. Nature genetics. 37(8), 806-8
• BROWN, JERRY, GYDESEN, SUSANNE, JOHANNSEN, PETER, GADE, ANDERS, SKIBINSKI, GAIA, CHAKRABARTI, LISA, BRUN, ARNE, SPILLANTINI, MARIA, YANCOPOULOU, DESPINA, THUSGAARD, TOVE, SORENSEN, ASGER and FISHER, ELIZ, 2004. Frontotemporal dementia linked to chromosome 3. Dementia and geriatric cognitive disorders. 17(4), 274-6
• YANCOPOULOU, DESPINA, CROWTHER, R ANTHONY, CHAKRABARTI, LISA, GYDESEN, SUSANNE, BROWN, JEREMY M and SPILLANTINI, MARIA GRAZIA, 2003. Tau protein in frontotemporal dementia linked to chromosome 3 (FTD-3). Journal of neuropathology and experimental neurology. 62(8), 878-82
• GYDESEN, S, BROWN, J M, BRUN, A, CHAKRABARTI, L, GADE, A, JOHANNSEN, P, ROSSOR, M, THUSGAARD, T, GROVE, A, YANCOPOULOU, D, SPILLANTINI, M G, FISHER, E M C, COLLINGE, J and SORENSEN, S A, 2002. Chromosome 3 linked frontotemporal dementia (FTD-3). Neurology. 59(10), 1585-94
• PETERS, M A, JARVIK, G P, JANER, M, CHAKRABARTI, L, KOLB, S, GOODE, E L, GIBBS, M, DUBOIS, C C, SCHUSTER, E F, HOOD, L, OSTRANDER, E A and STANFORD, J L, 2001. Genetic linkage analysis of prostate cancer families to Xq27-28. Human heredity. 51(1-2), 107-13
• GOODE, E L, STANFORD, J L, CHAKRABARTI, L, GIBBS, M, KOLB, S, MCINDOE, R A, BUCKLEY, V A, SCHUSTER, E F, NEAL, C L, MILLER, E L, BRANDZEL, S, HOOD, L, OSTRANDER, E A and JARVIK, G P, 2000. Linkage analysis of 150 high-risk prostate cancer families at 1q24-25. Genetic epidemiology. 18(3), 251-75
• XU, J, 2000. Combined analysis of hereditary prostate cancer linkage to 1q24-25: results from 772 hereditary prostate cancer families from the International Consortium for Prostate Cancer Genetics. American journal of human genetics. 66(3), 945-57
• GIBBS, M, STANFORD, J L, JARVIK, G P, JANER, M, BADZIOCH, M, PETERS, M A, GOODE, E L, KOLB, S, CHAKRABARTI, L, SHOOK, M, BASOM, R, OSTRANDER, E A and HOOD, L, 2000. A genomic scan of families with prostate cancer identifies multiple regions of interest. American journal of human genetics. 67(1), 100-9
• GIBBS, M, STANFORD, J L, MCINDOE, R A, JARVIK, G P, KOLB, S, GOODE, E L, CHAKRABARTI, L, SCHUSTER, E F, BUCKLEY, V A, MILLER, E L, BRANDZEL, S, LI, S, HOOD, L and OSTRANDER, E A, 1999. Evidence for a rare prostate cancer-susceptibility locus at chromosome 1p36. American journal of human genetics. 64(3), 776-87
• PARMANTIER, E, LYNN, B, LAWSON, D, TURMAINE, M, NAMINI, S S, CHAKRABARTI, L, MCMAHON, A P, JESSEN, K R and MIRSKY, R, 1999. Schwann cell-derived Desert hedgehog controls the development of peripheral nerve sheaths. Neuron. 23(4), 713-24
• GIBBS, M, CHAKRABARTI, L, STANFORD, J L, GOODE, E L, KOLB, S, SCHUSTER, E F, BUCKLEY, V A, SHOOK, M, HOOD, L, JARVIK, G P and OSTRANDER, E A, 1999. Analysis of chromosome 1q42.2-43 in 152 families with high risk of prostate cancer. American journal of human genetics. 64(4), 1087-95
• CHAKRABARTI, L, BRISTULF, J, FOSS, G S and DAVIES, K E, 1998. Expression of the murine homologue of FMR2 in mouse brain and during development. Human molecular genetics. 7(3), 441-8
• CHAKRABARTI, L and DAVIES, K E, 1997. Fragile X syndrome. Current opinion in neurology. 10(2), 142-7
• RITCHIE, R J, CHAKRABARTI, L, KNIGHT, S J, HARDING, R M and DAVIES, K E, 1997. Population genetics of the FRAXE and FRAXF GCC repeats, and a novel CGG repeat, in Xq28. American journal of medical genetics. 73(4), 463-9
• KNIGHT, S J, RITCHIE, R J, CHAKRABARTI, L, CROSS, G, TAYLOR, G R, MUELLER, R F, HURST, J, PATERSON, J, YATES, J R, DOW, D J and DAVIES, K E, 1996. A study of FRAXE in mentally retarded individuals referred for fragile X syndrome (FRAXA) testing in the United Kingdom. American journal of human genetics. 58(5), 906-13
• CHAKRABARTI, L, KNIGHT, S J, FLANNERY, A V and DAVIES, K E, 1996. A candidate gene for mild mental handicap at the FRAXE fragile site. Human molecular genetics. 5(2), 275-82