Nancy Bonini

Last updated
Nancy M. Bonini
Nancy Bonini 2012.jpg
Born1959 (age 64–65) [1]
NationalityAmerican
Alma mater Princeton University (AB)

University of Wisconsin-Madison (PhD)

California Institute of Technology (Postdoc)
Known forDeveloped the first Drosophila model of human neurodenerative disease
SpouseAnthony Cashmore
Awards
Scientific career
Fields
Institutions University of Pennsylvania
Doctoral advisor David L. Nelson
Website http://web.sas.upenn.edu/bonini-lab/

Nancy M. Bonini (born 1959) is an American neuroscientist and geneticist, best known for pioneering the use of Drosophila as a model organism to study neurodegeneration of the human brain. Using the Drosophila model approach, Bonini's laboratory has identified genes and pathways that are important in the development and progression of neurodegenerative diseases such as Amyotrophic lateral sclerosis (ALS, also called Lou Gehrig's Disease), [5] Alzheimer's disease, [6] and Parkinson's disease, [7] [8] as well as aging, neural injury and regeneration, [9] and response to environmental toxins. [8]

Contents

A professor of biology at the University of Pennsylvania since 1994, Bonini has held appointments as the inaugural Lucille B. Williams Term Professor of Biology (2006–2012), [10] an Investigator of the Howard Hughes Medical Institute (2000–2013), [2] [11] and the Florence RC Murray Professor of Biology (since 2012). [12] She was editor of the Annual Review of Genetics from 2018-2021. [13] [14]

Early life and education

Bonini was born in 1959 to parents Rose and William “Bill” Bonini. [1] Her father was a Professor of GeoScience and Civil Engineering at Princeton University from 1952 to 1996. [15] Nancy, her sister (Jennifer), brothers (Jack and Jamie), and father all attended Princeton University. [16]

Bonini earned an AB degree from Princeton University in 1981, studying Biology. [17] Her undergraduate thesis research, performed under the direction of William (Chip) Quinn, formed the basis for her first publication, "Reward Learning in Normal and Mutant Drosophila". [18] After graduation, Bonini entered the Neurosciences Training Program at the University of Wisconsin–Madison. There, she completed doctoral research in the laboratory of David L. Nelson, [19] graduating with a Doctorate (Ph.D.) in Neuroscience in 1987. [20] Bonini's post-doctoral research was performed in the laboratory of Seymour Benzer (behavioral geneticist) at the California Institute of Technology. [17] Focusing on using the fruit fly as a tool for understanding the genetic basis of the brain and behavior, Bonini was the first to demonstrate that Drosophila can be used as a model of human neurodegenerative disease. [21] [22]

Research

The fruit fly as a model for human neurodegenerative disease

In 1998, Bonini's research conclusively demonstrated that Drosophila could be used as an in vivo model for human neurodegenerative disease. [21] [22] Using this model, Bonini's research group subsequently discovered unexpected and novel pathways that play a role in normal biology, injury, and disease. [17] In the pioneering study that showed that the fruit fly can be used as a model of disease, Bonini's laboratory collaborated with human geneticists to examine the effects of expressing normal and mutant forms of a human neurodegenerative polyQ disease protein. Flies that expressed the mutant form of the protein showed symptoms and characteristics similar to those seen in human polyQ disease patients; flies that expressed the normal protein did not. [23] [24]

Chaperones and Polyglutamine Repeat Diseases

Studying Polyglutamine repeat diseases (polyQ diseases) in Drosophila neurodegeneration models, Bonini's research group elucidated an important role for molecular chaperones in polyQ diseases, [25] and subsequently Parkinson's disease. [7] [23] [26] In those studies, upregulation of the chaperone Hsp70 suppressed neurodegeneration, and this finding established chaperones as a new therapeutic target for Parkinson's disease and other neurodegenerative disorders. [7] [26] [27] Bonini's research team demonstrated the pharmacologic potential of chaperones in further Drosophila studies; administering geldanamycin (an antitumor antibiotic that acts on Hsp90) to mutant flies before symptoms of neural decline were visible averted the onset of neurodegeneration in the mutant flies, suggesting a new approach for people susceptible to Parkinson's disease and other neurodegenerative conditions. [28]

Amyotrophic lateral sclerosis (ALS/Lou Gehrig's Disease)

Bonini's research laboratory developed and validated a Drosophila model for familial ALS, [9] [29] [30] then used an ALS model to evaluate genes and pathways important for ALS onset, progression, and possible treatment. [31] [32] Through these studies, Bonini's team, in collaboration with Aaron Gitler, discovered that ATXN2 (the gene that encodes the protein Ataxin-2) was a disease susceptibility gene for ALS, and that interrupting the interaction between TDP-43 and Ataxin-2 was a promising target for treating ALS and other diseases. [30] [31] [32] [33] [34]

A role for brain microRNAs in aging and disease

The Bonini lab discovered that a conserved microRNA, miR-34, plays a neuroprotective role in the brains of aging Drosophila. [35] The loss of miR-34 resulted in a profile consistent with accelerated aging, late-onset brain neurodegeneration, and reduced survival, whereas upregulation of miR-34 enhanced survival and mitigated neurodegeneration. [35] [36]

An epigenetic basis for Alzheimer's disease

In 2018, Bonini, with collaborators Shelley Berger, Brad Johnson, and others, completed a study investigating the epigenetic landscape of tissue samples donated by individuals who did and did not have Alzheimer's disease. The findings established the basis for an epigenetic link between aging and Alzheimer's disease, suggesting a new model for the disease and a paradigm shift from the previously established view of Alzheimer's disease as an 'advanced state of normal aging'. Based on the study findings, Bonini and collaborators established that a set of normal aging changes that occur in the epigenome protect against Alzheimer's disease, and that disrupting those normal protective changes may be a trigger that predisposes people to the disease. [6] [37]

Honors and awards

A professor of biology at the University of Pennsylvania since 1994, Bonini has held appointments as the inaugural Lucille B. Williams Term Professor of Biology (2006–2012), [10] an Investigator of the Howard Hughes Medical Institute (2000–2013), [2] [11] and the Florence RC Murray Professor of Biology (2012-). [12] In 2012, she was elected to the National Academy of Sciences, [11] [38] and the National Academy of Medicine. [3] Also in 2012, Bonini became an elected Fellow of the American Association for the Advancement of Science. [39] In 2014, Bonini was elected to the American Academy of Arts and Sciences. [4]

Bonini was the recipient of a March of Dimes Basil O'Connor Award in 1996, [40] a Packard Fellowship for Science and Engineering in 1997, [41] an Ellison Medical Foundation Senior Scholar in Aging Research Award in 2009, [42] a Glenn Award for Research in the Biological Mechanisms of Aging in 2015, [43] and a National Institutes of Health Outstanding Investigator R35 Award in 2016. [44] [45] In 2010, she appeared as a panelist on Charlie Rose’s The Brain Series (Episode: The Disordered Brain). [46]

Personal

A.Cashmore Anthony R Cashmore Biochemist and Plant Molecular Biologist 2010 (cropped).jpg
A.Cashmore

Bonini is married to Anthony Cashmore, [16] a University of Pennsylvania Professor Emeritus best known for discovering the cryptochrome that serves as a blue light photoreceptor in Arabidopsis. [47]

Representative publications

Journal articles

Reviews

Commentary

Related Research Articles

<span class="mw-page-title-main">Hsp70</span> Family of heat shock proteins

The 70 kilodalton heat shock proteins are a family of conserved ubiquitously expressed heat shock proteins. Proteins with similar structure exist in virtually all living organisms. Intracellularly localized Hsp70s are an important part of the cell's machinery for protein folding, performing chaperoning functions, and helping to protect cells from the adverse effects of physiological stresses. Additionally, membrane-bound Hsp70s have been identified as a potential target for cancer therapies and their extracellularly localized counterparts have been identified as having both membrane-bound and membrane-free structures.

Molecular neuroscience is a branch of neuroscience that observes concepts in molecular biology applied to the nervous systems of animals. The scope of this subject covers topics such as molecular neuroanatomy, mechanisms of molecular signaling in the nervous system, the effects of genetics and epigenetics on neuronal development, and the molecular basis for neuroplasticity and neurodegenerative diseases. As with molecular biology, molecular neuroscience is a relatively new field that is considerably dynamic.

<span class="mw-page-title-main">Heat shock response</span> Type of cellular stress response

The heat shock response (HSR) is a cell stress response that increases the number of molecular chaperones to combat the negative effects on proteins caused by stressors such as increased temperatures, oxidative stress, and heavy metals. In a normal cell, proteostasis must be maintained because proteins are the main functional units of the cell. Many proteins take on a defined configuration in a process known as protein folding in order to perform their biological functions. If these structures are altered, critical processes could be affected, leading to cell damage or death. The heat shock response can be employed under stress to induce the expression of heat shock proteins (HSP), many of which are molecular chaperones, that help prevent or reverse protein misfolding and provide an environment for proper folding.

In genetics, trinucleotide repeat disorders, a subset of microsatellite expansion diseases, are a set of over 30 genetic disorders caused by trinucleotide repeat expansion, a kind of mutation in which repeats of three nucleotides increase in copy numbers until they cross a threshold above which they cause developmental, neurological or neuromuscular disorders. Depending on its location, the unstable trinucleotide repeat may cause defects in a protein encoded by a gene; change the regulation of gene expression; produce a toxic RNA, or lead to production of a toxic protein. In general, the larger the expansion the faster the onset of disease, and the more severe the disease becomes.

<span class="mw-page-title-main">Neurodegenerative disease</span> Central nervous system disease

A neurodegenerative disease is caused by the progressive loss of structure or function of neurons, in the process known as neurodegeneration. Such neuronal damage may ultimately involve cell death. Neurodegenerative diseases include amyotrophic lateral sclerosis, multiple sclerosis, Parkinson's disease, Alzheimer's disease, Huntington's disease, multiple system atrophy, tauopathies, and prion diseases. Neurodegeneration can be found in the brain at many different levels of neuronal circuitry, ranging from molecular to systemic. Because there is no known way to reverse the progressive degeneration of neurons, these diseases are considered to be incurable; however research has shown that the two major contributing factors to neurodegeneration are oxidative stress and inflammation. Biomedical research has revealed many similarities between these diseases at the subcellular level, including atypical protein assemblies and induced cell death. These similarities suggest that therapeutic advances against one neurodegenerative disease might ameliorate other diseases as well.

<span class="mw-page-title-main">Ataxin 1</span> Protein-coding gene in the species Homo sapiens

Ataxin-1 is a DNA-binding protein which in humans is encoded by the ATXN1 gene.

Ataxin 7 (ATXN7) is a protein of the SCA7 gene, which contains 892 amino acids with an expandable poly(Q) region close to the N-terminus. The expandable poly(Q) motif region in the protein contributes crucially to spinocerebellar ataxia (SCA) pathogenesis by the induction of intranuclear inclusion bodies. ATXN7 is associated with both olivopontocerebellar atrophy type 3 (OPCA3) and spinocerebellar ataxia type 7 (SCA7).

Lytico-bodig (also Lytigo-bodig) disease, Guam disease, or amyotrophic lateral sclerosis-parkinsonism-dementia (ALS-PDC) is a neurodegenerative disease of uncertain etiology endemic to the Chamorro people of the island of Guam in Micronesia. Lytigo and bodig are Chamorro language words for two different manifestations of the same condition. ALS-PDC, a term coined by Asao Hirano and colleagues in 1961, reflects its resemblance to amyotrophic lateral sclerosis (ALS), Parkinson's disease, and Alzheimer's disease.

<span class="mw-page-title-main">Proteinopathy</span> Medical condition

In medicine, proteinopathy, or proteopathy, protein conformational disorder, or protein misfolding disease, is a class of diseases in which certain proteins become structurally abnormal, and thereby disrupt the function of cells, tissues and organs of the body. Often the proteins fail to fold into their normal configuration; in this misfolded state, the proteins can become toxic in some way or they can lose their normal function. The proteinopathies include such diseases as Creutzfeldt–Jakob disease and other prion diseases, Alzheimer's disease, Parkinson's disease, amyloidosis, multiple system atrophy, and a wide range of other disorders. The term proteopathy was first proposed in 2000 by Lary Walker and Harry LeVine.

<span class="mw-page-title-main">Ataxin-2</span> Mammalian protein found in Homo sapiens

Ataxin-2 is a protein that in humans is encoded by the ATXN2 gene. Mutations in ATXN2 cause spinocerebellar ataxia type 2 (SCA2).

<span class="mw-page-title-main">Ataxin 3</span> Protein-coding gene in the species Homo sapiens

Ataxin-3 is a protein that in humans is encoded by the ATXN3 gene.

John Quinn Trojanowski was an American academic research neuroscientist specializing in neurodegeneration. He and his partner, Virginia Man-Yee Lee, MBA, Ph.D., are noted for identifying the roles of three proteins in neurodegenerative diseases: tau in Alzheimer's disease, alpha-synuclein in Parkinson's disease, and TDP-43 in Amyotrophic Lateral Sclerosis (ALS) and frontotemporal degeneration.

Richard I. Morimoto is a Japanese American molecular biologist. He is the Bill and Gayle Cook Professor of Biology and Director of the Rice Institute for Biomedical Research at Northwestern University.

<span class="mw-page-title-main">Hugo J. Bellen</span> American geneticist

Hugo J. Bellen is a professor at Baylor College of Medicine and an investigator emeritus at the Howard Hughes Medical Institute who studies genetics and neurobiology in the model organism, Drosophila melanogaster, the fruit fly.

<span class="mw-page-title-main">Epigenetics of neurodegenerative diseases</span> Field of study

Neurodegenerative diseases are a heterogeneous group of complex disorders linked by the degeneration of neurons in either the peripheral nervous system or the central nervous system. Their underlying causes are extremely variable and complicated by various genetic and/or environmental factors. These diseases cause progressive deterioration of the neuron resulting in decreased signal transduction and in some cases even neuronal death. Peripheral nervous system diseases may be further categorized by the type of nerve cell affected by the disorder. Effective treatment of these diseases is often prevented by lack of understanding of the underlying molecular and genetic pathology. Epigenetic therapy is being investigated as a method of correcting the expression levels of misregulated genes in neurodegenerative diseases.

David Chaim Rubinsztein FRS FMedSci is the Deputy Director of the Cambridge Institute of Medical Research (CIMR), Professor of Molecular Neurogenetics at the University of Cambridge and a UK Dementia Research Institute Professor.

<span class="mw-page-title-main">Virginia Man-Yee Lee</span> American neuroscientist and biochemist

Virginia Man-Yee Lee is a Chinese-born American biochemist and neuroscientist who specializes in the research of Alzheimer's disease. She is the current John H. Ware 3rd Endowed Professor in Alzheimer's Research at the Department of Pathology and Laboratory Medicine, and the director of the Center for Neurodegenerative Disease Research and co-director of the Marian S. Ware Alzheimer Drug Discovery Program at the Perelman School of Medicine, University of Pennsylvania. She received the 2020 Breakthrough Prize in Life Sciences.

<span class="mw-page-title-main">Bryce Vissel</span> Australian neuroscientist

Bryce Vissel is an Australian neuroscientist who is a professor of neuroscience at the University of New South Wales. He is the Director of the Centre for Neuroscience and Regenerative Medicine (CNRM) at St Vincent's Hospital Sydney. He is a specialist in neurodegenerative diseases, such as Alzheimer's, Parkinson's, and the neural basis of learning, memory and movement.

Michelle Gray is an American neuroscientist and assistant professor of neurology and neurobiology at the University of Alabama Birmingham. Gray is a researcher in the study of the biological basis of Huntington's disease (HD). In her postdoctoral work, she developed a transgenic mouse line, BACHD, that is now used worldwide in the study of HD. Gray's research now focuses on the role of glial cells in HD. In 2020 Gray was named one of the 100 Inspiring Black Scientists in America by Cell Press. She is also a member of the Hereditary Disease Foundation’s scientific board.

Hilal Lashuel is an American-Yemeni neuroscientist and chemist, currently an associate professor at the EPFL. His research focuses on protein misfolding and aggregation in the pathogenesis of Alzheimer's and Parkinson's diseases.

References

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  2. 1 2 3 "Our Investigators: Nancy M. Bonini, PhD". hhmi.org. Howard Hughes Medical Institute. 2019. Retrieved 15 Jul 2019.
  3. 1 2 "ASBMB Today" (PDF). USA: American Society for Biochemistry and Molecular Biology. 1 Dec 2012. Retrieved 15 Jul 2019.
  4. 1 2 "Ellison Medical Foundation Senior Scholar Nancy Bonini elected to American Academy of Arts and Sciences". ellisonfoundation.org. 2014. Retrieved 15 Jul 2019.
  5. ↑ "DC: New ALS Genetics Hog the Limelight at Satellite Conference". www.alzforum.org. FBRI LLC. 2011. Retrieved 21 Jul 2019.
  6. 1 2 "Penn Study Shows that the "Epigenetic Landscape" is Protective in Normal Aging, Impaired in Alzheimer's Disease". Penn Medicine News. USA. 5 Mar 2018. Retrieved 19 Jul 2019.
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  15. ↑ Kelly, Morgan (3 Jan 2017). "Geoscientist William Bonini, dedicated teacher and genial colleague, dies at 90". Princeton University News. Princeton, NJ, USA. Retrieved 12 Jul 2019.
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  17. 1 2 3 Nichols, Peter (1999). "A fly like thee. Studying the fruit fly, Nancy Bonini '81 unravels causes of neurodegenerative diseases". www.princeton.edu. Princeton University . Retrieved 18 Jul 2019.
  18. ↑ Tempel, Bruce L.; Bonini, Nancy; Dawson, Douglas R.; Quinn, William G. (1983). "Reward learning in normal and mutant Drosophila". Proceedings of the National Academy of Sciences of the United States of America . 80 (5): 1482–1486. Bibcode:1983PNAS...80.1482T. doi: 10.1073/pnas.80.5.1482 . PMC   393622 . PMID   6572401.
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  20. ↑ "Neuroscience Training Program – Alumni". www.ntp.neuroscience.wisc.edu. University of Wisconsin – Madison. 2019. Retrieved 18 Jul 2019.
  21. 1 2 Warrick, John M; Paulson, Henry L; Gray-Board, Gladys; Fischbeck, Kenneth H; Pittman, Randall N; Bonini, Nancy M. (12 Jun 1998). "Expanded Polyglutamine Protein Forms Nuclear Inclusions and Causes Neural Degeneration in Drosophila". Cell. 93 (6): 939–949. doi: 10.1016/S0092-8674(00)81200-3 . PMID   9635424. S2CID   17720790.
  22. 1 2 Max Perutz (1 Feb 1999). "Glutamine repeats and neurodegenerative diseases: molecular aspects". Trends in Biochemical Sciences. 24 (2): 58–63. doi:10.1016/S0968-0004(98)01350-4. PMID   10098399.
  23. 1 2 R. Horowski; Y. Mizuno; C.W. Olanow; W. Poewe; P. Riederer; J.A. Stoessel; M.B.H. Youdim (24 July 2003). Advances in Research on Neurodegeneration. Springer Science & Business Media. pp. 52–. ISBN   978-3-211-83907-2 . Retrieved 20 July 2019.
  24. ↑ Warrick, JM; Chan, HY; Gray-Board, GL; Paulson, H; Bonini, NM (1999). "Suppression of polyglutamine disease in Drosophila by the molecular chaperone hsp70". Nature Genetics. 23 (4): 425–428. doi:10.1038/70532. PMID   10581028. S2CID   24632055.
  25. ↑ Chai, Y; Koppenhafer, SL; Bonini, NM; Paulson, HL (1 Dec 1999). "Analysis of the role of heat shock protein (Hsp) molecular chaperones in polyglutamine disease". The Journal of Neuroscience . 19 (23): 10338–47. doi:10.1523/JNEUROSCI.19-23-10338.1999. PMC   6782415 . PMID   10575031.
  26. 1 2 Helfand, Stephen L. (1 Feb 2002). "Chaperones Take Flight". Science . 295 (5556): 809–810. doi:10.1126/science.1069544. PMID   11823628. S2CID   84002211.
  27. ↑ R. Horowski; Y. Mizuno; C.W. Olanow; W. Poewe; P. Riederer; J.A. Stoessel; M.B.H. Youdim (24 July 2003). "General Aspects of Neurodegeration". Advances in Research on Neurodegeneration. Springer Science & Business Media. p. 117. ISBN   978-3-211-83907-2 . Retrieved 20 July 2019.
  28. ↑ "Drug Averts Parkinson's Disease in Fruit Flies, Suggesting New Approaches to Human Neurodegenerative Diseases". www.penntoday.upenn.edu. University of Pennsylvania. 11 Nov 2002. Retrieved 22 Jul 2019.
  29. 1 2 "A Fly Model for ALS". Journal of Biological Chemistry. 283: e99948. 5 Sep 2008. doi: 10.1016/S0021-9258(19)49256-9 .
  30. 1 2 Varslag, Brian (Feb 2011). "Hope Floats: With a new arsenal of robust models of ALS, drug development may move to the fast track". www.hhmi.org. Howard Hughes Medical Institute . Retrieved 21 Jul 2019. In 1998, however, Bonini authored an idea that radically extended the scientific reach of the humble insect. She mused that inserting genes related to human brain diseases might yield critical insights into poorly understood neurodegenerative conditions, including Huntington's disease, Parkinson's disease, and ALS. "I saw it as, 'there are all these terrible diseases and nobody is really studying them in model organisms,'" Bonini says. "I knew it was a high-risk thing."
  31. 1 2 Flam, Faye (26 Aug 2010). "Researchers at University of Pennsylvania find possible genetic link to Lou Gehrig's disease". The Philadelphia Inquirer . Retrieved 16 Jul 2019.
  32. 1 2 Elden, Andrew C.; Kim, Hyung-Jun; Hart, Michael P.; Chen-Plotkin, Alice S.; Johnson, Brian S.; Fang, Xiaodong; Armakola, Maria; Geser, Felix; Greene, Robert; Lu, Min Min; Padmanabhan, Arun; Clay-Falcone, Dana; McCluskey, Leo; Elman, Lauren; Juhr, Denise; Gruber, Peter J.; Rüb, Udo; Auburger, Georg; Trojanowski, John Q.; Lee, Virginia M.-Y.; Van Deerlin, Vivianna M.; Bonini, Nancy M.; Gitler, Aaron D. (2010). "Ataxin-2 intermediate-length polyglutamine expansions are associated with increased risk for ALS". Nature . 466 (7310): 1069–1078. Bibcode:2010Natur.466.1069E. doi:10.1038/nature09320. PMC   2965417 . PMID   20740007.
  33. ↑ USA US20110142789A1,Aaron D. Gitler&Nancy M. Bonini,"Compositions and Methods for the Diagnosis and Treatment of Amyotrophic Lateral Sclerosis", assigned to University of Pennsylvania
  34. ↑ Clotilde Lagier-Tourenne; Don W. Cleveland (25 Aug 2010). "An expansion in ALS genetics". Nature . 466 (7310): 1052–1053. doi: 10.1038/4661052a . PMID   20740002. S2CID   205056924. "… present evidence on page 1069 of this issue that short expansions of glutamine (Q) amino-acid residues — a polyglutamine, or polyQ tract — in the ataxin-2 protein are associated with increased risk of ALS. This unexpected finding comes 15 years after the discovery that long polyQ expansions in ataxin-2 cause spinocerebellar ataxia type 2, a neurodegenerative disorder involving abnormalities of gait.
  35. 1 2 Aw, Sherry; Cohen, Stephen M. (Aug 2012). "Time is of the essence: microRNAs and age-associated neurodegeneration". Nature . 22 (8): 1218–1220. doi:10.1038/cr.2012.59. PMC   3411169 . PMID   22491478.
  36. ↑ Gwyneth Dickey Zakaib (17 Feb 2012). "Neurodegeneration and Aging: Could MicroRNA Be the Link?". www.alzforum.org. Retrieved 21 Feb 2019.
  37. ↑ Nativio, Raffaella; Donahue, Greg; Berson, Amit; Lan, Yemin; Amlie-Wolf, Alexandre; Tuzer, Ferit; Toledo, Jon B.; Gosai, Sager J.; Gregory, Brian D.; Torres, Claudio; Trojanowski, John Q.; Wang, Li-San; Johnson, F.Brad; Bonini, nancy M.; Berger, Shelley L. (2018). "Dysregulation of the epigenetic landscape of normal aging in Alzheimer's disease". Nature Neuroscience . 21 (4): 497–505. doi: 10.1038/s41593-018-0101-9 . PMC   6124498 . PMID   29507413.
  38. ↑ "National Academy of Sciences Members and Foreign Associates Elected". www.nasonline.org. National Academy of Sciences. 1 May 2012. Retrieved 20 Jul 2019.
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  40. ↑ Bui, Q. T.; Zimmerman, J. E.; Liu, H.; Bonini, N. M. (2000). "Molecular Analysis of Drosophila eyes absent Mutants Reveals Features of the Conserved Eya Domain". Genetics. 155 (2): 709–720. doi:10.1093/genetics/155.2.709. PMC   1461105 . PMID   10835393 . Retrieved 26 Jul 2019.
  41. ↑ "Nancy M. Bonini, 1997 Fellow". www.packard.org. David and Lucile Packard Foundation. 2019. Retrieved 26 Jul 2019.
  42. ↑ "2009 Senior Scholar Award in Aging". www.ellisonfoundation.org. Ellison Medical Foundation. 2009. Retrieved 20 Jul 2019.
  43. ↑ "Glenn Foundation for Medical Research: Award Recipients". www.glennfoundation.org. Glen Foundation. 2019. Retrieved 20 Jul 2019.
  44. ↑ "NINDS Research Program Award (R35) Recipients FY 2017". www.ninds.nih.gov. National Institutes of Health. 28 Jun 2018. Archived from the original on 21 March 2019. Retrieved 20 Jul 2019.
  45. ↑ "NIH initiates pilot grant program for innovative neurological research". www.nih.gov. National Institutes of Health. 26 Jan 2017. Retrieved 20 Jul 2019.
  46. ↑ Charlie Rose (talk show), Eric Kandel, John Donoghue (neuroscientist), John Krakauer, Nancy Bonini (22 Jul 2010). The Disordered Brain (video). Retrieved 21 Jul 2019. As part of Charlie's Brain Series, a panel of experts gives insight into disorders of the brain, such as Parkinson's disease, stroke, and paralysis, and describes the latest cutting-edge treatments.
  47. ↑ Nair, Prashant (11 Jan 2011). "Profile of Anthony R. Cashmore". Proceedings of the National Academy of Sciences . 108 (2): 443–445. Bibcode:2011PNAS..108..443N. doi: 10.1073/pnas.1018069108 . PMC   3021040 . PMID   21191100.
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