Profiles

Adele Woodhouse

UTAS Home Dr Adele Woodhouse

Adele Woodhouse

Research Fellow
Wicking Dementia Research & Education Centre

Room 417h (Level 4) , Medical Science Precinct

+61 3 6226 4708 (phone)

Adele.Woodhouse@utas.edu.au

Dr Woodhouse is a current Alzheimer's Australia Dementia Research Foundation research fellow working at the Wicking Dementia Research and Education Centre. Her PhD focused on the cellular pathology in Alzheimer's disease (AD), she was then awarded a NHMRC postdoctoral overseas training fellowship during which she investigated the homeostasis of intrinsic excitability in the lab of Dr Jean-Marc Goaillard (INSERM, UNIS 1072). She is now investigating neuronal activity alterations in ageing and AD, and the role of epigenetic dysfunction in AD.

Biography

Dr Woodhouse completed her PhD at the University of Tasmania in 2008, which focussed on the cellular pathology in Alzheimer's disease. She was then awarded a NHMRC postdoctoral overseas training fellowship and a Foundation pour la recherche medicale postdoctoral fellowship (France) to investigate the homeostasis of intrinsic excitability in the lab of Dr Jean-Marc Goaillard (INSERM, Marseille, France). 

Dr Woodhouse returned to the University of Tasmania to work at the Wicking Dementia Research and Education Centre, and was awarded an Alzheimer's Australia Dementia Research Foundation postdoctoral research fellowship to continue her research.

Career summary

Qualifications

  • PhD, University of Tasmania, Australia, 2008. Pathological changes leading to neuronal degeneration in Alzheimer's disease
  • BSc (1st Class Hons), University of Tasmania, Australia, 2003. Profileration and migration of ensheathing cells in response to spinal cord tissue
  • BSc, University of Tasmania, Australia, 2002

Languages (other than English)

  • French (basic)

Teaching

Neuroscience, Alzheimer's Disease (AD), Electrophysiology, Intrinsic Excitability

Teaching expertise

Dr Woodhouse has developed and delivered lectures, practicals and tutorials, including setting and marking assessments in undergraduate units offered by the School of Medicine.

Teaching responsibility

View more on Dr Adele Woodhouse in WARP

Expertise

  • Alzheimer's disease
  • Neuronal excitability
  • Epigenetics

Research Themes

Dr Woodhouse's work within the Wicking Dementia Research and Education Centre (WDREC) aligns with the University's strategic direction: Research - creating new ideas and new knowledge as well as with the University's research theme of Better Health. Dr Woodhouse is leading a project investigating how neurons regulate their activity in aging and in AD mouse models (supported by Yulgilbar postdoctoral excellence award and an Alzheimer's Australia Dementia Research Foundation postdoctoral scholarship).

She is also involved in a new project in collaboration with epigenetics experts (Dr Phillippa Taberlay, Dr Timothy Mercer) to investigate epigenetic reprogramming in AD. Dr Woodhouse also collaborates on several other research projects at the WDREC, including projects investigating the impact of brain injury and anaesthetics on the development of AD.

Collaboration

Local

Dr Woodhouse collaborates with her mentor Prof James Vickers (WDREC, University of Tasmania); and with Dr Anna King and Dr Carmen Fernandez-Martos (WDREC, University of Tasmania) to investigate aspects of AD.

National         

To tackle large research questions Dr Woodhouse is in collaboration with epigenetics and bioinformatics experts Dr Taberlay and Dr Mercer at the Garvan Institute (Sydney) to chart the epigenetic reprogramming that occurs in AD.

International   

Dr Woodhouse's collaboration and mentorship with Dr Jean-Marc Goaillard (INSERM, Marseille, France) continues.

Awards

  • UTAS University Career Development Scholarship (CIE) (2015)
  • Judith Jan Mason and Harold Stannett Williams Memorial Foundation National Medical Program grant (CIB) (2015)
  • Alzheimer's Australia Dementia Research Foundation postdoctoral fellowship (CIA) (2014)
  • Yulgilbar postdoctoral excellence award from the Yulgilbar Foundation (CIA) (2014)
  • UTAS Research Enhancement Scheme Grant (CIA) (2013)
  • Fondation pour la Recherche Medicale postdoctoral fellowship in France (2010)
  • NHMRC overseas postdoctoral training fellowship (2009)
  • Finalist in the Tasmanian Southern Cross Young Achiever Awards (2008, 2009)
  • Society for Neuroscience/ International Brain Research Organization International Travel Grant (2007)
  • Finalist in the inaugural Australian Society of Medical Research Medical Research Week Student Award (2007)
  • International Brain Research Organization School of Neuroscience, Hong Kong (2006)
  • Tasmanian Postgraduate Scholarship (2004-2007)
  • Masonic Lodge Medical Research Foundation Scholarship (2004-2007)

Current projects

Dr Woodhouse is leading a project investigating how neurons regulate their activity in aging and in AD mouse models (supported by Yulgilbar postdoctoral excellence award and an Alzheimer's Australia Dementia Research Foundation postdoctoral scholarship).

She is also involved in a new project in collaboration with epigenetics experts (Dr Phillippa Taberlay, Dr Timothy Mercer) to investigate epigenetic reprogramming in AD.

Dr Woodhouse also collaborates on several other research projects at the Wicking Dementia Research and Education Centre, including projects investigating the impact of brain injury and anaesthetics on the development of AD.

Fields of Research

  • Neurology and neuromuscular diseases (320905)
  • Cellular nervous system (320902)
  • Central nervous system (320903)
  • Animal physiology - biophysics (310908)
  • Neurosciences (320999)
  • Epigenetics (incl. genome methylation and epigenomics) (310504)
  • Animal physiology - cell (310909)
  • Neurogenetics (310511)
  • Cell development, proliferation and death (310102)
  • Other biological sciences (319999)
  • Anthropological genetics (310501)
  • Bioinformatic methods development (310201)
  • Autonomic nervous system (320901)
  • Biological mathematics (490102)
  • Sensory systems (320907)
  • Cell neurochemistry (310104)
  • Chiropractic (420801)
  • Biostatistics (490502)

Research Objectives

  • Clinical health (200199)
  • Expanding knowledge in the biological sciences (280102)
  • Expanding knowledge in the biomedical and clinical sciences (280103)
  • Expanding knowledge in the health sciences (280112)
  • Health related to ageing (200502)
  • Diagnosis of human diseases and conditions (200101)
  • Behaviour and health (200401)
  • Treatment of human diseases and conditions (200105)
  • Expanding knowledge in the mathematical sciences (280118)
  • Human pharmaceutical treatments (240803)
  • Ageing and older people (230102)

Publications

Dr Woodhouse's research on neurodegenerative diseases and intrinsic excitability includes 15 articles in international peer reviewed journals 8 of which are first author publications. There has been significant international interest in her work, as is indicated by her H-index of 11 (329 total citations, average citation count 23) and the publication of her articles in journals such as Elife and highly regarded specialty journals including Acta Neuropathologica (ranked 13/252 in Neuroscience), the Journal of Neuroscience (24/250), Neurobiology of Disease (43/252) and Neurobiology of Aging (50/252). Notably, her first author publication in The Journal of Neuroscience (Amendola*, Woodhouse* et al., 2012; The Journal of Neuroscience; *equal contribution) represented a conceptual advance in the field of intrinsic excitability and aroused significant interest in the neuroscience community, as is evidenced by a commentary on this article (Hamood and Goeritz, 2012; The Journal of Neuroscience).

Total publications

52

Journal Article

(26 outputs)
YearCitationAltmetrics
2021Dyer MS, Woodhouse A, Blizzard CA, 'Cytoplasmic human TDP-43 mislocalization induces widespread dendritic spine loss in mouse upper motor neurons', Brain Sciences, 11, (7) pp. 1-16. ISSN 2076-3425 (2021) [Refereed Article]

DOI: 10.3390/brainsci11070883 [eCite] [Details]

Citations: Scopus - 2Web of Science - 2

Co-authors: Dyer MS; Blizzard CA

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2021Pan G, King A, Wu F, Simpson-Yap S, Woodhouse A, et al., 'The potential roles of genetic factors in predicting ageing-related cognitive change and Alzheimer's disease', Ageing Research Reviews, 70 pp. 1-15. ISSN 1568-1637 (2021) [Refereed Article]

DOI: 10.1016/j.arr.2021.101402 [eCite] [Details]

Citations: Scopus - 2Web of Science - 2

Co-authors: King A; Wu F; Simpson-Yap S; Vickers JC

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2020Collins JM, Woodhouse A, Bye N, Vickers JC, King AE, et al., 'Pathological links between traumatic brain injury and dementia: Australian pre-clinical research', Journal of Neurotrauma, 37, (5) pp. 782-791. ISSN 0897-7151 (2020) [Refereed Article]

DOI: 10.1089/neu.2019.6906 [eCite] [Details]

Citations: Scopus - 4Web of Science - 4

Co-authors: Collins JM; Bye N; Vickers JC; King AE; Ziebell JM

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2020Dyer MS, Reale LA, Lewis KE, Walker AK, Dickson TC, et al., 'Mislocalisation of TDP‐43 to the cytoplasm causes cortical hyperexcitability and reduced excitatory neurotransmission in the motor cortex', Journal of Neurochemistry, 157, (4) pp. 1300-1315. ISSN 0022-3042 (2020) [Refereed Article]

DOI: 10.1111/jnc.15214 [eCite] [Details]

Citations: Scopus - 8Web of Science - 10

Co-authors: Dyer MS; Reale LA; Lewis KE; Walker AK; Dickson TC; Blizzard CA

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2019Collins JM, King AE, Woodhouse A, Kirkcaldie MTK, Vickers JC, 'Age moderates the effects of traumatic brain injury on beta-amyloid plaque load in APP/PS1 mice', Journal of Neurotrauma, 36, (11) pp. 1876-1889. ISSN 0897-7151 (2019) [Refereed Article]

DOI: 10.1089/neu.2018.5982 [eCite] [Details]

Citations: Scopus - 10Web of Science - 12

Co-authors: Collins JM; King AE; Kirkcaldie MTK; Vickers JC

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2019Dyer M, Phipps AJ, Mitew S, Taberlay PC, Woodhouse A, 'Age, but not amyloidosis, induced changes in global levels of histone modifications in susceptible and disease-resistant neurons in Alzheimer's disease model mice', Frontiers in Aging Neuroscience, 11 Article 68. ISSN 1663-4365 (2019) [Refereed Article]

DOI: 10.3389/fnagi.2019.00068 [eCite] [Details]

Citations: Scopus - 4Web of Science - 4

Co-authors: Dyer M; Phipps AJ; Taberlay PC

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2018Woodhouse A, Fernandez-Martos CM, Atkinson RAK, Hanson KA, Collins JM, et al., 'Repeat propofol anesthesia does not exacerbate plaque deposition or synapse loss in APP/PS1 Alzheimer's disease mice', BMC Anesthesiology, 18, (1) Article 47. ISSN 1471-2253 (2018) [Refereed Article]

DOI: 10.1186/s12871-018-0509-5 [eCite] [Details]

Citations: Scopus - 4Web of Science - 4

Co-authors: Fernandez-Martos CM; Atkinson RAK; Hanson KA; Collins JM; O'Mara AR; Terblanche N; Skinner MW; Vickers JC; King AE

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2016King AE, Woodhouse A, Kirkcaldie MTK, Vickers JC, 'Excitotoxicity in ALS: Overstimulation, or overreaction?', Experimental Neurology, 275 pp. 162-171. ISSN 0014-4886 (2016) [Refereed Article]

DOI: 10.1016/j.expneurol.2015.09.019 [eCite] [Details]

Citations: Scopus - 98Web of Science - 99

Co-authors: King AE; Kirkcaldie MTK; Vickers JC

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2016Phipps AJ, Vickers JC, Taberlay PC, Woodhouse A, 'Neurofilament-labeled pyramidal neurons and astrocytes are deficient in DNA methylation marks in Alzheimer's disease', Neurobiology of Aging, 45 pp. 30-42. ISSN 0197-4580 (2016) [Refereed Article]

DOI: 10.1016/j.neurobiolaging.2016.05.003 [eCite] [Details]

Citations: Scopus - 21Web of Science - 22

Co-authors: Phipps AJ; Vickers JC; Taberlay PC

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2016Vickers J, Mitew S, Woodhouse A, Fernandez-Martos CM, Kirkcaldie MT, et al., 'Defining the earliest pathological changes of Alzheimer's disease', Current Alzheimer research, 13, (3) pp. 281-287. ISSN 1567-2050 (2016) [Refereed Article]

DOI: 10.2174/1567205013666151218150322 [eCite] [Details]

Citations: Scopus - 50Web of Science - 49

Co-authors: Vickers J; Mitew S; Fernandez-Martos CM; Kirkcaldie MT; Canty AJ; McCormack GH; King AE

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2015Collins JM, King AE, Woodhouse A, Kirkcaldie MTK, Vickers JC, 'The effect of focal brain injury on beta-amyloid plaque deposition, inflammation and synapses in the APP/PS1 mouse model of Alzheimer's disease', Experimental Neurology, 267 pp. 219-29. ISSN 0014-4886 (2015) [Refereed Article]

DOI: 10.1016/j.expneurol.2015.02.034 [eCite] [Details]

Citations: Scopus - 37Web of Science - 38

Co-authors: Collins JM; King AE; Kirkcaldie MTK; Vickers JC

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2015Fernandez-Martos CM, King AE, Atkinson RAK, Woodhouse A, Vickers JC, 'Neurofilament light gene deletion exacerbates amyloid, dystrophic neurite, and synaptic pathology in the APP/PS1 transgenic model of Alzheimer's disease', Neurobiology of Aging, 36, (10) pp. 2757-2767. ISSN 0197-4580 (2015) [Refereed Article]

DOI: 10.1016/j.neurobiolaging.2015.07.003 [eCite] [Details]

Citations: Scopus - 21Web of Science - 19

Co-authors: Fernandez-Martos CM; King AE; Atkinson RAK; Vickers JC

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2014Dufour MA, Woodhouse A, Amendola J, Goaillard JM, 'Non-linear developmental trajectory of electrical phenotype in rat substantia nigra pars compacta dopaminergic neurons', eLife, 3 Article e04059. ISSN 2050-084X (2014) [Refereed Article]

DOI: 10.7554/eLife.04059 [eCite] [Details]

Citations: Scopus - 20Web of Science - 15

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2014Dufour MA, Woodhouse A, Goaillard J-M, 'Somatodendritic ion channel expression in substantia nigra pars compacta dopaminergic neurons across postnatal development', Journal of Neuroscience Research, 92, (8) pp. 981-99. ISSN 0360-4012 (2014) [Refereed Article]

DOI: 10.1002/jnr.23382 [eCite] [Details]

Citations: Scopus - 32Web of Science - 33

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2012Amendola J, Woodhouse A, Martin-Eauclaire M-F, Goaillard J-M, 'Ca2+/cAMP-sensitive covariation of IA and IH voltage dependences tunes rebound firing in dopaminergic neurons', Journal of Neuroscience, 32, (6) pp. 2166-2181. ISSN 0270-6474 (2012) [Refereed Article]

DOI: 10.1523/JNEUROSCI.5297-11.2012 [eCite] [Details]

Citations: Scopus - 67Web of Science - 67

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2011King AE, Dickson TC, Blizzard CA, Woodhouse A, Foster SS, et al., 'Neuron-glia interactions underlie ALS-like axonal cytoskeletal pathology', Neurobiology of Aging: Experimental and Clinical Research, 32, (3) pp. 459-469. ISSN 0197-4580 (2011) [Refereed Article]

DOI: 10.1016/j.neurobiolaging.2009.04.004 [eCite] [Details]

Citations: Scopus - 27Web of Science - 24

Co-authors: King AE; Dickson TC; Blizzard CA; Foster SS; Chung RS; Vickers JC

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2010Chung RS, Howells C, Eaton ED, Shabala L, Zovo K, et al., 'The Native Copper- and Zinc- Binding Protein Metallothionein Blocks Copper-Mediated Aβ Aggregation and Toxicity in Rat Cortical Neurons', P L o S One, 5, (8) EJ ISSN 1932-6203 (2010) [Refereed Article]

DOI: 10.1371/journal.pone.0012030 [eCite] [Details]

Citations: Scopus - 56Web of Science - 52

Co-authors: Chung RS; Howells C; Eaton ED; Shabala L; Bennett WR; Ray S; Vickers JC; West AK

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2009Vickers JC, King AE, Woodhouse A, Kirkcaldie MT, Staal JA, et al., 'Axonopathy and cytoskeletal disruption in degenerative diseases of the central nervous system ', Brain Research Bulletin, 80, (4-5) pp. 217-223. ISSN 0361-9230 (2009) [Refereed Article]

DOI: 10.1016/j.brainresbull.2009.08.004 [eCite] [Details]

Citations: Scopus - 53Web of Science - 51

Co-authors: Vickers JC; King AE; Kirkcaldie MT; Staal JA; McCormack GH; Blizzard CA; Musgrove RE; Mitew S; Liu Y; Chuckowree JA; Bibari O; Dickson TC

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2009Woodhouse A, Shepherd CE, Sokolova A, Carroll V, King AE, et al., 'Cytoskeletal alterations differentiate presenilin-1 and sporadic Alzheimer's disease', Acta Neuropathologica, 117, (1) pp. 19-29. ISSN 0001-6322 (2009) [Refereed Article]

DOI: 10.1007/s00401-008-0458-z [eCite] [Details]

Citations: Scopus - 23Web of Science - 21

Co-authors: Sokolova A; Carroll V; King AE; Dickson TC; Vickers JC

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2009Woodhouse A, Vickers JC, Adlard PA, Dickson TC, 'Dystrophic neurites in TgCRND8 and Tg2576 mice mimic human pathological brain aging', Neurobiology of Aging, 30, (6) pp. 864-874. ISSN 0197-4580 (2009) [Refereed Article]

DOI: 10.1016/j.neurobiolaging.2007.09.003 [eCite] [Details]

Citations: Scopus - 36Web of Science - 34

Co-authors: Vickers JC; Dickson TC

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2007Woodhouse A, Dickson TC, Vickers JC, 'Vaccination strategies for Alzheimer's disease: a new hope?', Drugs and Aging, 24, (2) pp. 107-119. ISSN 1170-229X (2007) [Refereed Article]

DOI: 10.2165/00002512-200724020-00003 [eCite] [Details]

Citations: Scopus - 25Web of Science - 22

Co-authors: Dickson TC; Vickers JC

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2006Woodhouse A, Dickson TC, West AK, McLean CA, Vickers JC, 'No difference in expression of apoptosis-related proteins and apoptotic morphology in control, pathologically aged and Alzheimer's disease cases', Neurobiology of Disease, 22, (2) pp. 323-333. ISSN 0969-9961 (2006) [Refereed Article]

DOI: 10.1016/j.nbd.2005.11.010 [eCite] [Details]

Citations: Scopus - 31Web of Science - 29

Co-authors: Dickson TC; West AK; Vickers JC

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2006Woodhouse A, Vickers JC, Dickson TC, 'Cytoplasmic cytochrome c immunolabelling in dystrophic neurites in Alzheimer's disease', Acta Neuropathologica, 112, (4) pp. 429-437. ISSN 0001-6322 (2006) [Refereed Article]

DOI: 10.1007/s00401-006-0107-3 [eCite] [Details]

Citations: Scopus - 9Web of Science - 8

Co-authors: Vickers JC; Dickson TC

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2005Woodhouse A, Vincent AJ, Kozel MA, Chung RS, Waite PME, et al., 'Spinal cord tissue affects ensheathing cell proliferation and apoptosis', NeuroReport, 16, (7) pp. 737-740. ISSN 0959-4965 (2005) [Refereed Article]

DOI: 10.1097/00001756-200505120-00016 [eCite] [Details]

Citations: Scopus - 17Web of Science - 14

Co-authors: Vincent AJ; Chung RS; Vickers JC; West AK; Chuah MI

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2005Woodhouse A, West AK, Chuckowree JA, Vickers JC, Dickson TC, 'Does Beta-Amyloid Plaque Formation Cause Structural Injury to Neuronal Processes?', Neurotoxicity Research, 7, (1,2) pp. 5-15. ISSN 1029-8428 (2005) [Refereed Article]

DOI: 10.1007/BF03033772 [eCite] [Details]

Citations: Scopus - 20Web of Science - 20

Co-authors: West AK; Chuckowree JA; Vickers JC; Dickson TC

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2004Chung RS, Woodhouse A, Fung SJ, Dickson TC, West AK, et al., 'Olfactory ensheathing cells promote neurite sprouting of injured axons in vitro by direct cellular contact and secretion of soluble factors', Cellular and Molecular Life Sciences, 61, (10) pp. 1238-1245. ISSN 1420-682X (2004) [Refereed Article]

DOI: 10.1007/s00018-004-4026-y [eCite] [Details]

Citations: Scopus - 97Web of Science - 82

Co-authors: Chung RS; Fung SJ; Dickson TC; West AK; Vickers JC; Chuah MI

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Conference Publication

(26 outputs)
YearCitationAltmetrics
2019Phipps A, Giles K, Mercer T, Vickers J, Robinson M, et al., 'id #12216 - Dysregulation of the neuronal epigenome occurs prior to pathology-onset and alters with progressive amyloidosis', Australasian Neuroscience Society (ANS) 2019 Conference, 2-5 December, Adelaide Convention Centre (2019) [Conference Extract]

[eCite] [Details]

Co-authors: Phipps A; Vickers J; Taberlay P

2019Phipps A, Giles K, Mercer T, Vickers JC, Robinson M, et al., 'Recapitulation of juvenile-like histone landscape in aged neurons', Australian Dementia Forum 2019, 13-14 June 2019, Hobart, Tasmania (2019) [Conference Extract]

[eCite] [Details]

Co-authors: Phipps A; Vickers JC; Taberlay PC

2016Phipps A, Vickers J, Mercer G, Woodhouse A, Taberlay P, 'Poster 299 - Epigenetic dysregulation of critical gene regulatory elements in AD mice', Australasian Neuroscience Society Annual Scientific Meeting 2016, 4-7 December, Hobart, Tasmania (2016) [Conference Extract]

[eCite] [Details]

Co-authors: Phipps A; Vickers J; Taberlay P

2016Phipps A, Woodhouse A, Taberlay P, 'Poster 341 - Simultaneous alterations in nucleosome positions and DNA methylation predict epigenome-wide changes in Alzheimer's disease', Australasian Neuroscience Society Annual Scientific Meeting 2016, 4-7 December, Hobart, Tasmania (2016) [Conference Extract]

[eCite] [Details]

Co-authors: Phipps A; Taberlay P

2016Woodhouse A, Stuart Kimberley, Vickers J, 'Poster 375 - Increased intrinsic excitability of cortical pyramidal neurons in healthy aging', Australasian Neuroscience Society Annual Scientific Meeting 2016, 4-7 December, Hobart, Tasmania (2016) [Conference Extract]

[eCite] [Details]

Co-authors: Stuart Kimberley; Vickers J

2015Phipps AJ, Vickers JC, Taberlay PC, Woodhouse A, 'No difference in DNA methylation and hydroxymethylation marks in cortical pyramidal neurons, interneurons and microglia in control, early- and late-stage sporadic AD cases', 9th Alzheimer's + Parkinson's Disease (A+PD) Symposium, 23-24 April, Queensland Brain Institute (St Lucia) (2015) [Conference Extract]

[eCite] [Details]

Co-authors: Phipps AJ; Vickers JC; Taberlay PC

2015Phipps AJ, Vickers JC, Taberlay PC, Woodhouse A, 'Neurofilament-labelled pyramidal neurons and astrocytes are deficient in DNA methylation marks in Alzheimer's disease', Epigenetics 2015 - Australian Scientific Conference, 12-14 November, Hobart, Tasmania (2015) [Conference Extract]

[eCite] [Details]

Co-authors: Phipps AJ; Vickers JC; Taberlay PC

2014Collins J, King A, Woodhouse A, Kirkcaldie M, Vickers J, 'The effect of focal brain injury on beta-amyloid plaque deposition, inflammation and synapses in the APP/PS1 mouse model of Alzheimer's disease', Society for Neuroscience Meeting 2014, November 2014, Washington DC (2014) [Conference Extract]

[eCite] [Details]

Co-authors: Collins J; King A; Kirkcaldie M; Vickers J

2014King AE, Fernandez-Martos CM, Hanson K, Woodhouse A, Vickers JC, 'The role of anesthesia in exacerbation of ad pathology in a transgenic mouse model of amyloid plaque deposition', Australian Neuroscience Society Conference, 28-31 January 2014, Adelaide (2014) [Conference Extract]

[eCite] [Details]

Co-authors: King AE; Fernandez-Martos CM; Hanson K; Vickers JC

2014King AE, Fernandez-Martos CM, Hanson K, Woodhouse A, Vickers JC, 'Anaesthetic exposure and dementia: What can we learn from studies in transgenic mice?', Australian Society of Anaesthetists, 1-2 Mar, Hobart, TAS (2014) [Conference Extract]

[eCite] [Details]

Co-authors: King AE; Fernandez-Martos CM; Hanson K; Vickers JC

2011Amendola J, Woodhouse A, Martin-Eauclaire M-F, Goaillard J-M, 'Co-variation of IA and IH voltage dependences tunes rebound firing in dopaminergic neurons', Society for Neurosciences, Washington DC (2011) [Conference Extract]

[eCite] [Details]

2011Amendola J, Woodhouse A, Martin-Eauclaire M-F, Goaillard J-M, 'Co-regulation of IA and IH voltage dependences flexibly tunes dopaminergic neuron rebound firing', Ion Channel Meeting, Presqu'ile de Geins, France (2011) [Conference Extract]

[eCite] [Details]

2011Woodhouse A, Amendola J, Martin-Eauclaire M-F, Goaillard J-M, 'Co-variation of voltage-dependence of A-type and H-type currents maximizes the dynamic range of rebound firing in dopaminergic neurons', Meeting of the Societe des Neurosciences, Marseille, France (2011) [Conference Extract]

[eCite] [Details]

2009Woodhouse A, Goaillard J-M, 'Biophysical properties of substantia nigra dopaminergic neurons in organotypic cultures', Society for Neuroscience, Chicago (2009) [Conference Extract]

[eCite] [Details]

2008King AE, Dickson TC, Blizzard CA, Foster SS, Woodhouse A, et al., 'Neuron-glia interactions underlying axonal health in an in vitro spinal culture model of relevance to ALS', Amyotrophic Lateral Sclerosis, 19th Symposium on ALS/MND, 3-5 November, Birmingham, pp. 85. (2008) [Conference Extract]

[eCite] [Details]

Co-authors: King AE; Dickson TC; Blizzard CA; Foster SS; Chung RS; Vickers JC

2008Vickers JC, King AE, Blizzard CA, Woodhouse A, Foster SS, et al., 'Murine spinal neurons in vitro develop proximal axonal transport abnormalities and swellings that are similar to early axonal changes in amyotrophic lateral sclerosis', Society for Neuroscience, 15-19 November, Washington, DC (2008) [Conference Extract]

[eCite] [Details]

Co-authors: Vickers JC; King AE; Blizzard CA; Foster SS; Chung RS; Dickson TC

2008Woodhouse A, Carroll V, Sokolova A, Shepherd CE, Halliday G, et al., 'Presenilin-1 familial Alzheimer's disease cases exhibit altered pathology in comparison to sporadic AD', Proceedings of the Australian Neuroscience Society Annual Conference 2008, 27-30 January 2008, Hobart, pp. 113. (2008) [Conference Extract]

[eCite] [Details]

Co-authors: Carroll V; Sokolova A; Shepherd CE; Halliday G; Dickson TC; Vickers JC

2007Woodhouse A, Vickers JC, Adlard PA, Dickson TC, 'Plaque-induced axonal pathology in transgenic mice expressing human mutant amyloid precursor protein genes replicates the dystrophic neurites characteristic of preclinical AD', Society for Neuroscience, San Diego (2007) [Conference Extract]

[eCite] [Details]

Co-authors: Vickers JC; Dickson TC

2007Woodhouse A, Vickers JC, Adlard PA, Dickson TC, 'The dystrophic neurite pathology exhibited by TgCRND8 and Tg2576 transgenic mice models preclinical Alzheimer's disease', IBRO World Congress of Neuroscience, Melbourne (2007) [Conference Extract]

[eCite] [Details]

Co-authors: Vickers JC; Dickson TC

2006Vickers JC, King AE, Dickson TC, Chung RS, Chuckowree JA, et al., 'In vitro models of the key pathological changes in axons associated with neurodegenerative disease and acquired brain injury', 4th Congress of Federation of Asian-Oceanain Neuroscience Societies, November, Hong Kong (2006) [Conference Extract]

[eCite] [Details]

Co-authors: Vickers JC; King AE; Dickson TC; Chung RS; Chuckowree JA; Haas MA; Staal JA; Blizzard C; West AK; Chuah I; McCormack G

2006Woodhouse A, Adlard PA, Dickson TC, Vickers JC, 'Mutant human APP transgenic mice demonstrate dystrophic neurite pathology identical to preclinical Alzheimer's disease', Congress of the Federation of the Asian-Oceanian Neuroscience Societies, Hong Kong (2006) [Conference Extract]

[eCite] [Details]

Co-authors: Dickson TC; Vickers JC

2005Woodhouse A, Dickson TC, West AK, Vickers JC, 'Proteins and genes related to apoptosis are not elevated in pathological brain aging or Alzheimer's disease', Society for Neuroscience, Washington DC (2005) [Conference Extract]

[eCite] [Details]

Co-authors: Dickson TC; West AK; Vickers JC

2004Woodhouse A, Vincent AJ, Chung RS, Vickers JC, West AK, et al., 'Proliferation, apoptosis and migration of ensheathing cells in response to spinal cord tissue', Proceedings of the Australian Neuroscience Society, Melbourne, pp. 85. ISSN 1034-3237 (2004) [Conference Extract]

[eCite] [Details]

Co-authors: Vincent AJ; Chung RS; Vickers JC; West AK; Chuah MI

2004Woodhouse A, Vincent AJ, Kozel M, Chung RS, Waite PME, et al., 'Olfactory ensheathing cells exhibit different rates of proliferation and apoptosis in the presence of uninjured and injured spinal cord tissue', The International Neurotrauma Symposium, pp. 189. (2004) [Conference Extract]

[eCite] [Details]

Co-authors: Vincent AJ; Chung RS; Vickers JC; West AK; Chuah MI

2003Chung RS, Woodhouse A, Fung SJ, Vincent AJ, West AK, et al., 'Olfactory ensheathing cells promote reactive neurite sprouting in vitro through both direct and indirect mechanisms', Society for Neuroscience, November 2003, New Orleans, pp. 42.20. (2003) [Conference Extract]

[eCite] [Details]

Co-authors: Chung RS; Fung SJ; Vincent AJ; West AK; Vickers JC; Chuah MI

2003Chung RS, Woodhouse A, Fung SJ, Vincent AJ, West AK, et al., 'Olfactory ensheathing cells promote reactive neurite sprouting in vitro through both direct and indirect mechanisms', Journal of Neurotrauma, USA, pp. 1099. ISSN 0897-7151 (2003) [Conference Extract]

[eCite] [Details]

Co-authors: Chung RS; Fung SJ; Vincent AJ; West AK; Vickers JC; Chuah MI

Grants & Funding

Dr Woodhouse has been awarded ~$800,000 in competitive funding from Australian and International funding schemes to support my research. This includes an Alzheimer's Australia Dementia Research Foundation postdoctoral fellowship ($220K), NHMRC overseas postdoctoral training fellowship ($366K) and the Foundation pour la Recherché Medicale postdoctoral fellowship ($35K) in France. To undertake my PhD I was awarded a Tasmanian Postgraduate and Tasmanian Masonic Centenary Medical Research Foundation Scholarships totalling ($84K). In 2015 I was awarded a Judith Jan Mason and Harold Stannett Williams Memorial Foundation National Medical Program grant (CIB, $50K) to chart the epigenetic reprogramming in AD mice. In 2014 I was awarded a Yulgilbar postdoctoral excellence award (CIA, $20K) for young investigators to pursue ambitious research projects from the Yulgilbar Foundation. I have also received 4 competitive travel awards, including the highly competitive Society for Neuroscience (SFN)/International Brain Research Organization (IBRO) International Travel Grant and the IBRO School of Neuroscience and FAONs congress grant.

Funding Summary

Number of grants

13

Total funding

$2,360,855

Projects

Identifying critical neuronal signatures of epigenetic modifier complexes alteration in human Alzheimer's disease (2019 - 2021)$30,000
Description
We aim to determine the key epigenetic changes that occur in neurons in early-sporadic and late-sporadic human Alzheimers disease (AD). We will use the chromatin immunoprecipitation and sequencing (ChIP-seq) technique to generate the first comprehensive genome wide maps of epigenetic modifying proteins in neurons from humans. We will identify the patterns of epigenetic modifying proteins that distinguish neurons normal ageing from those in sporadic AD brains, including differences that change in tandem with disease progression.
Funding
The Yulgilbar Foundation ($30,000)
Scheme
Contract Research
Administered By
University of Tasmania
Research Team
Woodhouse A; Perez Saurez T
Period
2019 - 2021
Delineating the epigenetic evolution of neurons in human sporadic Alzheimer's disease (2019 - 2021)$826,102
Description
Sporadic Alzheimer's disease (sAD) is not part of normal aging and we must determine how and why it occurs. The epigenome (meaning, 'above genes') ensures that our genes are expressed in the right cell type at the right time. Epigenetic defects are of great interest as they are reversible; but first, the epigenetic changes that characterise AD progression must be defined. Our overall aim is to identify how epigenetic programming is altered in the nerve cells that die in AD.
Funding
National Health & Medical Research Council ($826,102)
Scheme
Grant-Project
Administered By
University of Tasmania
Research Team
Taberlay PC; Woodhouse A; Robinson M; Mercer T
Period
2019 - 2021
Grant Reference
1161768
Turning back the clock on brain cell aging (2018 - 2021)$458,608
Description
This proposal aims to determine the role of fundamental epigenetic mechanisms in the process of aging. It combines the fields of epigenetics, neurosciences and mathematics to delineate the dynamics of DNA methylation and histone modification marking on the transcriptome during normal, healthy aging. This project will uniquely apply environmental enrichment to determine whether modulation of the epigenome underpins an improvement in cognitive function. Thus, whether an adult, rather than aged, epigenome can be maintained in neurons duringaging.
Funding
Australian Research Council ($458,608)
Scheme
Grant-Discovery Indigenous
Administered By
University of Tasmania
Research Team
Taberlay PC; Woodhouse A; Vickers JC
Period
2018 - 2021
Grant Reference
IN180100005
TDP-43 Misprocessing drives synaptic deficits that leads to ALS (2017)$249,861
Description
Disturbances in neuronal synapses may be an early event that potentially leads to the neuronal dysfunction and death that causes Amyotrophic Lateral Sclerosis (ALS). Mutations in the protein, transactive response DNA-binding protein 43 (TDP-43) causes a genetic form of ALS. TDP-43 has recently been shown to be involved in maintaining synapses between neurons; regulating the number and maturation of synapses. We will investigate how dysfunction TDP-43 protein alters synapses and determine how these synaptic changes can lead to the neuronal death that characterises ALS.
Funding
Motor Neurone Disease Research Australia ($249,861)
Scheme
Grant-Betty Laidlaw
Administered By
University of Tasmania
Research Team
Blizzard C; Woodhouse A; Walker A
Year
2017
Identifying critical neuronal signatures of epigenetic modifier complexes of Alzheimer's disease initiation and progression (2017)$33,000
Description
Aging causes our cells to decline in both integrity and function. As such, the incidence of disorders that affect nerve cells, including Alzheimers disease (AD), increases with aging. In healthy cells, our genes are tightly regulated so that the correct combination of genes are switched on, or off, at the proper time to allow for learning and memory to occur. This is achieved by the addition or removal of small chemical residues associated with DNA, and the study of these processes is known as epigenetics. Epigenetic marks can change during aging, and diseases occur when this happens too quickly or in an uncontrolled way. Proper epigenetic control must be maintained during aging and we raise the possibility that epigenetic dysregulation plays an important role in AD progression. Surprising though, existing knowledge of the epigenetic alterations in AD is extremely limited, highlighting that new knowledge in this area is critical and that the timing of our study is significant. We present striking preliminary data revealing that epigenetic changes are occurring in AD and that they are affecting important gene regulatory regions. Our overall aim is to investigate whether the proteins in charge of regulating epigenetic processes behave abnormally in AD. At completion we will understand whether certain epigenetic signatures are associated with different stages in sporadic AD, and whether they differ between sporadic and familial AD. Ours is the only study currently measuring epigenetic changes specifically in nerve cells. These findings will significantly advance our understanding of the role of epigenetic dysregulation in AD and ss epigenetic defects are reversible, this study could also identify new clinical targets to improve the outcomes for people living with AD.
Funding
Brain Foundation ($33,000)
Scheme
Grant-Research
Administered By
University of Tasmania
Research Team
Taberlay PC; Woodhouse A; Robinson M; Mercer T
Year
2017
New geNOMeC maps of neuronal epigenetic changes in Alzheimer's disease (2017)$24,971
Description
Every cell in our body contains an identical genetic code; yet, for example, our heart and brain are very different. This is made possible by a process called epigenetics, which describes the addition and removal of small chemical marks above (epi) our DNA (genetics). Epigenetic marks carefully build layers on top of each other and when this happens properly, the right genes are expressed in the right cells at the right time and allow them to function as they should. However, there are no techniques to measure more than two epigenetic marks at the same time. Our overall goal is to address this deficit by developing a new technique that measures three epigenetic marks simultaneously (DNA methylation, histone modifications, nucleosomes). The benefit will be unlimited because it will be applicable to all normal and disease states, and all organisms. Furthermore, we will use this capability to determine whether epigenetic mistakes could explain why certain cells in the brain (neurons) are dysfunctional and die in Alzheimers disease, while other cells are resistant. This is a critical question in the field and our new data may unlock vital clues about the molecular etiology of this currently incurable disease.
Funding
Rebecca L Cooper Medical Research Foundation ($24,971)
Scheme
Grant
Administered By
University of Tasmania
Research Team
Taberlay PC; Woodhouse A
Year
2017
Single-cell DNA Methylome Sequencing to detect epigenetic heterogeneity in aged pyramidal neurons (2016)$14,407
Description
Chemical and physical modification of DNA enables phenotypic variation within individuals built from a single genome. Thestudy of epigenetics has the potential to span the spectrum of biology, but has been somewhat limited to some fields (e.g. cancerand aging) or by virtue of the methods currently available to map epigenomes. DNA methylation is a major component of theepigenome and underpins normal development and survival. It is measured by whole genome bisulfite sequencing (WGBS), whichprovides information on the methylation status of DNA loci from the entire pools of cells sampled as a population; thus,knowledge regarding the cell-to-cell variation in epigenetic signatures is severely lacking. Single-cell WGBS experiments are atthe cutting edge of epigenetics research (Smallwood et al., 2014, Nature Methods, Farlik et al., 2015, Cell Reports) and will allowus to ascertain the heterogeneity in DNA methylation patterns from cell to cell. Our study will address a substantial gap in knowledge in the field by generating the first single-cell WGBS data from individual aged neurons. Pyramidal neurons are postmitotic long-lived cells with the ability to accrue epigenetic differences over time, thus, providing an ideal model to assess the heterogeneity in the DNA methylomes of individual cells in healthy aging.
Funding
University of Tasmania ($14,407)
Scheme
Grant-Research Enhancement (REGS)
Administered By
University of Tasmania
Research Team
Woodhouse A; Taberlay PC; Vickers JC
Year
2016
Charting epigenetic reprogramming in Alzheimer's disease mice (2015)$50,020
Description
Aging constitutes a time-dependent decline in cellular integrity and function. As we age, the incidence of neurodegenerative disorders, including Alzheimers disease (AD) increase. Ordinarily, the genome remains under exquisite control; epigenetic plasticity in neurons isimportant for continued learning and memory1,2 and is retained across lifespan3. Epigenetic mechanisms such as DNA methylation, and histone modifications are absolutely necessary for proper transcriptional output that underpins these normal cellular processes. Indeed, theimportance of epigenetics has now been well established in cancer field, yet other diseases have been largely overlooked.We hypothesize that epigenetic changes are hallmarks of Alzheimers disease.Here, we emphasize that proper epigenetic control must be maintained during aging and raise the possibility that epigenetic dysregulation plays an important role in AD progression. Striking observations from our preliminary study forms the basis of this new proposal. Foremost, epigenetic marks defining both enhancers (H3K4me1, H3K27Ac) and promoters (H3K4me3, H3K27me3) are lost from gene regulatory regions, revealing that epigenetic reprogramming does occur in AD. Existing knowledge of the epigenetic alterations in AD is extremely limited, highlighting that new knowledge in this area is critical and the timing of this work is highly significant.Our OVERALL AIM is to determine the repertoire of epigenetic aberrations associated with Alzheimers disease and to test whether the development of disease is underpinned by an abnormal epigenetic program.Our Overall Aim will be addressed by:1) Generating maps of activating and repressive epigenetic marks across a time course that encompasses pre-disease, disease onset and late disease stages in a mouse model of AD.2) Identifing the spatial epigenetic changes that occur in distinct cell types across a time course of disease progression in AD mice.At completion we will understand whether distinct epigenetic signatures are associated with different stages in disease progression in AD, and if epigenetic alterations are cell typespecific or dependent on proximity to AD pathology. These findings will significantly advance our understanding of the role of pigenetic dysregulation in AD and could identifying new clinical targets to improve the outcomes for AD patients.
Funding
The Mason Foundation ($50,020)
Scheme
Grant-Judith Jane Mason & Harold Stannett Williams
Administered By
Garvan Institute of Medical Research
Research Team
Taberlay PC; Woodhouse A; Mercer T; Phipps AJ
Year
2015
Selectively vulnerable neurons in Alzheimer's disease: functional and morphological changes in healthy ageing and early Alzheimer's disease (2015 - 2017)$220,000
Description
<p>AD is highly correlated with ageing. Alterations in neuron function are important in age-associated cognitive decline. In AD memory deficits are due to dysfunction, degeneration and death of a vulnerable subpopulation of neurons. Existing knowledge is extremely limited and does not identify why a subset of neurons are selectively vulnerable in AD.</p><p>Hypothesis: Vulnerable neurons in AD exhibit a distinct signature of alterations in healthy aging and early AD.</p><p>A multi-dimensional approach (patch-clamp electrophysiology, morphological analysis, cognitive assessment) will be used to:</p>1: Determine how neuronal activity, morphology and cognition are altered in neuron subpopulations in healthy ageing.<br>2: Examine how neuronal activity and morphology are altered in vulnerable neurons in early AD.<br>3: Identify and characterize alterations in currents underlying age- and AD-associated changes in neuronal activity.<br><p>This proposal will significantly advance our knowledge by producing data essential for understanding how neurons function across healthy ageing and how this is altered in the subpopulation of neurons vulnerable to AD, providing vital knowledge that will be valuable across key areas of neuroscience research. Understanding of the mechanisms underlying the selective vulnerability of this subset of neurons in AD will inform the design of therapeutics aimed at protecting these cells.</p>
Funding
Dementia Australia Research Foundation Ltd ($220,000)
Scheme
Fellowship-Postdoctoral Fellowship in Dementia
Administered By
University of Tasmania
Research Team
Woodhouse A; Vickers JC
Period
2015 - 2017
Selectively vulnerable neurons in Alzheimers disease: functional and morphological changes (2015)$20,000
Description
The overall aim of the project is to determine whether neurons vulnerable in AD exhibit a distinct signature of functional and morphological changes in healthy ageing and early AD.
Funding
The Yulgilbar Foundation ($20,000)
Scheme
Award-Postdoctoral Excellence
Administered By
University of Tasmania
Research Team
Woodhouse A; Vickers JC
Year
2015
Charting epigenetic reprogramming in Alzheimer's disease mice (2015 - 2017)$52,500
Description
Aging causes our cells to decline in both integrity and function. As such, the incidence of disorders that affect neurons, including AD, increase with aging. In healthy cells, our genes are tightly regulated so that the correct combination of genes are switched on, or off, at the proper time to allow for learning and memory to occur. This is achieved by the addition or removal of small chemical residues on top of the DNA, and the study of these processes is known as epigenetics. Epigenetic marks on our DNA can change during aging, and diseases occur when this happens too quickly or in an uncontrolled way. Proper epigenetic control must be maintained during aging and we raise the possibility that epigenetic dysregulation plays an important role in AD progression.
Funding
Dementia Australia Research Foundation Ltd ($52,500)
Scheme
Grant-Scholarship
Administered By
University of Tasmania
Research Team
Woodhouse A; Phipps AJ
Period
2015 - 2017
Assessing the alterations in cortical neuron activity in the vicinity of AB plaques in Alzheimer's disease model mice (2013)$15,400
Funding
University of Tasmania ($15,400)
Scheme
Grant-Research Enhancement (REGS)
Administered By
University of Tasmania
Research Team
Woodhouse A
Year
2013
Regulation of dendritic ion channels and its role in intrinsic neuronal excitability in health and disease (2009 - 2014)$365,986
Funding
National Health & Medical Research Council ($365,986)
Scheme
Fellowship-Overseas Based Biomedical
Administered By
University of Tasmania
Research Team
Woodhouse A
Period
2009 - 2014
Grant Reference
0544940

Research Supervision

Dr Woodhouse is currently supervising 2 PhD students, one as primary supervisor, due for completion in 2015 and 2018. She has successfully supervised one honours student to completion (2014, First Class Honours), despite being on maternity leave (August 2014-ongoing).

Current

3

Completed

2

Current

DegreeTitleCommenced
PhDInvestigating the Role of Mislocalised TDP-43 in Cortical Hyperexcitability in ALS2018
PhDDNA Methylation and Nucleosome Occupancy Landscapes of Excitatory Neurons in Human Sporadic Alzheimer's Disease2018
PhDDelineating the Epigenetic Evolution of Neurons in Human Alzheimer's Disease2020

Completed

DegreeTitleCompleted
PhDDNA Methylation and Histone Modification Dynamics in Neurons in Aging and Alzheimer's Disease
Candidate: Andrew James Phipps
2019
PhDThe Effect of Traumatic Brain Injury in Experimental Models of Alzheimer's Disease
Candidate: Jessica Marie Collins
2016