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Home: Community: Researcher Profiles
Researcher Profile

RESEARCHER INFORMATION
First Name:David
Last Name:Small
Title:Professorial Research Fellow
Advanced Degrees:BSc. PhD.
Affiliation:University of Tasmania
Department:Menzies Research Institute
Street Address 1:Private Bag 23
City:Hobart
State/Province:Tasmania
Zip/Postal Code:7001
Country/Territory:Australia
Phone:61-3-6226-7700
Fax:61-3-6226-7704
Email Address: 
Disclosure:
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View all comments by David Small
Clinical Interests:
Alzheimer Disease, Aging Process, Neuromuscular Disorders (ALS, etc.), Tauopathies, Neurodevelopmental Disorders (Down syndrome, etc.), Stroke and Trauma, Polyglutamine Disorders (Huntington's, etc.), Prion Diseases
Research Focus:
Protein structure/chemistry, Proteomics, Diagnosis, Neurobiology, A-beta PP/A-beta, Molecular and Cell biology
Work Sector(s):
University, Research institute
Web Sites:
Personal: http://www.alzweb.org
Professional: http://www.monash.edu.au
Lab: http://www.alzweb.org
Researcher Bio
PhD University of Melbourne, Australia, 1982.
Postdoctoral research, MIT 1982-1984, Flinders University of South Australia, 1984-1985.
University of Melbourne 1986-2002. Monash University 2003-present. Current appointment National Health and Medical Research Council of Australia Senior Research Fellow (Continuing) Level B. Approximately 110 publications (mostly in field of Alzheimer's disease and related disorders) as of 2003.
Top Papers
1. Small, D.H., Nurcombe, V., Clarris, H., Beyreuther, K. & Masters, C.L. (1994) A heparin-binding domain on the amyloid protein precursor of Alzheimer's disease is involved in the regulation of neurite outgrowth. J. Neuroscience 14, 2117-2127.

2. Small, D.H., Reed, G., Whitefield, B., Nurcombe, V. (1995) Cholinergic regulation of neurite outgrowth from isolated chick sympathetic neurons in culture. J. Neuroscience 15, 144-151.

3. Williamson, T., Mok, S.S., Henry, A., Cappai, R., Lander, A., Nurcombe, V., Beyreuther, K., Masters, C. and Small, D.H. (1996) Secreted glypican binds to the amyloid protein precursor (APP) of Alzheimer’s disease and inhibits APP-induced neurite outgrowth. J. Biol. Chem. 271, 31215-31221.

4. Mok, S.S., Evin, G., Li, Q.X., Smith, A.I., Beyreuther, K., Masters, C.L. and Small, D.H. (1997) A novel metalloprotease in rat brain cleaves the amyloid protein precursor of Alzheimer’s disease generating amyloidogenic fragments. Biochemistry 36, 156-163.

5. Sberna, G., Sáez-Valero, J., Beyreuther, K., Masters, C.L. and Small, D.H. (1997) The amyloid-b protein of Alzheimer’s disease increases acetylcholinesterase expression by increasing intracellular calcium in embryonal carcinoma P19 cells J. Neurochem. 69, 1177-1184.

6. Sáez-Valero, J., Sberna, G., McLean, C.A., Masters, C.L. and Small, D.H. (1997) Glycosylation of acetylcholinesterase as diagnostic marker for Alzheimer’s disease. Lancet 350, 929.

7. Sberna G., Sáez-Valero, J., Li, Q.-X., Czech, C., Beyreuther, K., McLean, C., Masters, C.L. and Small, D.H. (1998) Acetylcholinesterase is increased in the brains of transgenic mice expressing the C-terminal fragment (CT100) of the b-amyloid protein precursor of Alzheimer’s disease. J. Neurochem. 71, 723-731.

8. Small, D.H., Mok, S.S. and Bornstein, J.C. (2001) Alzheimer’s disease and Ab toxicity: from top to bottom. Nature Reviews Neuroscience 2, 595-598.

9. Nunan, J., Shearman, M.S., Checler, F., Cappai, R., Evin, G., Beyreuther, K., Masters, C.L. and Small, D.H. (2001) The C-terminal fragment of the Alzheimer’s disease amyloid protein precursor (APP-CTFb) is degraded by a proteasome-dependent mechanism distinct from g-secretase. Eur. J. Biochem. 268, 5329-5336.

10. Subasinghe, S., Unabia, S., Barrow, C.J., Mok, S.S., Aguilar, M.I. and Small, D.H. (2003) Cholesterol is necessary both for the toxic effect of Ab peptides on vascular smooth muscle cells and for Ab binding to vascular smooth muscle cell membranes. J. Neurochem. 84, 471-479.
What is the greatest void to date in our knowledge of Alzheimer's Disease?
Our understanding of the mechanism of Abeta toxicity.
If resources were not limited, what research projects would you pursue?
We are currently pursuing them.
What is your leading hypothesis?
That Alzheimer's disease is in essence a disease of altered synaptic plasticity.
What piece of missing evidence would help prove it?
There is no one single piece of evidence.
What is your fallback position?
There are many.

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