Dr. Walker Jackson

Group leader

German Center for Neurodegenerative Diseases (DZNE)
Sigmund-Freud-Str. 27 
53127 Bonn

walker.jackson(at)dzne.de
+49 (0) 228 / 43302-690
+49 (0) 228 / 43308-684 (Secretary)

Group members

Name Phone
Nancy El Deiry, Assistant +49 (0)228 / 43302-684
Dr. Lech Kaczmarczyk, Postdoc +49 (0)228 / 43302-693
Dr. Lars Dittrich, Postdoc +49 (0)228 / 43302-691
Melvin Schleif, PhD Student +49 (0)228 / 43302-692
Andrea Baral, Technical Assistant +49 (0)228 / 43302-696
Lisa Weidner, Technical Assistant +49 (0)228 / 43302-695
F.l.t.r.: Walker Jackson, Melvin Schleif, Chenna Galiveti, Alessandro Petese, Fabio Testaquadra, Lars Dittrich, and Lech Kaczmarczyk.

Publications

Spontaneous generation of prion infectivity in fatal familial insomnia knock-in mice.

#Jackson WS, Borkowski AW, Faas H, Steele AD, King OD, Watson N, Jasanoff A, Lindquist S. Neuron 63, 438-450 (2009).
#Article covered in Nature Reviews Neuroscience 10, 694 (2009)

Context-dependent perturbation of neural systems in transgenic mice expressing a cytosolic prion protein.

*Faas H, *Jackson WS, Borkowski A, Wang X, Ma J, Lindquist S, Jasanoff A. Neuroimage, online (2009 Oct 14)
* authors contributed equally

Context dependent neuroprotective properties of prion protein (PrP).

Steele AD, Zhou Z, Jackson WS, Zhu C, Auluck P, Moskowitz MA, Chesselet MF, Lindquist S. Prion 3, 240-9 (2009).

Lymphotoxin-dependent prion replication in inflammatory stromal cells of granulomas.

Heikenwalder M, Kurrer MO, Margalith I, Kranich J, Zeller N, Haybaeck J, Polymenidou M, Matter M, Bremer J, Jackson WS, Lindquist S, Sigurdson CJ, Aguzzi A. Immunity 29, 998-1008 (2008).

Heat shock factor 1 regulates lifespan as distinct from disease onset in prion disease.

Steele AD, Hutter G, Jackson WS, Heppner FL, Borkowski AW, King OD, Raymond GJ, Aguzzi A, Lindquist S. Proc Natl Acad Sci U S A 105, 13626-31 (2008).

Illuminating aggregate heterogeneity in neurodegenerative disease.

Jackson WS & Lindquist S. Nat Methods 4, 1000-1 (2007).

Diminishing apoptosis by deletion of Bax or overexpression of Bcl-2 does not protect against infectious prion toxicity in vivo.

Steele AD, King OD, Jackson WS, Hetz CA, Borkowski AW, Thielen P, Wollmann R, Lindquist S. J Neurosci 27, 13022-7 (2007).

The power of automated high-resolution behavior analysis revealed by its application to mouse models of Huntington’s and prion diseases.

Steele AD, Jackson WS, King OD, Lindquist S. Proc Natl Acad Sci U S A 104, 1983-8 (2007).

Prion pathogenesis is independent of caspase-12.

Steele AD, Hetz C, Yi CH, Jackson WS, Borkowski AW, Yuan J, Wollmann RH, and Lindquist S. Prion 1, 1-5 (2007).

Intraflagellar transport is essential for endochondral bone formation.

Haycraft CJ, Zhang Q, Song B, Jackson WS, Detloff PJ, Serra R, Yoder BK. Development, 134, 307-16 (2007).

Nucleocytoplasmic transport signals affect the age at onset of abnormalities in knock-in mice expressing polyglutamine within an ectopic protein context.

Jackson WS, Tallaksen-Greene SM, Albin RL, Detloff PJ. Human Molecular Genetics 12, 1621-1629 (2003).

HPRT(CAG)146 mice: age of onset of behavioral abnormalities, time course of neuronal intranuclear inclusion accumulation, neurotransmitter marker alterations, mitochondrial function markers, and susceptibility to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.

Tallaksen-Greene SM, Ordway JM, Crouse AB, Jackson WS, Detloff PJ, Albin RL. HPRT(CAG). Journal of Comparative Neurology 465, 205-219 (2003).

Neurological abnormalities in a knock-in mouse model of Huntington’s disease.

Lin CH, Tallaksen-Greene S, Chein WM, Cearley JA, Jackson WS, Crouse AB, Ren S, Li XJ, Albin RL, Detloff PJ. Human Molecular Genetics 10, 137-44 (2001).

Curriculum Vitae

Walker Jackson received B.S. degrees in Biochemistry and Biological Sciences from Florida State University, Tallahassee, FL in 1997.  He earned his Ph.D. in 2003 from the University of Alabama-Birmingham, Birmingham, AL with Dr. Peter Detloff, where he developed and characterized an allelic series of knock-in mice to address important mechanistic questions related to polyglutamine diseases.  His postdoctoral research was with Dr. Susan Lindquist at the Whitehead Institute for Biomedical Research/MIT, Cambridge, MA.  After creating a new allelic series of knock-in mice to study prion diseases, he worked on new behavioral and imaging methods to study the progression of disease in vivo.

In 2011 he left the USA to join the DZNE Bonn as a group leader.


Areas of investigation/research focus

The types of clinical signs present in people suffering from neurodegenerative diseases (NDs) are determined by which brain areas are affected.  For example, areas of the brain important for motor control are damaged in Parkinson’s disease while areas important for memory are damaged in Alzheimer’s disease.  Most NDs appear to be caused by misfolding of proteins and, although there is some variability in the spatial distribution of these disease-causing proteins, there is not a positive correlation between protein levels and the extent of degeneration.  That is, many brain areas express the proteins at relatively high levels but appear to be unaffected.  Why this happens is both a scientifically intriguing question as well as a potential window for the design of therapies.  If we can identify the properties that allow certain cells to naturally tolerate high levels of the misfolded proteins, introduction of these properties into otherwise vulnerable cells may preserve their functionality.