Troy Rohn

Associate Professor
Department of Biology
Year arrived at BSU:

Mailing Address:



Office Location:

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e-mail address:


 2000

Department of Biology Boise State University Boise, ID 83725

SN228

208-426-2396

208-426-4267

trohn@boisestate.edu
Background
Troy Rohn graduated in 1990 from the University of California at Davis with a B.S. in Physiology. He received his Ph.D. in Pharmacology from the University of Washington, Seattle in 1994. His interests include the role of apoptosis in neurodegenerative diseases. Dr. Rohn had several Postdoctoral stints including two plus years living in Paris, France, one year at Montana State University in Bozeman, Montana, and two years at UC Irvine at the Institute of Brain Aging and Dementia under the direction of Dr. Carl Cotman.


Research Interests
Treatment of living cortical neurons with an apoptotic insult, PGJ2, results in neurite degeneration and nuclear condensation and fragmentation, which are hallmarks of apoptosis.
The primary focus of my laboratory is involved in the research involving neurodegenerative diseases including to a large extent, Alzheimer's disease (AD). During the progression of Alzheimer’s disease, many neurons die particularly in the area of the hippocampus. Because the hippocampus is an area of the brain involved in memory, AD is primary a disease where afflicted individuals lose their capacity for memory. A primary question in this field is how are neurons dying during the progression of AD. Our lab, as well as many others, is convinced that the primary cause of neuronal cell death associated with AD is caused by neurons undergoing apoptosis. Apoptosis, or programmed cell death, is a genetically driven form of cell death that plays an important function for living organisms. Upon activation of apoptosis, a series of steps occur, ultimately leading to cell death. One of the most important early steps in apoptosis is the activation of a family of proteases termed, caspases. Thus, caspase cleavage of critical proteins is believed to be responsible for the morphological and functional changes observed when cells undergo apoptosis. Biochemical markers are being developed that are designed to follow specific cleavage products produced from caspases. In this way, we can use these markers as footprints to the contribution of apoptosis in certain neurodegenerative diseases including AD. More recently, we have begun to examine if caspases are in fact the link between NFTs and senile plaques due to their ability to cleave tau.

Another focus of the lab is examining the molecular mechanisms underlying Parkinson’s disease and dementia with Lewy bodies. More specifically, we are looking at the role that calpain-cleavage of alpha-synuclein contributes to Lewy body initiation and evolution using both animal models and post-mortem brain tissue.
 
Click on the icon to download a recent paper on apoptosis

 
Selected Publications (out of 30)

Acarin, L., Villapol, S., Faiz, M., Rohn, T.T., Castellano, B. and Gonzalez, B. (2007).  Caspae-3 activation in astrocytes following postnatal excitotoxic damage correlates with cytoskeletal remodeling but not with cell death or proliferation.  (Submitted)

Dufty, B.M., Warner, L.R., Hou, S.T., Jiang, S.X., Gomez-Isla, T., Leenhouts, K.M., Oxford, J.T., Masliah, E. and Rohn T.T. (2007).  Calpain-cleavage of alpha-synuclein: Connecting proteolytic processing to disease-linked aggregation (submitted).

Mouser, P.E., Head, E., Ha, K-H., and Rohn, T.T. (2006).  Caspase cleavage of GFAP within degenerating astrocytes of the Alzheimer’s disease brain. American Journal of Pathology 168(3): 936-46.

Newman, J., Rissman R.A., Sarsoza, F., Kim, R.C., Dick, M., Rohn T.T. and Head, E.  (2005) Caspase-cleaved tau accumulation in neurodegenerative diseases associated with the intracellular accumulation of tau or synuclein. Acta Neuropathol (Berl). 110(2): 135-44.

Rohn, T.T., Cusack, S.M., Kessinger, S.R., and Oxford, J.T. (2004). Caspase activation independent of cell death is required for proper cell dispersal and correct morphology in PC12 cells. Experimental Cell Research 299(2): 442-53.

Rissman, R.A., Poon, W.W., Blurton-Jones, M., Oddo, S., Torp, R., LaFerla, F.M., Rohn, T.T. and Cotman, C.W. (2004). Caspase-dependent cleavage of tau is an early event in Alzheimer’s disease tangle pathology. Journal of Clinical Investigation 114: 121-130 (See commentary, page 23).

Chung, C-W, Hong, Y-M, Song, Woo, H-N, Choi, Y-H, Rohn, T.T. and Jung, Y-K. (2003). Atypical role of proximal caspase-8 in truncated tau-induced neurite regression and neuronal cell death. Neurobiol Dis 14(3): 557-566.

Rohn, T.T., Rissman, R.A., Head, E. and Cotman, C.W. (2002). Caspase activiation in the Alzheimer's Disease Brain: Tortuous and Torturous. Drug News & Perspectives 15(9): 549-557.

Rohn, T.T., Rissman, R.A., Davis, M.C., Kim, Y., Cotman, C.W. and Head, E.  (2002).  Caspase-9 activation and caspase cleavage of tau in the Alzheimer’s disease brain.  Neurobiol Dis 11:341-354.

Head, E., Lott, I.T., Cribbs, D.H., Cotman, C.W. and Rohn, T.T. (2002).  b-Amyloid deposition and neurofibrillary tangle association with caspase activation in Down syndrome.  Neurosci. Lett 330: 99-103.

Mbebi, C., Rohn, T.T., Doyennette, M-A., Chevessier, F., Jandrot-Perrus, M., Hantai, D. and Verdiere-Sahuque, M. (2001). Thrombin receptor induction by injury-related factors in human skeletal muscle cells.  Experimental Cell Research 263: 77-87.

Rohn, T.T., Head, E., Su, J.H., Anderson, A.J., Bahr, B.A., Cotman, C.W. and Cribbs, D.H. (2001) Evidence for caspase activation in tangle-bearing neurons in Alzheimer’s disease.  American Journal of Pathology 158: 189-198 (See Commentary, page 1-2)

Rohn, T.T., Wong, S.M., Cotman, C.W. and Cribbs, D.H. (2001). 15-Deoxy-D12,14-prostaglandin J2, a specific ligand for peroxisome proliferator-activated receptor, induces neuronal apoptosis.  NeuroReport 12: 839-843.

Rohn, T.T., Head, E., Nesse, W.P., Cotman, C.W. and Cribbs, D.H. (2001).  Activation of caspase-8 in the Alzheimer’s disease brain.  Neurobiology of Disease 8:1006-1016.

Rohn, T.T., Ivins, K.J., Bahr, B.A., Cotman, C.W. and Cribbs, D.H. (2000)  A monoclonal antibody to amyloid precursor protein induces neuronal apoptosis.  J. Neurochem. 74: 2331-2342.


Ivins, K.J., Thornton, P.L., Rohn, T.T. and Cotman, C.W. (1999) Neuronal apoptosis by ß -amloid is mediated by caspase-8. Neurobiology of Disease 6(5): 440-449.
 


Opportunities in my lab:

There are no current openings in my lab for graduate students or lab technicians.

 

Courses Taught

Instructor for Biol. 442/542 at Boise State University. This is a molecular neurobiology course for undergraduate and graduate-students. Topics covered are all aspects of neuronal function at the molecular level.  A discussion of several neurodegenerative diseases including Parkinson's, Alzheimer’s, and Schizophrenia are a few of diseases covered.  

Instructor for Biol. 431/531 at Boise State University.  This is a general pharmacology course for undergraduate and graduate-students.  Topics include the pharmacokinetics and pharmacodynamics.  All major drug classes are covered in this course.

Both courses are taught in the fall semesters

Instructor for Biol. 100 at Boise State University (spring semesters). This is a non-majors course covering all aspects of biology. A two-hour weekly lab reinforces concepts taught in lecture.  I also teach the electronic course for this class during spring semesters.

   

To look at my Black Board courses click on one of the following courses and in the new window click on the "preview button" (it is not necessary to enter anything in the username or password fields).

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Concepts of Biology

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Molecular Neurobiology

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Pharmacology