Troy Rohn, Ph.D.
Professor, Department of Biological Sciences
Year arrived at BSU: 2000
Department of Biology
Boise State University
Boise, ID 83725-1515
Office Location: Science Building, Room 228
Office Number: 208-426-2396
Lab Location: Science Building, Room 216
E-Mail Address: email@example.com
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 ApoE4 in Alzheimer’s disease. 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. He has obtained extramural funding continuously since his arrival at BSU including grants from NIH, AFAR and AHAF.
BIOL442/542: 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.
BIOL 431/531: 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 including drugs that effect the heart, brain, vasculature and all other major organ systems.
Both courses are taught in the fall semesters
BIOL 100 at Boise State University (Electronic): This is a non-majors course covering all aspects of biology.
BIOL 320: A cell biology course that represents a core requirement for all biology majors.
UF 100: Brain Matters (coming spring of 2021)
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 and eventually other important cognitive skills involved in executive functions.
The primary focus of my lab currently is understanding how inheritance of the apolipoprotein E4 (APOE4) gene greatly enhances dementia risk. Although it is well established that inheritance of the APOE4 allele increases the risk of AD approximately tenfold, the mechanism of how this protein contributes to AD pathogenesis remains unknown. Emerging data from our lab suggests that the matrix metalloproteinase-9 can generate an amino-terminal fragment of ApoE4 that localizes to the nucleus in microglia of the human AD brain. We are currently assessing in vitro the mechanisms by which this fragment is taken up by microglia, traffics to the nucleus and ultimately alters gene expression. We have recently discovered that a fragment of ApoE4 is able to upregulate thousands of genes in microglia following a transcriptome analysis (see reference below). Many of these genes appear to be regulated to enhanced inflammation. Our data support the hypothesis that the link between harboring the APOE4 allele and dementia risk could be enhanced inflammation through the activation of microglia. We are also examining the in vivo effects of ApoE fragments in zebrafish and have shown that like in microglia, ApoE4 is toxic and causes gross malformations. In addition, we are seeing effects on the heart including a significant decrease in heart rate. We are now exploring these effects in young zebrafish to determine what effect sub-lethal effects of ApoE4 may have on swimming behavior and other brain functions.
Figure showing the nuclear localization of apoE4 fragments (green punctated labeling) within neurons of zebrafish embryos following in vivo exogenous treatment for 24 hours. Staining was primarily observed within the hypothalamus of developing zebrafish embryos.
RECENT PUBLICATIONS (selected from 70 total)
Pollock, T.B., Isho, N.F., Day, R.J., Suresh, T., Cholico, G.N., Stewart, E.S., McCarthy, M.M. and Rohn, T.T. (2020). Transcriptome analyses in BV2 microglial cells following treatment with amino-terminal fragments of apolipoprotein E. Front. Aging Neurosci., 13 August 2020 | https://doi.org/10.3389/fnagi.2020.00256 | https://doi.org/10.3389/fnagi.2020.00256
Oxford, A.E., Stewart, E.S., Rohn T.T. (2020). Clinical Trials in Alzheimer’s Disease: A Hurdle in the Path of Remedy. Int J Alzheimers Dis. Apr 1;2020:5380346. doi: 10.1155/2020/5380346. eCollection 2020.
Pollock, T.B., Mack, J.M., Day, R.J., Isho, N.F., Brown, R.J., Oxford, A.E., Morrison, B.E., Hayden, E.J. and Rohn T.T. (2019). A fragment of apolipoprotein E4 leads to the downregulation of CXorf56, a novel ER-protein, and activation of BV2 microglial cells. Oxidative Medicine and Cellular Longevity. Volume 2019, Article ID 5123565. https://doi.org/10.1155/2019/5123565
Rohn, T.T., Kim, N., Isho, N.F. and Mack, J.M. (2018). The potential of CRISPR/Cas9 gene editing as a treatment strategy for Alzheimer’s disease. J Alzheimers Dis Parkinsonism. 8(3). Pii: 439. Doi: 10.4172/2161-0460. Epub 2018 May 31.
Love, J.E., Day, R.J., Gause, J.W, Brown, R.J., Pu, X., Theis, D.I., Caraway, C.A., Poon, W.W., Rahman, A.A., Morrison, B.E., and Rohn T.T. (2017). Nuclear uptake of an amino-terminal fragment of apolipoprotein E4 promotes cell death and localizes within microglia of the Alzheimer’s disease brain. Int J Physiol Pathophysiol Pharmacol: 9(2): 40-57
Gause J.W., Day, R.J., Caraway, C.A., Poon, W.W. and Rohn T.T. (2017). Evaluation of apolipoprotein E fragmentation as a biomarker for Alzheimer’s disease. J. of Neurology and Neurological Disorders. 3(2): 204. DOI: 10.15744/2454- 4981.3.204
Rohn, T.T. and Moore, Z.D. (2017). Nuclear localization of apolipoprotein E4: A new trick for an old protein. Int. J. Neurol. Neurother. 4(2): DOI: 10.23937/2378-3001/1410067.