Mailing Address: Department of Biology
Boise State University
Boise, ID 83725-1515 Office Location: Science Building, Room 117 Office Number: 208-426-2396 Lab Location: Science Building, Room 216 E-Mail Address:trohn@boisestate.edu
Academic Degrees
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. He has obtained extramural funding continuously since his arrival at BSU including grants from NIH, AFAR, and AHAF. Dr. Rohn recently was awarded a 3-year renewal of his NIH NIA R15 grant he has held since 2013.
Teaching
BIOL 442: 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 just a few of the diseases covered.
BIOL 431: This is a general pharmacology course for undergraduate and graduate students. Topics include pharmacokinetics and pharmacodynamics. All major drug classes are covered in this course including drugs that affect the heart, brain, vasculature, and all other major organ systems.
BIOL 100 at Boise State University (Electronic): This is a non-major course covering all aspects of biology (taught online in the summers).
BIOL 320: A cell biology course that represents a core requirement for all biology majors.
UF 100: Brain Matters: A survey of the brain covering behavior, plasticity, genetics, and many diseases and disorders.
RESEARCH INTERESTS
The Rohn lab has a long-standing interest in understanding the molecular underpinnings of Alzheimer’s disease (AD). During the progression of Alzheimer’s disease, many brain cells die particularly in the area of the hippocampus. Because the hippocampus is an area of the brain involved in memory, AD is primarily 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. We have recently discovered that a fragment of ApoE4 in the human AD brain when produced is toxic and inflammatory.
We are excited to currently be examining the in vivo effects of ApoE fragments in zebrafish a new model system for the lab where we have recently shown that following treatment of embryos with an amino-terminal fragment of ApoE4, leads to toxicity and effects on the heart including a significant decrease in heart rate. We have also generated a mutant zebrafish strain that specifically expresses this ApoE4 fragment and are in the process of characterizing these fish through molecular techniques and behavioral analyses.
Figure showing the expression of an amino-terminal fragment of ApoE4. Representative expression of mCherry (red) in the brain and notochord following injection into one-cell stage zebrafish. The expression of enhanced green fluorescent protein under the cardiac myosin light chain 2 promoter (green), allows for easy screening of zebrafish for the mutant ApoE4 gene. These pictures were obtained by a current undergraduate student, Alex LaFollette who is working in the lab as a B2B student.
RECENT PUBLICATIONS (selected from 77 total)
H-index 40
Troy T. Rohn, Dean Radin, Tracy Brandmeyer, Peter G. Seidler, Barry J. Linder, Tom Lytle, John L. Mee and Fabio Macciardi. (2024). Intranasal Delivery of shRNA to Knockdown the 5HT-2A receptor Enhances Memory and Alleviates Anxiety (2024). Translational Psychiatry: Published 20 March 2024. Volume 14: 154.
Troy T. Rohn and Dean Radin (2024). Long-lasting genetic therapeutics for debilitating neurological conditions. Nature Biopharmdeal, March 2024.
McCarthy, M.M., Hardy, M.J., Leising, S.E., LaFollette, A., Stewart, E.S., Cogan, A.S., Sanghal, T., Matteo, K., Oxford, J.T., and Rohn T.T. (2022). An amino-terminal fragment of apolipoprotein E4 leads to behavioral deficits, increased PHF-1 immunoreactivity, and mortality in zebrafish. PLOS One Dec 15;17(12):e0271707. doi: 10.1371/journal.pone.0271707. eCollection 2022
Rohn, T.T., Beck, J.D., Galla, S.J., Isho, N.F., Pollock, T.B., Suresh, T., Kulkarni A., Sanghal, T. and Hayden, E.J. (2021). Fragmentation of apolipoprotein E4 is required for differential expression of inflammation and activation related genes in microglia cells. Int J Neurodegener Dis. (2021),4(1): 020.doi: 10.23937/2643-4539/1710020. Epub 2021 Sep 10.
Rohn, T.T. (2021). The new FDA-approved drug for Alzheimer’s disease, aducanumab, and what patients should know. J Alzheimers Dis Parkinsonism, DOI: 10.4172/2161-0460.s5.1000019
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 |Â 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.
RESEARCH OPPORTUNITIES
The lab is not accepting any positions for the 2024-25 academic year for both undergraduate and graduate students
OTHER ACTIVITIES
Associate Editor
Associate Editor for the scientific journal, Frontiers in Dementia
Associate Editor for the scientific journal, Frontiers in Aging Neuroscience
Anxiety, CRISPR, and Serotonin
Research update
Recently, I have become interested in finding better treatments for anxiety. Why? About three years ago, I was diagnosed with anxiety, which really became worse during the Covid-19 epidemic. I have had counseling and I take medication daily. Even my dog Bailey helps me a ton. Interestingly, about the same time, I was contacted by John Mee to see if I was interested in building a new biotech company. John is the current CEO of Cognigenics and at that time the company had no capital or data, but they had a great idea and a blue-ribbon team. I joined the team and became director of their preclinical studies. RCA-101 was our first asset and is an unusual biologic “drug” that utilizes CRISPR/Cas9. CRISPR is the new, precision gene-editing tool poised to cure many disorders and diseases in the 21st century. We proposed to permanently lower anxiety by targeting the serotonin receptor (5HT-2A) gene using CRISPR. This receptor has been known to be linked to anxiety for decades. Today, 39 million Americans suffer from anxiety disorders and ~30-40% do not respond to current treatments including SSRIs, Zoloft, and Cipramil the standard long-term medications. A few weeks ago, our proof-of-concept paper on this concept was published in PNAS Nexus, a top notch journal. Currently, this paper is in the top 5% of all research outputs as scored by Altermic (Altmetric tracks millions of published articles) and is one of the most-read articles at PNAS Nexus. In less than two weeks since it has been published, it has already been viewed over 3,200 times and our findings have generated a buzz on the internet:
Here are images showing proof-of-concept data. One important finding was the similar efficacy of RCA-101 to Valium (diazepam), a gold standard for lowering anxiety.
These data we believe put us on track for human clinical trials shortly. For me, having anxiety and trying to find new treatments for anxiety has been a personal journey that has been very rewarding. As a result of my connection both in research and my own anxiety.