Prajwal Ciryam, MD, PhD

1. O’Brien EP, Ciryam P, Vendruscolo M, Dobson CM. Understanding the Influence of Codon Translation Rates on Cotranslational Folding. Chem. Res. 47(5): 1536-1544, 2014.

2. Freer R, Sormanni P, Vecchi G, Ciryam P, Dobson CM, Vendruscolo M. A protein homeostasis signature in healthy brain recapitulates tissue vulnerability to Alzheimer’s disease. Advances. 2(8): e1600947, 2016.

3. Kundra R, Ciryam P, Morimoto RI, Dobson CM, Vendruscolo M. Protein homeostasis of a metastable subproteome is associated with Alzheimer’s disease. Natl. Acad. Sci. 114 (28): E5703-E5711, 2017.

4. Farawell NE, Lambert-Smith I, Mitchell K, McKenna J, McAlary L, Ciryam P, Vine KL, Saunders DN, Yerbury JJ. SOD1A4V aggregation alters ubiquitin hemostasis in a cell model of ALS. J Cell Sci. jcs.209122, 2018.

5. Radmard S, Reid S, Ciryam P, Boubour A, Ho N, Zucker J, Sayre D, Greendyke WG, Miko BA, Pereira MR, Whittier S, Green DA, Thakur KT. Clinical utilization of the FilmArray meningitis/encephalitis (ME) multiplex polymerase chain reaction (PCR) assay. Front Neurol 10: 281, 2019.

6. Yerbury JJ, Ooi L, Blair IP, Ciryam P, Dobson CM, Vendruscolo M. The metastability of the proteome of spinal motor neurons underlies their vulnerability in ALS. Lett. 704: 89-94, 2019.

7. Ahmed N, Sormanni P, Ciryam P, Vendruscolo M, Dobson CM, O’Brien EP. Identifying A- and P-site locations on ribosome protected mRNA fragments using Integer Programming. Rep. 9(1): 6256, 2019.

8. Sharma AK, Sormanni P, Ahmed N, Ciryam P, Friedrich UA, Kramer K, O’Brien EP. A chemical kinetic basis for measuring translation initiation and elongation rates from ribosome profiling data. PLoS Comput Biol. 15(5): e1007070, 2019.

9. Freer R, Sormanni P, Ciryam P, Rammer B, Rizzoli SO, Dobson CM, Vendruscolo M. Supersaturated proteins are enriched at synapses and underlie cell and tissue vulnerability in Alzheimer’s disease. Heliyon 5(11): e02589, 2019.

10. Miller EH, Namale VS, Kim C, Dugue R, Waldrop G, Ciryam P, Chong AM, Zucker J, Miller EC, Bain JM, Joshua ZW, Doyle K, Boehme A, Claassen J, Uhlemann A-C, Thakur KT. Cerebrospinal analysis in patients with COVID-19. Open forum infectious diseases. 7(11): ofaa501, 2020.

11. Ahmed N, Friedrich UA, Sormanni P, Ciryam P, Altman NS, Bukau B, Kramer G, O’Brien EP. Pairs of amino acids at the P- and A-sites of the ribosome predictably and causally modulate translation-elongation rates. J Mol Biol. 432(24): 166696, 2020.

My graduate work addressed chronic neurodegeneration, but my current interests are focused on acute brain injury. These areas of work address a common fundamental question: After an initial injury to the nervous system, a cascade of mechanisms gives rise to secondary injury; what pathways are involved, how can we quantify them, and how can we reverse them? In acute neurological injury, such as traumatic brain injury (TBI) and subarachonid hemorrhage, I am asking how the complex immune response, involving numerous cell types and soluble signaling molecules, alters outcomes to disease.

To study this question, I have two main approaches:

1. How do specific cytokines modulate contusion volume and functional outcome in a mammalian model of traumatic brain injury? Using the controlled cortical impact model in mice, I am interested in determining the role that specific cytokines play in stimulating the CNS innate immune response and recruiting innate immune cells such as neutrophils and macrophages to the brain. Establishing these pathways is part of a program to determine how the innate immune response after TBI affects contusion volume and neurological function.
2. Can a time-dependent multimodal immune response after TBI and subarachnoid hemorrhage predict the onset of delayed cerebral ischemia? Using genomic and proteomic approaches on patient samples, I am interested in establishing a temporal map of the immune response in the cerebrospinal fluid after TBI and subarachnoid hemorrhage. The hypothesis is that specific cellular phenotypes of the innate immune system in the cerebrospinal fluid are associated with the release of a network of key inflammatory proteins and give rise to and can predict the onset of delayed neurological deterioration.

I am a clinical neurointensivist, working in neurocritical care units at the University of Maryland and providing inpatient neurocritical care consultation in our system. To me, providing high-quality care to our patients is my number one responsibility. This is a team effort, and I see my clinical role as helping to lead and coordinate critical care by our multidisciplinary team and working with colleagues across specialties to ensure that patients gets timely and appropriate diagnosis and treatment. High-quality care is individualized care, ensuring that we offer the treatments that are most likely to help patients in line with their values and wishes. I strive to take care of my patients and their families as individuals, not only offering my expertise, but also listening to their needs. I recognize the structural barriers that can limit access to care in our society and am dedicated in my practice to providing equitable, respectful treatment to all patients.

• Center for Neuroscience and Regenerative Medicine Traumatic Brain Injury Fellowship (2022)
• Ciryam et al PNAS 2016 — One of “25 Milestones” in Australian ALS research, MND Australia (2017)
• Benefactors’ Scholarship, St John’s College, University of Cambridge (2010)
• Fulbright Scholarship, United Kingdom (2009)
• Finalist, Rhodes Scholarship (2005)
• National Merit Scholarship (2002)