Clinician guide to motorcycle helmet safety.

Motorcyclists' increased likelihood of involvement in motor vehicle collisions increases their risk of brain injury or death. Despite irrefutable evidence of the protective capabilities of motorcycle helmets, their use among riders is not ubiquitous. This paper is a functional guide to motorcycle helmet safety, assisting clinicians in promoting helmet use and treating patients with motorcycle-related injuries. First, five commonly held myths that promote unhelmeted riding are dispelled. Then, clinicians are prepared to assist their patients in choosing an appropriate helmet through an in-depth presentation of motorcycle helmet construction, testing, and sizing. Discussion of patient care considerations for first responders, emergency medicine practitioners, and primary care providers will empower all-level clinicians to act as patient advocates. Finally, ethical and legal considerations regarding motorcycle helmet use are clarified. Equipping clinicians with applicable knowledge of motorcycle helmet safety will translate to safer roads and fewer motorcyclist patients.

Kollidon VA64 Treatment in Traumatic Brain Injury: Operation Brain Trauma Therapy.

Loss of plasmalemmal integrity may mediate cell death after traumatic brain injury (TBI). Prior studies in controlled cortical impact (CCI) indicated that the membrane resealing agent Kollidon VA64 improved histopathological and functional outcomes. Kollidon VA64 was therefore selected as the seventh therapy tested by the Operation Brain Trauma Therapy consortium, across three pre-clinical TBI rat models: parasagittal fluid percussion injury (FPI), CCI, and penetrating ballistic-like brain injury (PBBI). In each model, rats were randomized to one of four exposures (7-15/group): (1) sham; (2) TBI+vehicle; (3) TBI+Kollidon VA64 low-dose (0.4 g/kg); and (4) TBI+Kollidon VA64 high-dose (0.8 g/kg). A single intravenous VA64 bolus was given 15 min post-injury. Behavioral, histopathological, and serum biomarker outcomes were assessed over 21 days generating a 22-point scoring matrix per model. In FPI, low-dose VA64 produced zero points across behavior and histopathology. High-dose VA64 worsened motor performance compared with TBI-vehicle, producing -2.5 points. In CCI, low-dose VA64 produced intermediate benefit on beam balance and the Morris water maze (MWM), generating +3.5 points, whereas high-dose VA64 showed no effects on behavior or histopathology. In PBBI, neither dose altered behavior or histopathology. Regarding biomarkers, significant increases in glial fibrillary acidic protein (GFAP) levels were seen in TBI versus sham at 4 h and 24 h across models. Benefit of low-dose VA64 on GFAP was seen at 24 h only in FPI. Ubiquitin C-terminal hydrolase-L1 (UCH-L1) was increased in TBI compared with vehicle across models at 4 h but not at 24 h, without treatment effects. Overall, low dose VA64 generated +4.5 points (+3.5 in CCI) whereas high dose generated -2.0 points. The modest/inconsistent benefit observed reduced enthusiasm to pursue further testing.

The Impact of Traumatic Brain Injury on Microbiome Composition: A Systematic Review.

Traumatic brain injuries (TBIs) are a significant health problem, impacting millions of people every year. Although emerging evidence suggests that the composition of the gut microbiome is altered after TBI, no systematic review has been published on this topic. The objective of the present systematic review is to analyze publications that evaluate the impact of TBI on gut microbiome composition. Research articles were pulled from seven databases. The systematic review was performed following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. In order for publications to be eligible for this review, they had to (1) report on original human- or animal-subjects research, (2) evaluate the impact of TBI on the microbiome, and (3) be written in English and (4) be published in a peer-reviewed journal. Of the seven articles that met these criteria, one involved human participants, while the other six reported on experimental animal studies. All studies found changes in the gut microbiome following TBI, with similar changes in bacterial populations observed across studies. The limitations of these studies included the use of primarily male animals, limitations of 16 S rRNA gene sequencing, and small sample sizes. This review was also limited by the small pool of studies conducted in this area. In summary, changes in bacterial populations of the gut microbiome, specifically increases in proteobacteria and firmicutes, were observed across the studies. By evaluating the changes in the microbiome resulting from TBI, potential therapeutic interventions could be explored.

Genetic Variation in the TP53 Gene and Patient Outcomes Following Severe Traumatic Brain Injury.

Traumatic brain injury (TBI) is a leading cause of death and disability, with more than 5 million people in the United States living with long-term complications related to TBI. This study examined the relationship between TP53, the gene that codes for the protein p53, and outcome variability following severe TBI. The p53 protein impacts neuronal apoptosis following TBI, thus investigation into TP53 genetic variability as a prognosticator for TBI outcomes (mortality, Glasgow Outcome Scale [GOS], Neurobehavioral Rating Scale [NRS], and Disability Rating Scale [DRS]) is warranted. Participants (N = 429) with severe TBI (Glasgow Coma Scale score ≤8) were enrolled into a prospective study with outcomes assessed over 24 months following injury. The single-nucleotide polymorphism Arg72Pro (rs1042522), a functional missense polymorphism for which the CC homozygous genotype is most efficient at inducing apoptosis, was investigated. Individuals with the CC genotype (arginine homozygotes) were more likely to have poorer outcomes at 24 months following TBI compared to individuals with CG/GG genotypes (GOS: p = .048, DRS: p = .022). These findings add to preliminary evidence that p53 plays a role in recovery following TBI and, if further replicated, could support investigations into p53-based therapies for treating TBI.

A Moderate Blast Exposure Results in Dysregulated Gene Network Activity Related to Cell Death, Survival, Structure, and Metabolism.

Blast exposure is common in military personnel during training and combat operations, yet biological mechanisms related to cell survival and function that coordinate recovery remain poorly understood. This study explored how moderate blast exposure influences gene expression; specifically, gene-network changes following moderate blast exposure. On day 1 (baseline) of a 10-day military training program, blood samples were drawn, and health and demographic information collected. Helmets equipped with bilateral sensors worn throughout training measured overpressure in pounds per square inch (psi). On day 7, some participants experienced moderate blast exposure (peak pressure ≥5 psi). On day 10, 3 days post-exposure, blood was collected and compared to baseline with RNA-sequencing to establish gene expression changes. Based on dysregulation data from RNA-sequencing, followed by top gene networks identified with Ingenuity Pathway Analysis, a subset of genes was validated (NanoString). Five gene networks were dysregulated; specifically, two highly significant networks: (1) Cell Death and Survival (score: 42), including 70 genes, with 50 downregulated and (2) Cell Structure, Function, and Metabolism (score: 41), including 69 genes, with 41 downregulated. Genes related to ubiquitination, including neuronal development and repair: UPF1, RNA Helicase and ATPase (UPF1) was upregulated while UPF3 Regulator of Nonsense Transcripts Homolog B (UPF3B) was downregulated. Genes related to inflammation were upregulated, including AKT serine/threonine kinase 1 (AKT1), a gene coordinating cellular recovery following TBIs. Moderate blast exposure induced significant gene expression changes including gene networks involved in (1) cell death and survival and (2) cellular development and function. The present findings may have implications for understanding blast exposure pathology and subsequent recovery efforts.

Elevated cerebrospinal fluid concentrations of N-acetylaspartate correlate with poor outcome in a pilot study of severe brain trauma.

Primary objective: Examine the correlation between acute cerebrospinal fluid (CSF) levels of N-acetylaspartate (NAA) and injury severity upon admission in addition to long-term functional outcomes of severe traumatic brain injury (TBI). Design and rationale: This exploratory study assessed CSF NAA levels in the first four days after severe TBI, and correlated these findings with Glasgow Coma Scale (GCS) score and long-term outcomes at 3, 6, 12, and 24 months post-injury. Methods: CSF was collected after passive drainage via an indwelling ventriculostomy placed as standard of care in a total of 28 people with severe TBI. NAA levels were assayed using triple quadrupole mass spectrometry. Functional outcomes were assessed using the Glasgow Outcomes Scale (GOS) and Disability Rating Scale (DRS). Results: In this pilot study, better functional outcomes, assessed using the GOS and DRS, were found in individuals with lower acute CSF NAA levels after TBI. Key findings were that average NAA level was associated with GCS (p = .02), and GOS at 3 (p = .01), 6 (p = .04), 12 (p = .007), and 24 months (p = .002). Implications: The results of this study add to a growing body of neuroimaging evidence that raw NAA values are reduced and variable after TBI, potentially impacting patient outcomes, warranting additional exploration into this finding. This line of inquiry could lead to improved diagnosis and prognosis in patients with TBI.

Gene expression differences in PTSD are uniquely related to the intrusion symptom cluster: A transcriptome-wide analysis in military service members.

Posttraumatic stress disorder (PTSD) is associated with wide-spread immune dysregulation; however, little is known about the gene expression differences attributed to each PTSD symptom cluster. This is an important consideration when identifying diagnostic and treatment response markers in highly comorbid populations with mental and physical health conditions that share symptoms. To this aim, we utilized a transcriptome-wide analysis of differential gene expression in peripheral blood by comparing military service members: (1) with vs. without PTSD, (2) with high vs. low PTSD cluster symptom severity, and (3) with improved vs. not improved PTSD symptoms following 4-8 weeks of evidenced-based sleep treatment. Data were analyzed at a ±2.0-fold change magnitude with subsequent gene ontology-based pathway analysis. In participants with PTSD (n = 39), 89 differentially expressed genes were identified, and 94% were upregulated. In participants with high intrusion symptoms (n = 22), 1040 differentially expressed genes were identified, and 98% were upregulated. No differentially expressed genes were identified for the remaining two PTSD symptom clusters. Ten genes (C5orf24, RBAK, CREBZF, CD69, PMAIP1, AGL, ZNF644, ANKRD13C, ESCO1, and ZCCHC10) were upregulated in participants with PTSD and high intrusion symptoms at baseline and downregulated in participants with improved PTSD symptoms following treatment. Pathway analysis identified upregulated immune response systems and metabolic networks with a NF-kB hub, which were downregulated with symptom reduction. Molecular biomarkers implicated in intrusion symptoms and PTSD symptom improvement may inform the development of therapeutic targets for precise treatment of PTSD.

Best Practices for Obtaining Genomic Consent in Pediatric Traumatic Brain Injury Research.

BACKGROUND: Precision health relies on large sample sizes to ensure adequate power, generalizability, and replicability; however, a critical first step to any study is the successful recruitment of participants. OBJECTIVES: This study seeks to explore how the enrollment strategies used in a parent study contributed to the high consent rates, establish current best practices that can be used in future studies, and identify additional factors that contribute to consent into pediatric traumatic brain injury biobanks. METHODS: Retrospective secondary analysis of data from a parent study with high consent rates was examined to explore factors affecting consent into biobanking studies. RESULTS: Of the 76 subjects who were approached, met the eligibility criteria, and reviewed the consent form, only 16 (21.1%) declined to participate. The consented group (n = 60) represents 64.5% of those who met the eligibility criteria upon initial screening (n = 93) and 78.9% of those with confirmed eligibility (n = 76). Analysis of screening data suggested there were no major barriers to consenting individuals into this pediatric traumatic brain injury biobank. DISCUSSION: There were no demographic or research-related characteristics that significantly explained enrollment. Ethically, to obtain true informed consent, parents need to understand only their child's diagnosis, prognosis, and medical care, as well as the purpose of the proposed research and its risks and benefits. Researchers need to implement best practices, including a comprehensive review of census data to identify eligible participants to approach, a prescreening protocol, and effective consenting process to obtain informed consent so that precision care initiatives can be pursued.

Direct to consumer versus clinical genetic testing.

There are approximately 250 direct to consumer (DTC) genetic testing companies marketing different testing options such as genetic health risk, carrier status, ancestry, wellness, traits, noninvasive prenatal genetic testing, athleticism, and many others. As a result, choosing the most appropriate test may be daunting when compared with a focused genetic test ordered by a clinician. A wealth of information may be discovered and care must be taken by both consumers and clinicians when deciphering test results. This column highlights considerations when proceeding forward with a DTC genetic test.

Variation in Candidate Traumatic Brain Injury Biomarker Genes Are Associated with Gross Neurological Outcomes after Severe Traumatic Brain Injury.

Diagnostic and prognostic biomarkers of traumatic brain injury (TBI) are actively being pursued; potential candidates include glial fibrillary acid protein (GFAP), S100 calcium-binding protein B (S100B), and ubiquitin C-terminal hydrolase L1 (UCHL1), two of which the United States Food and Drug Administration (FDA) recently approved for marketing of blood tests for adult concussion. The relationship between biomarker-encoding genes and TBI outcomes remains unknown. This pilot study explores variation in 18 single nucleotide polymorphisms (SNPs) in biomarker-encoding genes as predictors of neurological outcome in a population of adults with severe TBI. Participants (n = 305) were assessed using the Glasgow Outcome Scale (GOS) at 3, 6, 12, and 24 months post-injury. Multivariate logistical regression was used to calculate the odds ratio (OR) and determine the odds of having a lower score on the GOS ( = 1-2 vs. 3-5) based on variant allele presence, while controlling for confounders. Possession of the variant allele of one S100B SNP (rs1051169) was associated with higher scores on the GOS at 3 months (OR = 0.39; p = 0.04), 6 months (OR = 0.34; p = 0.02), 12 months (OR = 0.32; p = 0.02), and 24 months (OR = 0.30; p = 0.02) post-severe TBI. The relationship among these polymorphisms, protein levels, and biomarker utility, merits examination. These findings represent a novel contribution to the evidence that can inform future studies aimed at enhancing interpretation of biomarker data, identifying novel biomarkers, and ultimately harnessing this information to improve clinical outcomes and personalize care.

Higher exosomal tau, amyloid-beta 42 and IL-10 are associated with mild TBIs and chronic symptoms in military personnel.

OBJECTIVE: Identify biomarkers in peripheral blood that relate to chronic post-concussive and behavioural symptoms following traumatic brain injuries (TBIs) to ultimately improve clinical management. RESEARCH DESIGN: We compared military personnel with mild TBIs (mTBIs) (n = 42) to those without TBIs (n = 22) in concentrations of tau, amyloid-beta (Aß42) and cytokines (tumour necrosis factor alpha (TNFα, interleukin (IL)-6 and -10) in neuronal-derived exosomes from the peripheral blood. We utilized nanosight technology coupled with ultra-sensitivity immunoassay methods. We also examined the impact of post-concussive and behavioural symptoms including depression and post-traumatic stress disorder (PTSD) on these neuronal-derived markers. RESULTS: We report that concentrations of exosomal tau (F1, 62 = 10.50), Aß42 (F1, 61 = 5.32) and IL-10 (F1, 59 = 4.32) were elevated in the mTBI group compared to the controls. Within the mTBI group, regression models show that post-concussive symptoms were most related to exosomal tau elevations, whereas exosomal IL-10 levels were related to PTSD symptoms. CONCLUSIONS: These findings suggest that chronic post-concussive symptoms following an mTBI relate to altered exosomal activity, and that greater tau pathology may underlie chronic post-concussive symptoms that develop following mTBIs. It also suggests that central inflammatory activity contributes to PTSD symptoms following an mTBI, providing necessary insights into the role of inflammation in chronic PTSD symptoms.

Melatonin as a Therapy for Traumatic Brain Injury: A Review of Published Evidence.

Melatonin (MEL) is a hormone that is produced in the brain and is known to bind to MEL-specific receptors on neuronal membranes in several brain regions. MEL's documented neuroprotective properties, low toxicity, and ability to cross the blood-brain-barrier have led to its evaluation for patients with traumatic brain injury (TBI), a condition for which there are currently no Food and Drug Administration (FDA)-approved therapies. The purpose of this manuscript is to summarize the evidence surrounding the use of melatonin after TBI, as well as identify existing gaps and future directions. To address this aim, a search of the literature was conducted using Pubmed, Google Scholar, and the Cochrane Database. In total, 239 unique articles were screened, and the 22 preclinical studies that met the a priori inclusion/exclusion criteria were summarized, including the study aims, sample (size, groups, species, strain, sex, age/weight), TBI model, therapeutic details (preparation, dose, route, duration), key findings, and conclusions. The evidence from these 22 studies was analyzed to draw comparisons across studies, identify remaining gaps, and suggest future directions. Taken together, the published evidence suggests that MEL has neuroprotective properties via a number of mechanisms with few toxic effects reported. Notably, available evidence is largely based on data from adult male rats and, to a lesser extent, mice. Few studies collected data beyond a few days of the initial injury, necessitating additional longer-term studies. Other future directions include diversification of samples to include female animals, pediatric and geriatric animals, and transgenic strains.

Exosomes in Acquired Neurological Disorders: New Insights into Pathophysiology and Treatment.

Exosomes are endogenous nanovesicles that play critical roles in intercellular signaling by conveying functional genetic information and proteins between cells. Exosomes readily cross the blood-brain barrier and have promise as therapeutic delivery vehicles that have the potential to specifically deliver molecules to the central nervous system (CNS). This unique feature also makes exosomes attractive as biomarkers in diagnostics, prognostics, and therapeutics in the context of multiple significant public health conditions, including acquired neurological disorders. The purpose of this review is to summarize the state of the science surrounding the relevance of extracellular vesicles (EVs), particularly exosomes, to acquire neurological disorders, specifically traumatic brain injury (TBI), spinal cord injury (SCI), and ischemic stroke. In total, ten research articles were identified that examined exosomes in the context of TBI, SCI, or stroke; these manuscripts were reviewed and synthesized to further understand the current role of exosomes in the context of acquired neurological disorders. Of the ten published studies, four focused exclusively on TBI, one on both TBI and SCI, and five on ischemic stroke; notably, eight of the ten studies were limited to pre-clinical samples. The present review is the first to discuss the current body of knowledge surrounding the role of exosomes in the pathophysiology, diagnosis, and prognosis, as well as promising therapeutic strategies in TBI, SCI, and stroke research.

Pro- and anti-inflammatory biomarkers and traumatic brain injury outcomes: A review.

Traumatic Brain Injury (TBI) triggers a cascade of secondary biological and physiological effects that are variable, depending on the severity, location, and complexity of the injury. Improved diagnosis and prognosis of brain injury may be possible by examining changes in protein biomarker concentrations and, determining their role in long-term outcomes may improve treatment. One promising direction for biomarker research surrounds pro- and anti-inflammatory cytokines which may have utility for predicting short and long-term prognosis after TBI, and may also be therapeutic targets in shaping neuronal recovery following a TBI. The purpose of this review is to examine the relationship between TBI symptoms and changes in pro- and anti- inflammatory biomarkers. Eighteen (18) published articles met criteria for inclusion. Fourteen studies focused on individuals with severe TBI. Increased levels of interleukin (IL)-6, IL-1, IL-8, IL-10 and tumor necrosis factor alpha (TNFα) were associated with worse outcomes, with most studies focusing on morbidity and mortality. It is important to identify the biochemical changes that may influence or initiate the presentation of health outcomes after a TBI. Earlier identification of symptoms associated with these biochemical changes can be used to support better treatment planning, targeted interventions and ultimately, improvement in patient outcomes.

Moderate blast exposure alters gene expression and levels of amyloid precursor protein.

OBJECTIVE: To explore gene expression after moderate blast exposure (vs baseline) and proteomic changes after moderate- (vs low-) blast exposure. METHODS: Military personnel (N = 69) donated blood for quantification of protein level, and peak pressure exposures were detected by helmet sensors before and during a blast training program (10 days total). On day 7, some participants (n = 29) sustained a moderate blast (mean peak pressure = 7.9 psi) and were matched to participants with no/low-blast exposure during the training (n = 40). PAXgene tubes were collected from one training site at baseline and day 10; RNA-sequencing day 10 expression was compared with each participant's own baseline samples to identify genes and pathways differentially expressed in moderate blast-exposed participants. Changes in amyloid precursor protein (APP) from baseline to the day of blast and following 2 days were evaluated. Symptoms were assessed using a self-reported form. RESULTS: We identified 1,803 differentially expressed genes after moderate blast exposure; the most altered network was APP. Significantly reduced levels of peripheral APP were detected the day after the moderate blast exposure and the following day. Protein concentrations correlated with the magnitude of the moderate blast exposure on days 8 and 9. APP concentrations returned to baseline levels 3 days following the blast, likely due to increases in the genetic expression of APP. Onset of concentration problems and headaches occurred after moderate blast. CONCLUSIONS: Moderate blast exposure results in a signature biological profile that includes acute APP reductions, followed by genetic expression increases and normalization of APP levels; these changes likely influence neuronal recovery.

Mini Review of Controlled Cortical Impact: A Well-Suited Device for Concussion Research.

Mild traumatic brain injury (mTBI) is increasingly recognized as a significant public health problem which warrants additional research. Part of the effort to understand mTBI and concussion includes modeling in animals. Controlled cortical impact (CCI) is a commonly employed and well-characterized model of experimental TBI that has been utilized for three decades. Today, several commercially available pneumatic- and electromagnetic-CCI devices exist as do a variety of standard and custom injury induction tips. One of CCI's strengths is that it can be scaled to a number of common laboratory animals. Similarly, the CCI model can be used to produce graded TBI ranging from mild to severe. At the mild end of the injury spectrum, CCI has been applied in many ways, including to study open and closed head mTBI, repeated injuries, and the long-term deficits associated with mTBI and concussion. The purpose of this mini-review is to introduce the CCI model, discuss ways the model can be applied to study mTBI and concussion, and compare CCI to alternative pre-clinical TBI models.

Brain injury results in lower levels of melatonin receptors subtypes MT1 and MT2.

BACKGROUND: Traumatic brain injury (TBI) is a devastating and costly acquired condition that affects individuals of all ages, races, and geographies via a number of mechanisms. The effects of TBI on melatonin receptors remain unknown. PURPOSE: The purpose of this study is to explore whether endogenous changes in two melatonin receptor subtypes (MT1 and MT2) occur after experimental TBI. SAMPLE: A total of 25 adult male Sprague Dawley rats were used with 6 or 7 rats per group. METHODS: Rats were randomly assigned to receive either TBI modeled using controlled cortical impact or sham surgery and to be sacrificed at either 6- or 24-h post-operatively. Brains were harvested, dissected, and flash frozen until whole cell lysates were prepared, and the supernatant fluid aliquoted and used for western blotting. Primary antibodies were used to probe for melatonin receptors (MT1 and MT2), and beta actin, used for a loading control. ImageJ and Image Lab software were used to quantify the data which was analyzed using t-tests to compare means. RESULTS: Melatonin receptor levels were reduced in a brain region- and time point- dependent manner. Both MT1 and MT2 were reduced in the frontal cortex at 24h and in the hippocampus at both 6h and 24h. DISCUSSION: MT1 and MT2 are less abundant after injury, which may alter response to MEL therapy. Studies characterizing MT1 and MT2 after TBI are needed, including exploration of the time course and regional patterns, replication in diverse samples, and use of additional variables, especially sleep-related outcomes. CONCLUSION: TBI in rats resulted in lower levels of MT1 and MT2; replication of these findings is necessary as is evaluation of the consequences of lower receptor levels.

Moderate blast exposure results in increased IL-6 and TNFα in peripheral blood.

A unique cohort of military personnel exposed to isolated blast was studied to explore acute peripheral cytokine levels, with the aim of identifying blast-specific biomarkers. Several cytokines, including interleukin (IL) 6, IL-10 and tumor necrosis factor alpha (TNFα) have been linked to pre-clinical blast exposure, but remained unstudied in clinical blast exposure. To address this gap, blood samples from 62 military personnel were obtained at baseline, and daily, during a 10-day blast-related training program; changes in the peripheral concentrations of IL-6, IL-10 and TNFα were evaluated using an ultrasensitive assay. Two groups of trainees were matched on age, duration of military service, and previous history of blast exposure(s), resulting in moderate blast cases and no/low blast controls. Blast exposures were measured using helmet sensors that determined the average peak pressure in pounds per square inch (psi). Moderate blast cases had significantly elevated concentrations of IL-6 (F1,60=18.81, p<0.01) and TNFα (F1,60=12.03, p<0.01) compared to no/low blast controls; levels rebounded to baseline levels the day after blast. On the day of the moderate blast exposure, the extent of the overpressure (psi) in those exposed correlated with IL-6 (r=0.46, p<0.05) concentrations. These findings indicate that moderate primary blast exposure results in changes, specifically acute and transient increases in peripheral inflammatory markers which may have implications for neuronal health.

Symptom Science: Repurposing Existing Omics Data.

Omics approaches, including genomics, transcriptomics, proteomics, epigenomics, microbiomics, and metabolomics, generate large data sets. Once they have been used to address initial study aims, these large data sets are extremely valuable to the greater research community for ancillary investigations. Repurposing available omics data sets provides data to address research questions, generate and test hypotheses, replicate findings, and conduct mega-analyses. Many well-characterized, longitudinal, epidemiological studies collected extensive phenotype data related to symptom occurrence and severity. While the main phenotype of interest for many of these studies was often not symptom related, these data were collected to better understand the primary phenotype of interest. A search for symptom data (i.e., cognitive impairment, fatigue, gastrointestinal distress/nausea, sleep, and pain) in the database of genotypes and phenotypes (dbGaP) revealed many studies that collected symptom and omics data. There is thus a real possibility for nurse scientists to be able to look at symptom data over time from thousands of individuals and use omics data to identify key biological underpinnings that account for the development and severity of symptoms without recruiting participants or generating any new data. The purpose of this article is to introduce the reader to resources that provide omics data to the research community for repurposing, provide guidance on using these databases, and encourage the use of these data to move symptom science forward.