TBI initiates a cascade of biological responses that extend beyond the initial injury, including neuroinflammation, neuroaxonal damage, and neurodegenerative processes that can persist long after the acute event. As blood-based biomarkers emerge in TBI research, investigators are using complementary biomarker strategies to assess injury severity, monitor recovery, and better understand factors that influence long-term outcomes.
TBI involves a sequence of biological events that extend beyond the initial injury. Combining biomarkers associated with acute tissue damage, neuroinflammation, neuroaxonal injury, and long-term neurological outcomes can provide a more complete understanding of injury severity, recovery, and biological responses over time. The Simoa portfolio provides biomarker solutions to investigate the evolution of TBI within a single research workflow.
GFAP and UCH-L1 are among the most widely studied biomarkers of acute brain injury. GFAP reflects astrocytic injury and has demonstrated strong diagnostic accuracy for mild TBI, particularly in the early phase following injury. UCH-L1 provides complementary information related to neuronal cell body injury.
The Neurology 4-Plex D combines GFAP and UCH-L1 with Nf-L and BD-Tau, enabling comprehensive assessment of neuronal damage from the acute phase through long-term recovery.
Available Simoa assays:
Neurology 4-Plex D (BD-Tau Nf-L, GFAP, UCH-L1) Advantage PLUS
Following impact, neuroinflammatory responses contribute to acute tissue damage and secondary injury following TBI. IL-1β is a potent pro-inflammatory cytokine that activates the inflammatory response to protect the body against traumatic insults. However, excessive levels of IL-1β have been implicated in the progression of neuroinflammatory disorders. IL-6 rapidly upregulates in response to tissue damage and stimulates acute immune reactions. However, dysregulated IL-6 levels have been liked to chronic inflammatory conditions.
Available Simoa assays:
Neuroaxonal injury biomarkers provide insight into neuronal damage following TBI. Nf-L is a widely studied marker of axonal injury and may remain elevated from the acute phase through long-term recovery. BD-Tau provides brain-specific information related to neuronal injury and has been associated with clinical outcomes following severe TBI.
The Neurology 4-Plex D enables simultaneous assessment of neuronal injury and glial responses through measurement of BD-Tau, NfL, GFAP, and UCH-L1.
Available Simoa assays:
Neurology 4-Plex D (BD-Tau Nf-L, GFAP, UCH-L1) Advantage PLUS
Neurobiological consequences of TBI may extend years beyond the initial injury. Growing evidence suggests that TBI may initiate biological processes associated with ongoing neurodegeneration. NfL, GFAP, and p-Tau 181 enable researchers to study complementary aspects of this response, such as neuroaxonal damage, astrogliosis, and tau-related pathology.
Available Simoa assays:
Assess Acute Brain Injury
Learn how blood-based biomarkers are helping researchers identify and characterize traumatic brain injury.
Featured Blog: Blood-Based Brain Injury Biomarkers: Revealing the Hidden Story of Brain Health
Predict Clinical Outcomes
Discover how serum BD-Tau measurements are being used to investigate recovery trajectories and clinical outcomes following severe injury.
Featured Case Study: Association of Serum Brain-Derived Tau With Clinical Outcome and Longitudinal Change in Patients With Severe Traumatic Brain Injury
Investigate Neuroinflammatory Responses
Explore how cytokine biomarkers can provide insight into inflammatory signaling associated with neurological injury.
Featured Resource: Cytokine Biomarker Analysis with Simoa® for Neurology Research
Advance Precision Medicine Approaches
Learn how biomarker strategies may support patient stratification and precision medicine approaches in TBI research.
Featured Resource: Precision Medicine-Based Biomarkers for Traumatic Brain Injury
Connect with a Quanterix expert to identify the biomarkers, assays, and research strategies best suited for your neurological disease area and study objectives.
