Summary: A new study reveals that moderate-to-severe traumatic brain injuries (TBI) can have long-lasting effects, persisting for decades. Using advanced MRI scans, blood biomarkers, and cognitive tests, researchers found that survivors show signs of chronic brain pathology even 22 years after their injury.
This chronic condition can increase the risk of neurodegenerative diseases like Alzheimer’s. The study emphasizes the need for long-term management strategies to prevent cognitive decline in TBI survivors.
Key Facts:
- MRI and blood tests show the long-term effects of moderate-to-severe TBI.
- Chronic brain pathology linked to TBI increases the risk of neurodegenerative diseases.
- The study calls for better long-term care and management of TBI survivors.
Source: Monash University
Monash University-led research, believed to be the first of its kind, has used blood tests and MRI scans to show that the effects of traumatic brain injuries (TBI) can last decades.
Published in Brain, and involving researchers from the University of Melbourne and Austin Health, the Monash-Epworth Rehabilitation Research Center (MERRC) TBI Aging Study integrated a range of techniques to understand the enduring consequences of moderate to severe TBI.
The team included imaging to measure the integrity of the brain microstructure, blood biomarkers to determine ongoing brain pathology, and cognitive tests to understand how blood markers might be linked to a person’s cognitive health and clinical condition.
It’s one of few global studies on participants with moderate-severe TBI due to a single incident that have also been living with their injury for an average of 22 years, as opposed to experiencing repetitive injury.
Senior author Professor Sandy Shultz, from the Monash School of Translational Medicine, said, “Our finding of chronic pathology in the brains of traumatic brain injury survivors, and the ability to identify this with imaging and blood tests, not only provides us with methods to detect these changes but also a foundation to develop treatments that might prevent or slow evolving pathology and improve recovery.”
While TBI is a potential risk factor for neurodegenerative disorders, including Alzheimer’s Disease and Parkinson’s Disease, there is a critical need for comprehensive knowledge about long-term impacts.
This involves delineating the biological and clinical characteristics of any lasting neurodegeneration and identifying who is at risk, and then using this information to develop long-term management strategies.
First author Dr. Gershon Spitz, from the Monash-Epworth Rehabilitation Research Center (MERRC), the Monash School of Psychological Sciences, and the School of Translational Medicine Department of Neuroscience, said the findings supported the hypothesis that the effects of a moderate-severe TBI could be felt decades following the initial injury.
“We found that elevated levels of blood biomarkers are related to poorer brain microstructure and poor cognition,” Dr. Spitz said.
“Traditionally, TBI was viewed as an isolated event with a fixed recovery trajectory. Over the last decade, TBI has been redefined as a chronic, ongoing health condition.
“This redefinition is a crucial first step in overhauling our health care models, which presently allocate the bulk of resources to the immediate post-injury phase and leave long-term symptoms inadequately treated.”
Dr. Spitz said further work was needed on the connection between blood biomarkers and symptoms/improvement. “We need to see whether the biological signatures of possible ongoing neuropathology can also tell us about people who may be at higher risk of experiencing progressive decline in functions like memory,” he said.
About this concussion and TBI research news
Author: Sandy Shultz
Source: Monash University
Contact: Sandy Shultz – Monash University
Image: The image is credited to Neuroscience News
Original Research: Open access.
“Plasma biomarkers in chronic single moderate–severe traumatic brain injury” by Sandy Shultz et al. Brain
Abstract
Plasma biomarkers in chronic single moderate–severe traumatic brain injury
Blood biomarkers are an emerging diagnostic and prognostic tool that reflect a range of neuropathological processes following traumatic brain injury (TBI). Their effectiveness in identifying long-term neuropathological processes after TBI is unclear.
Studying biomarkers in the chronic phase is vital because elevated levels in TBI might result from distinct neuropathological mechanisms during acute and chronic phases.
Here, we examine plasma biomarkers in the chronic period following TBI and their association with amyloid and tau PET, white matter microarchitecture, brain age and cognition.
We recruited participants ≥40 years of age who had suffered a single moderate–severe TBI ≥10 years previously between January 2018 and March 2021.
We measured plasma biomarkers using single molecule array technology [ubiquitin C-terminal hydrolase L1 (UCH-L1), neurofilament light (NfL), tau, glial fibrillary acidic protein (GFAP) and phosphorylated tau (P-tau181)]; PET tracers to measure amyloid-β (18F-NAV4694) and tau neurofibrillary tangles (18F-MK6240); MRI to assess white matter microstructure and brain age; and the Rey Auditory Verbal Learning Test to measure verbal-episodic memory.
A total of 90 post-TBI participants (73% male; mean = 58.2 years) were recruited on average 22 years (range = 10–33 years) post-injury, and 32 non-TBI control participants (66% male; mean = 57.9 years) were recruited.
Plasma UCH-L1 levels were 67% higher {exp(b) = 1.67, P = 0.018, adjusted P = 0.044, 95% confidence interval (CI) [10% to 155%], area under the curve = 0.616} and P-tau181 were 27% higher {exp(b) = 1.24, P = 0.011, adjusted P = 0.044, 95% CI [5% to 46%], area under the curve = 0.632} in TBI participants compared with controls. Amyloid and tau PET were not elevated in TBI participants.
Higher concentrations of plasma P-tau181, UCH-L1, GFAP and NfL were significantly associated with worse white matter microstructure but not brain age in TBI participants.
For TBI participants, poorer verbal-episodic memory was associated with higher concentration of P-tau181 {short delay: b = −2.17, SE = 1.06, P = 0.043, 95% CI [−4.28, −0.07]; long delay: bP-tau = −2.56, SE = 1.08, P = 0.020, 95% CI [−4.71, −0.41]}, tau {immediate memory: bTau = −6.22, SE = 2.47, P = 0.014, 95% CI [−11.14, −1.30]} and UCH-L1 {immediate memory: bUCH-L1 = −2.14, SE = 1.07, P = 0.048, 95% CI [−4.26, −0.01]}, but was not associated with functional outcome.
Elevated plasma markers related to neuronal damage and accumulation of phosphorylated tau suggest the presence of ongoing neuropathology in the chronic phase following a single moderate–severe TBI.
Plasma biomarkers were associated with measures of microstructural brain disruption on MRI and disordered cognition, further highlighting their utility as potential objective tools to monitor evolving neuropathology post-TBI.
