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, body biomarkers, and cognitive tests, researchers found that survivors show signs of serious mental disease also 22 years after their damage.
This persistent problem can make you more susceptible to degenerative conditions like Alzheimer’s. The investigation emphasizes the need for long-term management techniques to stop mental decline in those who have TBI.
Important Information:
- MRI and blood testing show the long-term results of moderate-to-severe TBI.
- The risk of degenerative diseases is increased by serious brain pathology and TBI.
- The review calls for better long-term care and management of TBI individuals.
Origin: 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 also conducted cognitive tests to know how blood markers may be related to a person’s mental health and clinical condition, as well as imaging to evaluate the integrity of the brain microstructure, blood biomarkers to track continued brain pathology, and mental tests to track down how blood markers may be related to a person’s mental health and clinical condition.
One of the few international studies on moderate-severe TBI caused by a single event that also had an average of 22 years of follow-up care rather than repeated injury.
Our findings of severe pathology in the brains of traumatic, brain injury, and survivors, and the ability to determine this with imaging and blood tests, according to senior author Professor Sandy Shultz from the Monash School of Translational Medicine,” not only provides us with methods to identify these changes but even a foundation to develop treatments that may prevent or slow growing pathology and improve recovery,” said said Dr. Shultz.
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 identifying the biological and clinical characteristics of any long-lasting neurodegeneration, identifying the person at risk, and using this information to create long-term management plans.
The findings, according to 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, support the hypothesis that a moderate-severe TBI could have lasting effects for many years.
According to Dr. Spitz,” we found that elevated levels of blood biomarkers are related to poorer brain microstructure and poor cognition.”
” 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 the overhaul of our healthcare systems, which currently allocate the majority of resources to the post-injury phase and leave the majority of long-term symptoms untreated.
Dr. Spitz said further work was needed on the connection between blood biomarkers and symptoms/improvement”. We need to know whether the biological markers of potential ongoing neuropathology can also reveal information about people who may be more susceptible to a progressive decline in cognitive functions, he said.
About this news about TBI research and concussion
Author: Sandy Shultz
Source: Monash University
Contact: Sandy Shultz – Monash University
Image: The image is credited to Neuroscience News
Original Research: Open access.
By Sandy Shultz and colleagues,” Plasma biomarkers in chronic single, moderate, and severe traumatic brain injuries.” Brain
Abstract
Plasma biomarkers in chronic single moderate–severe traumatic brain injury
A variety of neuropathological processes that have emerged as a result of a traumatic brain injury ( TBI ) are being captured by blood biomarkers, a new diagnostic and prognostic tool. Their ability to identify long-term neuropathological processes following TBI is unknown.
Because elevated TBI levels could be caused by different neuropathological mechanisms during the acute and chronic phases, it is crucial to study biomarkers in the chronic phase.
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 sought out 40-year-old individuals who had experienced a single moderate-severe TBI ten years prior, 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.
In TBI participants, higher plasma concentrations of P-tau181, UCH-L1, GFAP, and NfL were statistically related to worse white matter microstructure but not brain age.
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:  , b
The presence of ongoing neuropathology in the chronic phase following a single moderately severe TBI may be attributed to elevated plasma markers for neuronal damage and phosphorylated tau accumulation.
Further highlighting their utility as potential objective tools to monitor evolving neuropathology post-TBI, plasma biomarkers were linked to MRI and MRI measurements of microstructural brain disruption, which further demonstrated their relevance as potential objective tools.
