Traumatic brain injury and the risk of dementia diagnosis: A nationwide cohort study

Nordström, Anna; Nordström, Peter

doi:10.1371/journal.pmed.1002496

Cited by 173 publications

(158 citation statements)

References 26 publications

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“…Data from a US cohort of older veterans found that even mild TBI without loss of consciousness was associated with an increased risk of dementia . In general, these investigations have observed a small but significant increase in risk of dementia with mild TBI and support a dose–response effect with increasing TBI severity . Future research, based on biomarker‐based diagnoses, is warranted to examine whether TBI specifically increases the risk of AD pathology (i.e.…”

Section: How Common Is Mild Tbi?mentioning

confidence: 95%

Head trauma in sports – clinical characteristics, epidemiology and biomarkers

et al. 2018

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Traumatic brain injury (TBI) is clinically divided into a spectrum of severities, with mild TBI being the least severe form and a frequent occurrence in contact sports, such as ice hockey, American football, rugby, horse riding and boxing. Mild TBI is caused by blunt nonpenetrating head trauma that causes movement of the brain and stretching and tearing of axons, with diffuse axonal injury being a central pathogenic mechanism. Mild TBI is in principle synonymous with concussion; both have similar criteria in which the most important elements are acute alteration or loss of consciousness and/or post‐traumatic amnesia following head trauma and no apparent brain changes on standard neuroimaging. Symptoms in mild TBI are highly variable and there are no validated imaging or fluid biomarkers to determine whether or not a patient with a normal computerized tomography scan of the brain has neuronal damage. Mild TBI typically resolves within a few weeks but 10–15% of concussion patients develop postconcussive syndrome. Repetitive mild TBI, which is frequent in contact sports, is a risk factor for a complicated recovery process. This overview paper discusses the relationships between repetitive head impacts in contact sports, mild TBI and chronic neurological symptoms. What are these conditions, how common are they, how are they linked and can they be objectified using imaging or fluid‐based biomarkers? It gives an update on the current state of research on these questions with a specific focus on clinical characteristics, epidemiology and biomarkers.

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Section: How Common Is Mild Tbi?mentioning

confidence: 95%

Head trauma in sports – clinical characteristics, epidemiology and biomarkers

et al. 2018

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“…Accumulation and aggregation of both tau NFTs and Aβ plaques are hallmarks of chronic traumatic encephalopathy (CTE), Alzheimer's disease (AD), and related dementias. Sustaining a TBI, including mTBI, has been implicated as a risk factor for dementia (Barnes et al., ; Nordström & Nordström, ; Shively, Scher, Perl, & Diaz‐Arrastia, ). Indeed, evidence from postmortem brains in short‐ (6 hr–7 days postinjury) and long‐term TBI survivors (1–47 years) suggests that even a single moderate‐to‐severe TBI is associated with an increase of Aβ deposits (Gentleman et al., ; Johnson, Stewart, & Smith, ).…”

mentioning

confidence: 99%

Concurrent Mild Traumatic Brain Injury and Posttraumatic Stress Disorder Is Associated With Elevated Tau Concentrations in Peripheral Blood Plasma

Pattinson

Gill

Lippa

et al. 2019

Journal of Traumatic Stress

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Concurrent mild traumatic brain injury (mTBI) and posttraumatic stress disorder (PTSD) are common in U.S. military service members and veterans. Tau and amyloid‐beta‐42 (Aβ42) are proteins that have been linked to cognitive impairment, neurological hallmarks of Alzheimer's disease, and may also relate to recovery from mTBI. However, the role of these proteins in the maintenance or resolution of chronic symptoms has not yet been determined. Participants in the current study were 102 service members and veterans who had sustained an mTBI (n = 84) or injured controls (IC) without TBI (n = 18). They were categorized into three groups based on the presence or absence of mTBI and PTSD: IC/PTSD‐Absent (n = 18), mTBI/PTSD‐Absent (n = 63), and mTBI/PTSD‐Present (n = 21). Concentrations of tau and Aβ42 in peripheral blood plasma were measured using SimoaTM, an ultrasensitive technology, and compared across groups. Tau concentrations were highest in the mTBI/PTSD‐Present group, F(2, 99) = 4.33, p = .016, compared to the other two groups. Linear multiple regression was conducted to determine the independent effects of PTSD and mTBI on tau concentrations, controlling for gender and sleep medication. PTSD was a significant and independent predictor of tau concentrations, β = .25, p = .009, ηp2 = .26. Aβ42 concentrations did not differ between the groups. The results indicated that PTSD was associated with an elevation of tau in peripheral blood and suggest that there may be increased biological effects of PTSD in this young cohort of service members and veterans following mTBI.

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“…5A, B). Interestingly, quantifying synaptic elements diffusely in cortex revealed only modest alterations in pre-or postsynaptic puncta compared to controls ( Fig TBI is associated through unknown pathological mediators with a substantially and dose-dependent increased risk of developing a dementing illness, particularly AD 9,44,45 . To evaluate potential neuropathological connections between brain trauma and AD, we examined synaptic health after TBI using SEQUIN.…”

Section: Pathological Loss Of Synaptic Loci Measured With Sequinmentioning

confidence: 97%

SEQUIN multiscale imaging of mammalian central synapses reveals loss of synaptic microconnectivity resulting from diffuse traumatic brain injury

Sauerbeck

Gangolli

Reitz

et al. 2019

Preprint

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The complex microconnectivity of the mammalian brain underlies its computational abilities, and its vulnerability to injury and disease. It has been challenging to illuminate the features of this synaptic network due in part to the small size and exceptionally dense packing of its elements. Here we describe a rapid and accessible super-resolution imaging and image analysis workflow-SEQUIN-that identifies, quantifies, and characterizes central synapses in animal models and in humans, enabling automated volumetric imaging of mesoscale synaptic networks without the laborious production of large histological arrays. Using SEQUIN, we identify delayed cortical synapse loss resulting from diffuse traumatic brain injury. Similar synapse loss is observed in an Alzheimer disease model, where SEQUIN mesoscale mapping of excitatory synapses across the hippocampus identifies region-specific synaptic vulnerability to neurodegeneration. These results establish a novel, easily implemented and robust nano-to-mesoscale synapse quantification and molecular characterization method. They furthermore identify a mechanistic link-synaptopathy-between Alzheimer neurodegeneration and its bestestablished epigenetic risk factor, brain trauma.

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Traumatic brain injury and the risk of dementia diagnosis: A nationwide cohort study

Abstract: Background

Cited by 173 publications

References 26 publications

Head trauma in sports – clinical characteristics, epidemiology and biomarkers

Head trauma in sports – clinical characteristics, epidemiology and biomarkers

Concurrent Mild Traumatic Brain Injury and Posttraumatic Stress Disorder Is Associated With Elevated Tau Concentrations in Peripheral Blood Plasma

SEQUIN multiscale imaging of mammalian central synapses reveals loss of synaptic microconnectivity resulting from diffuse traumatic brain injury

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