A meta-analysis of cohort studies: Traumatic brain injury and risk of Alzheimer’s Disease

Zhang, Jieyu; Zhang, Yongkang; Zou, Juntao; Cao, Fei

doi:10.1371/journal.pone.0253206

Cited by 17 publications

(15 citation statements)

References 17 publications

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“…The mechanisms underlying this risk are unclear and no clear link has notably been evidenced with heading the ball 28 . However, prolonged and repetitive exposure to traumatic head impacts from collisions and the ball might alter intracranial hypertension causing diffuse amyloid plaques and augmenting the risk of developing Alzheimer's disease 29 . Confirmation via prospective studies is necessary while research registering former footballers for brain donation autopsy at their time of death would be useful to inform on the existence of neurodegenerative pathologies especially as it is currently weak to non‐existent evidence for the link between football participation and long‐term neurological or cognitive deficits 8 .…”

Section: Discussionmentioning

confidence: 99%

“…28 However, prolonged and repetitive exposure to traumatic head impacts from collisions and the ball might alter intracranial hypertension causing diffuse amyloid plaques and augmenting the risk of developing Alzheimer's disease. 29 Confirmation via prospective studies is necessary while research registering former footballers for brain donation autopsy at their time of death would be useful to inform on the existence of neurodegenerative pathologies especially as it is currently weak to non-existent evidence for the link between football participation and long-term neurological or cognitive deficits. 8 Arguably, it is also important to continue the present research as it is possible that certain risk factors potentially associated in the past with the development of neurodegenerative disease might no longer exist or will, to a lesser extent, influence the future risk.…”

Section: Mortality Due To Neurodegenerative Diseasesmentioning

confidence: 99%

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A retrospective analysis of all‐cause and cause‐specific mortality rates in French male professional footballers

Orhant

Carling

Chapellier

et al. 2022

Scandinavian Med Sci Sports

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This study retrospectively compared all‐cause and cause‐specific mortality in French male professional football players with data from France's national population. Altogether, 6114 individuals born in Metropolitan France or in one of its overseas territories who played at least one competitive match in France's professional football championships between January 1, 1968 and December 31, 2015, were identified and followed up for vital status obtained from a national reference database until December 31, 2015. Data on all‐cause and cause‐specific mortality were subsequently compared to the expected number of deaths for the national population after standardization for the year, age, and sex. Ratios between observed and expected deaths provided standardized mortality ratios (SMR) along with 95% confidence intervals (95% CI). Linear trends were investigated using the Poisson trend test. Altogether, 662 player deaths were observed. All‐cause mortality overall was lower than that of the national population (SMR: 0.69, 95% CI 0.64–0.75). An excess of deaths from dementia was observed in the players (SMR: 3.38, 95% CI: 2.49–4.50) whereas mortality from diseases of the nervous (SMR: 0.64, 95% CI: 0.35–1.08) and cardiovascular systems (SMR: 0.82, 95% CI: 0.70–0.96), and cancer (SMR: 0.67, 95% CI: 0.58–0.76) was lower. Lower overall mortality and that owing to common cardiovascular and cancer‐related diseases were reported in French professional football players compared to France's national population. In line with previous studies, however, excess mortality from dementia was observed in the players. Career length was not associated with all‐cause or cause‐specific mortality. Prospective matched‐cohort studies are necessary to identify the neurologic impact of participation in professional football.

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Section: Discussionmentioning

confidence: 99%

Section: Mortality Due To Neurodegenerative Diseasesmentioning

confidence: 99%

A retrospective analysis of all‐cause and cause‐specific mortality rates in French male professional footballers

Orhant

Carling

Chapellier

et al. 2022

Scandinavian Med Sci Sports

View full text Add to dashboard Cite

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“…In this context, our findings suggest that there is substantial overlap between the brain's spatial patterns of vulnerability to (A) AD-related cortical thinning, (B) AD-related white matter demyelination, and (C) mTBI-related intracortical demyelination. Thus, because mTBI increases the risk of AD and related dementias ( 47 , 48 ) through uncertain mechanisms, further study on how post-traumatic demyelination patterns can translate into higher AD risk is warranted.…”

Section: Discussionmentioning

confidence: 99%

Mild Traumatic Brain Injury Results in Significant and Lasting Cortical Demyelination

et al. 2022

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Despite contributing to neurocognitive deficits, intracortical demyelination after traumatic brain injury (TBI) is understudied. This study uses magnetic resonance imaging (MRI) to map intracortical myelin and its change in healthy controls and after mild TBI (mTBI). Acute mTBI involves reductions in relative myelin content primarily in lateral occipital regions. Demyelination mapped ~6 months post-injury is significantly more severe than that observed in typical aging (p < 0.05), with temporal, cingulate, and insular regions losing more myelin (30%, 20%, and 16%, respectively) than most other areas, although occipital regions experience 22% less demyelination. Thus, occipital regions may be more susceptible to primary injury, whereas temporal, cingulate and insular regions may be more susceptible to later manifestations of injury sequelae. The spatial profiles of aging- and mTBI-related chronic demyelination overlap substantially; exceptions include primary motor and somatosensory cortices, where myelin is relatively spared post-mTBI. These features resemble those of white matter demyelination and cortical thinning during Alzheimer's disease, whose risk increases after mTBI.

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“…It remains unclear on why early TBI experience increases the chance of dementia and neurodegeneration in later life. A recent meta-analysis showed that TBI increases the rate of AD about 1.5 times [ 47 ]. A study from military veterans shows that TBI increases the risk of having Parkinson’s disease by approximately 56% [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

Early Aβ42 Exposure Causes Learning Impairment in Later Life

2022

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Amyloid cascade hypothesis proposes that amyloid β (Aβ) accumulation is the initiator and major contributor to the development of Alzheimer’s disease (AD). However, this hypothesis has recently been challenged by clinical studies showing that reduction of Aβ accumulation in the brain does not accompany with cognitive improvement, suggesting that therapeutically targeting Aβ in the brain may not be sufficient for restoring cognitive function. Since the molecular mechanism underlying the progressive development of cognitive impairment after Aβ clearance is largely unknown, the reason of why there is no behavioral improvement after Aβ clearance remains elusive. In the current study, we demonstrated that transient Aβ expression caused learning deficit in later life, despite the accumulated Aβ was soon being removed after the expression. Early Aβ exposure decreased the cellular expression of XBP1 and both the antioxidants, catalase, and dPrx5, which made cells more vulnerable to oxidative stress in later life. Early induction of XBP1, catalase, and dPrx5 prevented the overproduction of ROS, improved the learning performance, and preserved the viability of cells in the later life with the early Aβ induction. Treating the early Aβ exposed flies with antioxidants such as vitamin E, melatonin and lipoic acid, after the removal of Aβ also preserved the learning ability in later life. Taken together, we demonstrated that early and transient Aβ exposure can have a profound impact on animal behavior in later life and also revealed the cellular and molecular mechanism underlying the development of learning impairment by the early and transient Aβ exposure.

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A meta-analysis of cohort studies: Traumatic brain injury and risk of Alzheimer’s Disease

Cited by 17 publications

References 17 publications

A retrospective analysis of all‐cause and cause‐specific mortality rates in French male professional footballers

A retrospective analysis of all‐cause and cause‐specific mortality rates in French male professional footballers

Mild Traumatic Brain Injury Results in Significant and Lasting Cortical Demyelination

Early Aβ42 Exposure Causes Learning Impairment in Later Life

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