scholarly journals Traumatic brain injury may not increase the risk of Alzheimer disease

Neurology ◽  
2017 ◽  
Vol 89 (18) ◽  
pp. 1923-1925 ◽  
Author(s):  
Michael W. Weiner ◽  
Paul K. Crane ◽  
Thomas J. Montine ◽  
David A. Bennett ◽  
Dallas P. Veitch

Traumatic brain injury (TBI) commonly occurs in civilian and military populations. Some epidemiologic studies previously have associated TBI with an increased risk of Alzheimer disease (AD). Recent clinicopathologic and biomarker studies have failed to confirm the relationship of TBI to the development of AD dementia or pathologic changes, and suggest that other neurodegenerative processes might be linked to TBI. Additional studies are required to determine the long-term consequences of TBI.

2015 ◽  
Vol 148 (4) ◽  
pp. S-384
Author(s):  
Elise L. Ma ◽  
Allen Smith ◽  
Neemesh Desai ◽  
Alan Faden ◽  
Terez Shea-Donohue

2020 ◽  
pp. 1-12
Author(s):  
Cindy Santiago-Castañeda ◽  
Marysol Segovia-Oropeza ◽  
Luis Concha ◽  
Sandra Adela Orozco-Suárez ◽  
Luisa Rocha

Background: Severe traumatic brain injury (TBI), an important risk factor for Alzheimer’s disease, induces long-term hippocampal damage and hyperexcitability. On the other hand, studies support that propylparaben (PPB) induces hippocampal neuroprotection in neurodegenerative diseases. Objective: Experiments were designed to evaluate the effects of subchronic treatment with PPB on TBI-induced changes in the hippocampus of rats. Methods: Severe TBI was induced using the lateral fluid percussion model. Subsequently, rats received subchronic administration with PPB (178 mg/kg, TBI+PPB) or vehicle (TBI+PEG) daily for 5 days. The following changes were examined during the experimental procedure: sensorimotor dysfunction, changes in hippocampal excitability, as well as neuronal damage and volume. Results: TBI+PEG group showed sensorimotor dysfunction (p <  0.001), hyperexcitability (64.2%, p <  0.001), and low neuronal preservation ipsi- and contralateral to the trauma. Magnetic resonance imaging (MRI) analysis revealed lower volume (17.2%; p <  0.01) and great damage to the ipsilateral hippocampus. TBI+PPB group showed sensorimotor dysfunction that was partially reversed 30 days after trauma. This group showed hippocampal excitability and neuronal preservation similar to the control group. However, MRI analysis revealed lower hippocampal volume (p <  0.05) when compared with the control group. Conclusion: The present study confirms that post-TBI subchronic administration with PPB reduces the long-term consequences of trauma in the hippocampus. Implications of PPB as a neuroprotective strategy to prevent the development of Alzheimer’s disease as consequence of TBI are discussed.


2018 ◽  
Vol 20 (5) ◽  
pp. 566-576 ◽  
Author(s):  
Karin Reuter-Rice ◽  
Michael Regier ◽  
Ellen Bennett ◽  
Daniel Laskowitz

Background: Pediatric traumatic brain injury (TBI) is a leading cause of death and disability. Polymorphisms in the apolipoprotein E ( APOE) gene have been linked to cerebral vasospasm (CV) and poor outcomes in adults with TBI, yet these associations remain poorly defined in children. Objective: We examined the effect of the relationship between APOE polymorphisms and CV on functional outcomes in children with a TBI. Method: This prospective, descriptive study examined 60 children (aged 10 days to 15 years) with a TBI. Data included demographic information, genetic sampling for the APOE gene and single-nucleotide polymorphisms (SNPs; rs405509, rs429358, rs7412), and daily transcranial Doppler ultrasounds to evaluate for CV. We examined Glasgow Outcome Scale–Extended Pediatrics (GOS-E Peds) scores at the time of discharge and 4–6 weeks after discharge. Results: More than half (56.7%) of the 60 children ( Mage = 5.9 years) were male. Twenty-six participants (43.3%) experienced an occurrence of CV. There were significant differences in injury mechanism (unadjusted p = .048) and age (unadjusted p = .02) between those with and without CV. Also, the noncoding promoter SNP rs405509 T/T, when considered with injury severity, appeared to modify the relationship of APOE genotype to CV. The relationship between APOE and CV had no significant effect on GOS-E Peds scores. Conclusion: Injury severity and the APOE noncoding promoter SNP rs405509 may modify the relationship between APOE and CV in children with TBI. More studies are needed to understand the role of APOE polymorphisms in outcomes in children with TBI.


2016 ◽  
Vol 39 (3) ◽  
pp. 1229-1238 ◽  
Author(s):  
Qi-tao Huang ◽  
Yun-fei Gao ◽  
Mei Zhong ◽  
Yan-hong Yu

Background: Preterm birth (PTB) has been recognized as a crucial long term risk factor for multiple non-communicable diseases. However, studies between the relationship of PTB and the risk of acute childhood leukemia have yielded inconclusive results. Therefore, we performed a meta-analysis to systematically review the current literature to investigate whether PTB is associated with increased risk of acute childhood leukemia. Methods: Three electronic databases (PubMed, Web of Science, and EMBASE) were searched up to December 1st, 2015. Relevant studies reporting the association between PTB and subsequent risk of acute childhood leukemia were included for further evaluation. Statistical analysis was performed using Revmen 5.3 and Stata 10.0. Results: A total of 12 studies for acute childhood leukemia, eight studies for acute lymphoblastic leukemia (ALL), and seven studies for acute myeloid leukemia (AML) were included in the current meta-analyses. We calculated pooled odds ratio (OR) and 95% confidence interval (CI) to evaluate the relationship between PTB and acute childhood leukemia as well as its two subtypes: ALL and AML. Our results suggested that PTB was significantly associated with increased risk of acute childhood leukemia (OR = 1.09, 95% CI = 1.02-1.17, P = 0.01) and AML (OR = 1.42, 95% CI = 1.21-1.67, P < 0.01). However, PTB was not significantly associated with an increased risk of ALL (OR = 1.04, 95% CI = 0.96-1.13, P = 0.29). Conclusion: Our data showed that PTB increased the risk of AML. Further studies are required to explore causality and dissect the biological mechanisms involved.


2020 ◽  
Vol 16 (4) ◽  
pp. 564-570
Author(s):  
V. A. Dadaeva ◽  
A. A. Aleksandrov ◽  
A. S. Orlova ◽  
O. M. Drapkina

Epidemiologic studies demonstrate that both prolonged and reduced sleep duration is associated with increased risk of excessive weight and obesity. The aim of the review was to analyze probable mechanisms of association of sleep duration and obesity elucidated in current scientific literature. Several proposed mechanisms of such an association exist: an imbalance of appetite regulating hormones resulting from decreased sleep duration; fatigue or decreased activity during the daytime, leading to sedentary behavior with decreased energy expenditure; changes in eating behavior with increased daily calorie intake. The article gives a comprehensive review of factors, mediating the association of sleep duration and obesity (age, gender, ethnic origin), studies of neurohormonal regulation of sleep in association with obesity (the influence of sleep duration on thermoregulation, appetite center – increased grelin-to-leptin ratio); the relationship of sleep with growth hormone and insulin-like growth factor-1, with hypothalamic-pituitary-adrenal axis, and non-hormonal factors, stimulating food intake. Data indicating that increased sleep duration is often associated with decreased sleep quality are presented. Besides traditional risk factors – unhealthy diet and decreased physical exercise, specific attention should be given to the problems, associated with sleep disorders to increase the efficacy of treatment and prevention of obesity.


Sign in / Sign up

Export Citation Format

Share Document