Objective: To synthesize the best available evidence regarding the risk of dementia and chronic cognitive impairment (CCI) after mild traumatic brain injury (MTBI).
Data Sources: MEDLINE and other databases were searched (2001-2012) using a previously published search strategy and predefined criteria. Peer-reviewed reports in 6 languages were considered.
Study Selection: Systematic reviews, meta-analyses, randomized controlled trials, cohort studies, and case-control studies, with a minimum of 30 MTBI cases in subjects of any age, assessing the risk of dementia or CCI after MTBI were selected.
Data Extraction: Eligible studies were critically appraised using a modification of the Scottish Intercollegiate Guidelines Network criteria. Two reviewers independently reviewed each study and extracted data from accepted articles (ie, with a low risk of bias) into evidence tables.
Data Synthesis: Evidence from accepted studies was synthesized qualitatively according to modified Scottish Intercollegiate Guidelines Network criteria, and prognostic information was prioritized as exploratory or confirmatory according to design. Of 77,914 records screened, 299 articles were eligible and reviewed. Methodological quality was acceptable for 101 (34%) articles, of which 1 article considered dementia and 7 articles considered CCI. The study examining the risk of dementia after MTBI did not find an association. One randomized controlled trial found that being informed about possible cognitive dysfunction after MTBI was associated with worse cognitive performance on standard tests. Children with MTBI and intracranial pathology ("complicated" MTBI) performed worse than did children without intracranial pathology. Children showed higher rates of cognitive symptoms a year after MTBI than did a control group.
Conclusions: There is a lack of evidence of an increased risk of dementia after MTBI. In children, objective evidence of CCI exists only for complicated MTBI. More definitive studies are needed to inform clinical decisions, assessment of prognosis, and public health policy.
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http://dx.doi.org/10.1016/j.apmr.2013.06.036 | DOI Listing |
J Histotechnol
January 2025
Mechanical Engineering, Orthopedic Bioengineering Research Laboratory, Colorado State University, Fort Collins, CO, USA.
With an increasing concentration of microplastics (MPs) in every biome, laboratories with a focus on creating histology slides from resin-embedded specimens could be partially responsible for expanding the emission of microscopic resinous particles into the environment. With current research elucidating harmful health impacts from MPs, releasing them incautiously is arguably unethical and, in the near future, plausibly illegal. The Orthopedic Bioengineering Research Laboratory (OBRL) is in Colorado, a state known not only for its natural beauty but also for its increasing number of legislative amendments aimed at reducing plastic pollution.
View Article and Find Full Text PDFEClinicalMedicine
August 2024
Department of Psychiatry, University of Oxford, Warneford Hospital, Warneford Lane, Oxford, OX3 7JX, United Kingdom.
Background: While semaglutide, approved for type-2 diabetes mellitus (T2DM), is being investigated as a treatment for brain disorders, concerns over adverse neuropsychiatric events have emerged. More data are therefore needed to assess the effects of semaglutide on brain health. This study provides robust estimates of the risk of neurological and psychiatric outcomes following semaglutide use compared to three other antidiabetic medications.
View Article and Find Full Text PDFGBA is the major risk gene for Parkinson's disease (PD) and Dementia with Lewy Bodies (DLB), two common α-synucleinopathies with cognitive deficits. We investigated the role of mutant GBA in cognitive decline by utilizing Gba (L444P) mutant, SNCA transgenic (tg), and Gba-SNCA double mutant mice. Notably, Gba mutant mice showed early cognitive deficits but lacked PD-like motor deficits or α-synuclein pathology.
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Objective: To stratify AD patients based on baseline clinical profiles (up to two years prior to AD diagnosis) and update the model after AD diagnosis to prognosticate future AD-related outcomes.
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Objectives: To investigate the potential causal impact of OUD on later life brain health outcomes, including dementia, stroke and brain structure.
Methods: Observational and Mendelian randomization (MR) analyses were conducted.
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