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Background: Mild traumatic brain injury (mTBI) is a putative risk factor for dementia; however, despite having apparent face validity, the evidence supporting this hypothesis remains inconclusive. Understanding the role of mTBI as a risk factor is becoming increasingly important given the high prevalence of mTBI, and the increasing societal burden of dementia. Objective: Our objective was to use the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) format to determine if an association exists between mTBI and dementia and related factors, and to quantify the degree of risk. Methods: In this format, two authors conducted independent database searches of PubMed, PsycInfo, and CINAHL using three search blocks to find relevant papers published between 2000 and 2020. Relevant studies were selected using pre-defined inclusion/exclusion criteria, and bias scoring was performed independently by the two authors before a subset of studies was selected for meta-analysis. Twenty-one studies met the inclusion criteria for this systematic review. Results: The meta-analysis yielded a pooled odds ratio of 1.96 (95% CI 1.698–2.263), meaning individuals were 1.96 times more likely to be diagnosed with dementia if they had a prior mTBI. Most studies examining neuropsychiatric and neuroimaging correlates of dementia found subtle, persistent changes after mTBI. Conclusion: These results indicate that mTBI is a risk factor for the development of dementia and causes subtle changes in performance on neuropsychiatric testing and brain structure in some patients.

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Preclinical models for mild traumatic brain injury (mTBI) need to recapitulate several essential clinical features associated with mTBI, including a lack of significant neuropathology and the onset of neurocognitive symptoms normally associated with mTBI. Here we show how to establish a protocol for reliably and repeatedly inducing a mild awake closed head injury (ACHI) in rats, with no mortality or clinical indications of persistent pain. Moreover, we implement a new rapid neurological assessment protocol (NAP) that can be completely conducted within 1 min of each impact. This ACHI model will help to rectify the paucity of data on how repeated mTBI (r-mTBI) impacts the juvenile brain, an area of significant concern in clinical populations where there is evidence that behavioral sequelae following injury can be more persistent in juveniles. In addition, the ACHI model can help determine if r-mTBI early in life can predispose the brain to exhibiting greater neuropathology (i.e., chronic traumatic encephalopathy) later in life and can facilitate the identification of critical periods of vulnerability to r-mTBI across the lifespan. This article describes the protocol for administering an awake closed head mTBI (i.e., ACHI) to rats, as well as how to perform a rapid NAP following each ACHI. Methods for administering the ACHI to individual subjects repeatedly are described, as are the methods and scoring system for the NAP. The goal of this article is to provide a standardized set of procedures allowing the ACHI and NAP protocols to be used reliably by different laboratories. C 2019 by John Wiley & Sons, Inc.Keywords: behavior r concussion r head trauma r mild traumatic brain injury (2019). A rapid neurological assessment protocol for repeated mild traumatic brain injury in awake rats.

Background: It is becoming increasingly recognized that there is significant interneuron degeneration in Alzheimer's disease. As the hippocampus is integral for learning and memory, we performed a systematic review of primary literature focused on the relationship between Alzheimer's and hippocampal interneurons. In this study, we summarize the experimental work performed to date and identify opportunities for future experiments. Objectives: This PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses)-style systematic review seeks to summarize the findings of all accessible research focused on cholecystokinin (CCK), neuropeptide Y (NPY), parvalbumin (PV), and somatostatin (SOM) interneurons in the hippocampal formation. Results: One thousand five hundred ninety-three articles were pulled from PubMed, PsycInfo, and Web of Science, based on three blocks of search terms. There were 45 articles that met all the predetermined inclusion/exclusion criteria. There is strong evidence that PV interneurons are affected early in the disease by toxic amyloid beta (Ab) fragments; SOM interneurons are affected indirectly while the SOM neuropeptide may act to slowly worsen toxic Ab fragment accumulation, whereas NPY-and CCK-positive interneurons are affected later in the progression of the disease. Conclusions: Fewer studies have been performed on NPY and CCK interneurons, and there is room for further investigations regarding the role of PV interneurons in Alzheimer's to help resolve contradictory findings. This review found that PV interneurons are affected early in the disease, but only in Alzheimer's precursor protein but not tau models. NPY and CCK interneurons were found to be affected later in the disease, and SOM interneurons vary greatly. Future studies may consider reporting immunohistochemical studies inclusive of either cell location or morphology-as well as marker to give a more robust picture of the disease.