Association of traumatic brain injury and Alzheimer disease onset: A systematic review

Abstract

Failure to establish such a link may be related to methodological problems in the studies. To shed light on this dilemma, future studies should use a prospective design, define the types and severities of TBI and use standardized AD and TBI diagnostic criteria. Ultimately, an AD prediction model, based on several variables, would be useful for clinicians detecting TBI patients at risk of AD.

Advance of sporadic Alzheimer's disease animal models

“…100 Besides, the amount of activated microglial cells, the immune reaction of astrocyte, the level of cytokines, chemokines, and complements were increased both in AD patients and TBI patients. 101 were not persistent at 6 months in s-mTBI mice. 121 Villaopl et al 122 found that male mice showed more severe brain neuroinflammation than female mice during an acute and subacute period after injury in moderate to severe CCI models.…”

“…According to the severity of the injury, mild, moderate, and severe TBI can be selected. In general, the elevated level of phosphorylated Tau, the expression of Aβ, degradation of white matter, BBB dysfunction as well as neurogenic inflammation in hippocampus were observed in TBI models …”

“…Patients suffered from TBI might show the common features in pathology, which includes amyloid plaques, NFTs, and inflammatory response induced by activated microglial cells and inflammatory cytokines . Besides, the amount of activated microglial cells, the immune reaction of astrocyte, the level of cytokines, chemokines, and complements were increased both in AD patients and TBI patients . TBI‐induced AD models have been developed to mimic the sAD pathological changes in the brain.…”

“…According to the severity of the injury, mild, moderate, and severe TBI can be selected. In general, the elevated level of phosphorylated Tau, the expression of Aβ, degradation of white matter, BBB dysfunction as well as neurogenic inflammation in hippocampus were observed in TBI models [101][102][103][104][105][106][107][108][109][110][111][112][113][114][115][116][117][118]. Wang et al discovered that TBI induced the activation of the calpain-2-PTPN13-c-Abl pathway contributed to promoted abnormal Tau aggregation and NFTs formation.…”

Potential biomarkers to detect traumatic brain injury by the profiling of salivary extracellular vesicles

“…or saliva(Gonzalez-Begne et al, 2009;Kapsogeorgou, Abu-Helu, Moutsopoulos, & Manoussakis, 2005), as seen in brain cancer, poses an exciting avenue to painlessly diagnose disease.In the present study, we report the isolation and characterization of EVs from saliva and for the first time profiled the expression of Alzheimer disease genes in three groups of patients: acutely head injured emergency department (ED) patients, patients diagnosed with a concussion from an outpatient concussion clinic, and controls. Given the literature surrounding head injury and Alzheimer's disease(Becker, Kapogiannis, & Greig, 2018;Grinberg et al, 2016;Julien et al, 2017;Mendez, Paholpak, Lin, Zhang, & Teng, 2015;Ramos-Cejudo et al, 2018), we hypothesized that patients with mTBI would express Alzheimer's disease genes at significantly greater levels than controls. Our aim is to determine whether those gene expression profiles changed after mTBI and if the changes of the biomarkers could be potentially used to diagnose mTBI to prognosticate future development of postconcussion syndrome (PCS) or CTE, a disease characterized by tau protein deposition and amyloid beta plagues similar to those seen in Alzheimer's disease(Gavett et al, 2010).2 | MATERIALS AND METHODSAll participants and/or their relatives in addition to normal healthy control subjects gave written informed consent.…”