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This study seeks to identify Alzheimer’s and related dementias (ADRD) biomarkers associated with postoperative delirium (POD) via meta-analysis.
A comprehensive search was conducted. Studies met the following inclusion criteria: >18 years of age, identified POD with standardized assessment, and biomarker measured in the AT(N)-X (A = amyloid, T = tau, (N)=neurodegeneration, X-Other) framework. Exclusion criteria: focus on prediction of delirium, delirium superimposed on dementia, other neurologic or psychiatric disorders, or terminal delirium. Reviewers extracted and synthesized data for the meta-analysis.
Meta-analysis.
Patients with POD.
Primary outcome: association between POD and ATN-X biomarkers. Secondary outcomes involved sample heterogeneity.
28 studies were included in this meta-analysis. Studies focused on inflammatory and neuronal injury biomarkers; there were an insufficient number of studies for amyloid and tau biomarker analysis. Two inflammatory biomarkers (IL-6, and CRP) showed a significant relationship with POD (IL-6 n = 10, standardized mean difference (SMD): 0.53, 95% CI: 0.36–0.70; CRP n = 14, SMD: 0.53, 95% CI: 0.33–0.74). Two neuronal injury biomarkers (blood-based S100B and NfL) were positively associated with POD (S100B n = 5, SMD: 0.40, 95% CI: 0.11–0.69; NFL n = 2, SMD: 0.93, 95% CI: 0.28–1.57). Of note, many analyses were impacted by significant study heterogeneity.
This meta-analysis identified an association between certain inflammatory and neuronal injury biomarkers and POD. Future studies will need to corroborate these relationships and include amyloid and tau biomarkers in order to better understand the relationship between POD and ADRD.
Extensive research over the past several years has led to the elucidation of genetic and biochemical pathways involved in apoptosis (from the Greek apo = away from, and ptosis = falling), which is often referred to as the program for cell death. Concurrently, studies in stroke and degenerative diseases have sought to address the underlying mechanisms of neural cell death in these disease states. Interestingly, initial attempts to map the results from apoptosis mechanistic studies onto the patterns observed in neurological diseases have resulted in something of a paradox. On the one hand, the expression of genes associated with neurodegenerative diseases, such as mutants of sod 1 associated with amyotrophic lateral sclerosis or mutants of β-amyloid precursor protein associated with Alzheimer's disease, has been shown to induce apoptosis in cultured cells; on the other hand, studies in vivo have not disclosed classic apoptosis as the major route of neuronal cell death in any of the major neurodegenerative diseases. Initially, it was thought that this may simply be because the rate of cell death in neurodegenerative diseases is slow enough that it is difficult to capture enough neurons in the act of apoptosis (which is typically a relatively rapid program, occurring over minutes to a few hours in cultured cells) to demonstrate a clear increase in disease states.
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