Nontraumatic Myositis Ossificans After Spontaneous Subarachnoid Hemorrhage: A Case Report.

Myositis ossificans is uncommon in patients with nontraumatic brain injuries. This report presents a challenging case in which myositis ossificans was diagnosed and treated by medical management in a patient who was unable to complain of any symptoms due to akinetic mutism that occurred after nontraumatic subarachnoid hemorrhage. The patient had intermittent high-grade fever, and laboratory tests showed elevated C-reactive protein and D-dimer levels without clinical signs of infection two months after subarachnoid hemorrhage. Lower-extremity venography using computed tomography was performed to rule out deep venous thrombosis. There was no thrombus, but right vastus medialis muscle showed inflammatory change with faint multilayered curvilinear hyperdense rims. The administration of indomethacin helped prevent abnormal bone formation. For the early detection of myositis ossificans, careful observation of clinical presentation and a high index of clinical suspicion is necessary in brain-injured patients. Further, elevated serum inflammatory markers accompanied by elevated alkaline phosphatase can be a critical clue. Early computed tomography helps identify early 'string sign' prior to characteristic ossification. Our report highlights that the myositis ossificans is remediable by early detection and appropriate nonsurgical management.

Identification of IGF-1 Effects on White Adipose Tissue and Hippocampus in Alzheimer's Disease Mice via Transcriptomic and Cellular Analysis.

Alzheimer's disease (AD) stands as the most prevalent neurodegenerative disorder, characterized by a multitude of pathological manifestations, prominently marked by the aggregation of amyloid beta. Recent investigations have revealed a compelling association between excessive adiposity and glial activation, further correlating with cognitive impairments. Additionally, alterations in levels of insulin-like growth factor 1 (IGF-1) have been reported in individuals with metabolic conditions accompanied by memory dysfunction. Hence, our research endeavors to comprehensively explore the impact of IGF-1 on the hippocampus and adipose tissue in the context of Alzheimer's disease. To address this, we have conducted an in-depth analysis utilizing APP/PS2 transgenic mice, recognized as a well-established mouse model for Alzheimer's disease. Upon administering IGF-1 injections to the APP/PS2 mice, we observed notable alterations in their behavioral patterns, prompting us to undertake a comprehensive transcriptomic analysis of both the hippocampal and adipose tissues. Our data unveiled significant modifications in the functional profiles of these tissues. Specifically, in the hippocampus, we identified changes associated with synaptic activity and neuroinflammation. Concurrently, the adipose tissue displayed shifts in processes related to fat browning and cell death signaling. In addition to these findings, our analysis enabled the identification of a collection of long non-coding RNAs and circular RNAs that exhibited significant changes in expression subsequent to the administration of IGF-1 injections. Furthermore, we endeavored to predict the potential roles of these identified RNA molecules within the context of our study. In summary, our study offers valuable transcriptome data for hippocampal and adipose tissues within an Alzheimer's disease model and posits a significant role for IGF-1 within both the hippocampus and adipose tissue.

Circular RNA circSMAD4 regulates cardiac fibrosis by targeting miR-671-5p and FGFR2 in cardiac fibroblasts.

Heart failure is a leading cause of death and is often accompanied by activation of quiescent cardiac myofibroblasts, which results in cardiac fibrosis. In this study, we aimed to identify novel circular RNAs that regulate cardiac fibrosis. We applied transverse aortic constriction (TAC) for 1, 4, and 8 weeks in mice. RNA sequencing datasets were obtained from cardiac fibroblasts isolated by use of a Langendorff apparatus and then further processed by use of selection criteria such as differential expression and conservation in species. CircSMAD4 was upregulated by TAC in mice or by transforming growth factor (TGF)-ß1 in primarily cultured human cardiac fibroblasts. Delivery of si-circSMAD4 attenuated myofibroblast activation and cardiac fibrosis in mice treated with isoproterenol (ISP). si-circSmad4 significantly reduced cardiac fibrosis and remodeling at 8 weeks. Mechanistically, circSMAD4 acted as a sponge against the microRNA miR-671-5p in a sequence-specific manner. miR-671-5p was downregulated during myofibroblast activation and its mimic form attenuated cardiac fibrosis. miR-671-5p mimic destabilized fibroblast growth factor receptor 2 (FGFR2) mRNA in a sequence-specific manner and interfered with the fibrotic action of FGFR2. The circSMAD4-miR-671-5p-FGFR2 pathway is involved in the differentiation of cardiac myofibroblasts and thereby the development of cardiac fibrosis.

Low-Dose Ionizing Radiation-Crosslinking Immunoprecipitation (LDIR-CLIP) Identified Irradiation-Sensitive RNAs for RNA-Binding Protein HuR-Mediated Decay.

Although ionizing radiation (IR) is widely used for therapeutic and research purposes, studies on low-dose ionizing radiation (LDIR) are limited compared with those on other IR approaches, such as high-dose gamma irradiation and ultraviolet irradiation. High-dose IR affects DNA damage response and nucleotide-protein crosslinking, among other processes; however, the molecular consequences of LDIR have been poorly investigated. Here, we developed a method to profile RNA species crosslinked to an RNA-binding protein, namely, human antigen R (HuR), using LDIR and high-throughput RNA sequencing. The RNA fragments isolated via LDIR-crosslinking and immunoprecipitation sequencing were crosslinked to HuR and protected from RNase-mediated digestion. Upon crosslinking HuR to target mRNAs such as PAX6, ZFP91, NR2F6, and CAND2, the transcripts degraded rapidly in human cell lines. Additionally, PAX6 and NR2F6 downregulation mediated the beneficial effects of LDIR on cell viability. Thus, our approach provides a method for investigating post-transcriptional gene regulation using LDIR.

Human lncRNA SUGCT-AS1 Regulates the Proinflammatory Response of Macrophage.

Macrophages are the major primary immune cells that mediate the inflammatory response. In this process, long non-coding RNAs (lncRNAs) play an important, yet largely unknown role. Therefore, utilizing several publicly available RNA sequencing datasets, we predicted and selected lncRNAs that are differentially expressed in M1 or M2 macrophages and involved in the inflammatory response. We identified SUGCT-AS1, which is a human macrophage-specific lncRNA whose expression is increased upon M1 macrophage stimulation. Conditioned media of SUGCT-AS1-depleted M1 macrophages induced an inflammatory phenotype of vascular smooth muscle cells, which included increased expression of inflammatory genes (IL1B and IL6), decreased contractile marker proteins (ACTA2 and SM22α), and increased cell migration. Depletion of SUGCT-AS1 promoted the expression and secretion of proinflammatory cytokines, such as TNF, IL1B, and IL6, in M1 macrophages, and transcriptomic analysis showed that SUGCT-AS1 has functions related to inflammatory responses and cytokines. Furthermore, we found that SUGCT-AS1 directly binds to hnRNPU and regulates its nuclear-cytoplasmic translocation. This translocation of hnRNPU altered the proportion of the MALT1 isoforms by regulating the alternative splicing of MALT1, a mediator of NF-κB signaling. Overall, our findings suggest that lncRNAs can be used for future studies on macrophage regulation. Moreover, they establish the SUGCT-AS1/hnRNPU/MALT1 axis, which is a novel inflammatory regulatory mechanism in macrophages.

Clinical Practice Guidelines for Oropharyngeal Dysphagia.

OBJECTIVE: Dysphagia is a common clinical condition characterized by difficulty in swallowing. It is sub-classified into oropharyngeal dysphagia, which refers to problems in the mouth and pharynx, and esophageal dysphagia, which refers to problems in the esophageal body and esophagogastric junction. Dysphagia can have a significant negative impact one's physical health and quality of life as its severity increases. Therefore, proper assessment and management of dysphagia are critical for improving swallowing function and preventing complications. Thus a guideline was developed to provide evidence-based recommendations for assessment and management in patients with dysphagia. METHODS: Nineteen key questions on dysphagia were developed. These questions dealt with various aspects of problems related to dysphagia, including assessment, management, and complications. A literature search for relevant articles was conducted using Pubmed, Embase, the Cochrane Library, and one domestic database of KoreaMed, until April 2021. The level of evidence and recommendation grade were established according to the Grading of Recommendation Assessment, Development and Evaluation methodology. RESULTS: Early screening and assessment of videofluoroscopic swallowing were recommended for assessing the presence of dysphagia. Therapeutic methods, such as tongue and pharyngeal muscle strengthening exercises and neuromuscular electrical stimulation with swallowing therapy, were effective in improving swallowing function and quality of life in patients with dysphagia. Nutritional intervention and an oral care program were also recommended. CONCLUSION: This guideline presents recommendations for the assessment and management of patients with oropharyngeal dysphagia, including rehabilitative strategies.

Accuracy of Measurements of the Structural Reserve for Upper Limb Function in Patients With Moderate-to-Severe Stroke.

BACKGROUND: The structural integrity of the corticospinal tract (CST) is an important biomarker of poststroke upper limb recovery. Injured CST undergoes Wallerian degeneration rostrocaudally during the first few months. However, there is no standardized measurement of the structural integrity of the CST. This study aimed to determine the measurement accuracy of the structural integrity of the CST. METHODS: This cross-sectional study included 50 consecutive patients with middle cerebral artery stroke who underwent diffusion tensor imaging upon transfer from the acute stroke unit to the inpatient rehabilitation facility (2018-2022). We evaluated hemiplegic upper limb function using Shoulder Abduction and Finger Extension (SAFE) scores. Fractional anisotropy values representing the structural integrity of the CST were evaluated using 4 region of interest-based and 2 tract-based measurements, including the posterior limb of internal capsule, cerebral peduncle, pons, pontomedullary junction, entire CST, and CST in the brainstem. Multivariate linear regression models and the area under the curve (AUC) were used to determine measurement accuracy for hemiplegic upper limb function. RESULTS: The structural integrity of the CST at the pontomedullary junction showed the highest explanatory power, followed by the entire CST, in the multivariate linear regression models (adjusted R2=0.459 and 0.425, respectively). The structural integrity of the CST at the pontomedullary junction also showed the highest AUC, followed by the entire CST, in discriminating patients with a SAFE score of <8 or 5 from those with SAFE ≥8 or 5 (SAFE <8: AUC, 0.90 [95% CI, 0.80-1.00]; AUC, 0.83 [0.66-0.99]; SAFE <5: AUC, 0.87 [0.77-0.96]; AUC, 0.83, [0.72-0.95], respectively). CONCLUSIONS: The structural integrity of the CST measured at the pontomedullary junction or entire CST demonstrated the highest accuracy for hemiplegic upper limb function in the subacute phase of stroke.

Structural Integrity of the Cerebellar Outflow Tract Predicts Long-Term Motor Function After Middle Cerebral Artery Ischemic Stroke.

BACKGROUND: The cerebellum plays a crucial role in functional movement by influencing sensorimotor coordination and learning. However, the effects of cortico-cerebellar connectivity on the recovery of upper extremity motor function after stroke have not been investigated. We hypothesized that the integrity of the cortico-cerebellar connections would be reduced in patients with a subacute middle cerebral artery (MCA) stroke, and that this reduction may help to predict chronic upper extremity motor function. METHODS: We retrospectively analyzed the diffusion-tensor imaging of 25 patients with a subacute MCA stroke (mean age: 62.2 ± 2.7 years; 14 females) and 25 age- and sex-matched healthy controls. We evaluated the microstructural integrity of the corticospinal tract (CST), dentatothalamocortical tract (DTCT), and corticopontocerebellar tract (CPCT). Furthermore, we created linear regression models to predict chronic upper extremity motor function based on the structural integrity of each tract. RESULTS: In stroke patients, the affected DTCT and CST showed significantly impaired structural integrity compared to unaffected tracts and the tracts in controls. When all models were compared, the model that used the fractional anisotropy (FA) asymmetry indices of CST and DTCT as independent variables best predicted chronic upper extremity motor function (R2 = .506, P = .001). The extent of structural integrity of the CPCT did not significantly differ between hemispheres or groups and was not predictive of motor function. CONCLUSIONS: We found evidence that microstructural integrity of the DTCT in the subacute phase of an MCA stroke helped to predict chronic upper extremity motor function, independent of CST status.

Roles of non-coding RNAs in intercellular crosstalk in cardiovascular diseases.

Complex diseases including cardiovascular disease are caused by a combination of the alternation of many genes and the influence of environments. Recently, non-coding RNAs (ncRNAs) have been shown to be involved in diverse diseases, and the functions of various ncRNAs have been reported. Many researchers have elucidated the mechanisms of action of these ncRNAs at the cellular level prior to in vivo and clinical studies of the diseases. Due to the characteristics of complex diseases involving intercellular crosstalk, it is important to study communication between multiple cells. However, there is a lack of literature summarizing and discussing studies of ncRNAs involved in intercellular crosstalk in cardiovascular diseases. Therefore, this review summarizes recent discoveries in the functional mechanisms of intercellular crosstalk involving ncRNAs, including microRNAs, long non-coding RNAs, and circular RNAs. In addition, the pathophysiological role of ncRNAs in this communication is extensively discussed in various cardiovascular diseases.

H19X-encoded microRNAs induced by IL-4 in adipocyte precursors regulate proliferation to facilitate differentiation.

Adipose tissue, an organ critical for systemic energy homeostasis, is influenced by type 2 immunity in its development and function. The type 2 cytokine interleukin (IL)-4 induces the proliferation of bipotential adipocyte precursors (APs) in white fat tissue and primes these cells for differentiation into beige adipocytes, which are specialized for thermogenesis. However, the underlying mechanisms have not yet been comprehensively examined. Here, we identified six microRNA (miRNA) genes upregulated upon IL-4 stimulation in APs, miR-322, miR-503, miR-351, miR-542, miR-450a, and miR-450b; these are encoded in the H19X locus of the genome. Their expression is positively regulated by the transcription factor Klf4, whose expression also increases upon IL-4 stimulation. These miRNAs shared a large set of target genes, of which 381 genes were downregulated in mRNA expression upon IL-4 stimulation and enriched in Wnt signaling pathways. Two genes with downregulated expression, Ccnd1 and Fzd6, were repressed by H19X-encoded miRNAs. Additionally, the Wnt signaling activator LiCl downregulated the expression of this group of miRNAs in APs, indicating that Wnt signaling-related genes and these miRNAs form a double-negative feedback regulatory loop. This miRNA/Wnt feedback regulation modulated the elevated proliferation of APs induced by IL-4 stimulation and contributed to priming them for beige adipocyte differentiation. Moreover, the aberrant expression of these miRNAs attenuates the differentiation of APs into beige adipocytes. Collectively, our results suggest that H19X-encoded miRNAs facilitate the transition of APs from proliferation to differentiation in the IL-4-mediated regulation.

Evidence of lateralised white matter plasticity: A longitudinal study of balance performance in nonexpert healthy adults.

Training-induced plasticity by practicing expert skills has been of particular interest; however, little is known about white matter plasticity for improving a fundamental element of body function, such as balance or postural control. This study explored white matter plasticity in nonexpert healthy adults, based on stepwise balance training. Seventeen participants were included and performed a home-based balance training program for 4 weeks (30 min/day, 3 days/week). Before commencing training, they underwent a baseline diffusion tensor imaging scan. A second scan was acquired at the end of the 4-week training. Lateralised balance load was applied on the right leg to contrast any lateralised effect on the white matter tracts. The balance function was assessed using the Community Balance & Mobility Scale. We examined changes in the fractional anisotropy values of the tracts of interest between pre- and post-training. After the 4-week training, the fractional anisotropy values were enhanced in the right superior cerebellar peduncle, transverse pontine fibre, body of the corpus callosum, left fornix and left uncinate fasciculus. The Community Balance & Mobility Scale score improved after 4-week training, but an association with changes in fractional anisotropy values cannot be evaluated due to the ceiling effect of the balance assessment tools. Balance training can strengthen the cerebro-cerebellar and interhemispheric structural connections and induce microstructural changes in the limbic structures, including the fornix and uncinate fasciculus. The effect of a lateralised balance load could be projected to the specific white matter tracts in a lateralised manner.

Circular RNA Tmcc1 improves astrocytic glutamate metabolism and spatial memory via NF-κB and CREB signaling in a bile duct ligation mouse model: transcriptional and cellular analyses.

BACKGROUND: Hepatic encephalopathy-induced hyperammonemia alters astrocytic glutamate metabolism in the brain, which is involved in cognitive decline. To identify specific therapeutic strategies for the treatment of hepatic encephalopathy, various molecular signaling studies, such as non-coding RNA functional study, have been conducted. However, despite several reports of circular RNAs (circRNAs) in the brain, few studies of circRNAs in hepatic encephalopathy-induced neuropathophysiological diseases have been conducted. METHODS: In this study, we performed RNA sequencing to identify whether the candidate circRNA cirTmcc1 is specifically expressed in the brain cortex in a bile duct ligation (BDL) mouse model of hepatic encephalopathy. RESULTS: Based on transcriptional and cellular analysis, we investigated the circTmcc1-dysregulation-induced changes in the expression of several genes that are associated with intracellular metabolism and astrocyte function. We found that the circTmcc1 binds with the NF-κB p65-CREB transcriptional complex and regulates the expression of the astrocyte transporter EAAT2. Furthermore, circTmcc1 contributed to the secretion of proinflammatory mediators and glutamate metabolism in astrocytes and subsequently modulated an improvement in spatial memory by mediating neuronal synaptic plasticity. CONCLUSIONS: Thus, circTmcc1 may be a promising circRNA candidate for targeted interventions to prevent and treat the neuropathophysiological complications that occur due to hepatic encephalopathy.

Post-Stroke Infections: Insights from Big Data Using Clinical Data Warehouse (CDW).

This study analyzed a digitized database of electronic medical records (EMRs) to identify risk factors for post-stroke infections. The sample included 41,236 patients hospitalized with a first stroke diagnosis (ICD-10 codes I60, I61, I63, and I64) between January 2011 and December 2020. Logistic regression analysis was performed to examine the effect of clinical variables on post-stroke infection. Multivariable analysis revealed that post-stroke infection was associated with the male sex (odds ratio [OR]: 1.79; 95% confidence interval [CI]: 1.49-2.15), brain surgery (OR: 7.89; 95% CI: 6.27-9.92), mechanical ventilation (OR: 18.26; 95% CI: 8.49-44.32), enteral tube feeding (OR: 3.65; 95% CI: 2.98-4.47), and functional activity level (modified Barthel index: OR: 0.98; 95% CI: 0.98-0.98). In addition, exposure to steroids (OR: 2.22; 95% CI: 1.60-3.06) and acid-suppressant drugs (OR: 1.44; 95% CI: 1.15-1.81) increased the risk of infection. On the basis of the findings from this multicenter study, it is crucial to carefully evaluate the balance between the potential benefits of acid-suppressant drugs or corticosteroids and the increased risk of infection in patients at high risk for post-stroke infection.

Profiling and Cellular Analyses of Obesity-Related circRNAs in Neurons and Glia under Obesity-like In Vitro Conditions.

Recent evidence indicates that the pathogenesis of neurodegenerative diseases, including Alzheimer's disease, is associated with metabolic disorders such as diabetes and obesity. Various circular RNAs (circRNAs) have been found in brain tissues and recent studies have suggested that circRNAs are related to neuropathological mechanisms in the brain. However, there is a lack of interest in the involvement of circRNAs in metabolic imbalance-related neuropathological problems until now. Herein we profiled and analyzed diverse circRNAs in mouse brain cell lines (Neuro-2A neurons, BV-2 microglia, and C8-D1a astrocytes) exposed to obesity-related in vitro conditions (high glucose, high insulin, and high levels of tumor necrosis factor-alpha, interleukin 6, palmitic acid, linoleic acid, and cholesterol). We observed that various circRNAs were differentially expressed according to cell types with many of these circRNAs conserved in humans. After suppressing the expression of these circRNAs using siRNAs, we observed that these circRNAs regulate genes related to inflammatory responses, formation of synaptic vesicles, synaptic density, and fatty acid oxidation in neurons; scavenger receptors in microglia; and fatty acid signaling, inflammatory signaling cyto that may play important roles in metabolic disorders associated with neurodegenerative diseases.

Circular RNAs as a promising biomarker for heart disease.

Heart-related diseases account for a high proportion of deadly pathologies, so a large number of studies have been conducted to discover potential biomarkers for the early detection of heart disease. Circular RNAs (circRNAs) are known to be involved in various human diseases, and several circRNAs associated with heart disease have been reported recently. However, there is a lack of literature summarizing the potential of circRNAs as biomarkers of heart disease and suggesting future research prospects. In this review, the history of circRNA research and important studies on circRNAs are described. In addition, the biogenesis process of circRNAs and the applicability of circRNA as a biomarker of heart disease are introduced, and select studies that monitored circRNAs circulating in human blood as biomarkers of heart disease are summarized. The contents of this review may help the researchers interested in the detection and prevention of heart disease at an early stage.

Comparing the long non-coding RNA expression profiles of skeletal muscle and kidney tissues from patients with diabetes.

BACKGROUND: Diabetes causes the dysregulation of several organs, and these effects are often closely associated with changes in the expression of long non-coding RNAs (lncRNAs), a group of non-coding RNAs, within these tissues. Previous studies have described a variety of changes in the expression profile of several lncRNAs from different organs in response to the pathogenesis of diabetes. However, none of these studies compared the expression profiles of these lncRNAs between these organs. This study was designed to identify common and specific lncRNAs involved in the progression of diabetes in the skeletal muscles and kidneys. METHODS: Publicly available RNA sequencing data of diabetic patients was obtained from the Gene Expression Omnibus database. By analyzing the expression of lncRNAs in these datasets, differentially expressed lncRNAs in each tissue between non-diabetic and diabetic patients were identified. To identify any lncRNAs changed in common in both kidney and muscle tissues, those lncRNAs that are significantly dysregulated in both datasets were selected. RESULTS: These evaluations identified a series of novel lncRNAs unique to each organ and several transcripts that were common to both skeletal muscle and kidney tissues in these patients. Interestingly, the genomic location of these lncRNAs suggests that they reside in close proximity to several protein-coding genes known to be related to diabetes suggesting that these lncRNAs may have a regulatory relationship with their neighboring genes. CONCLUSION: These results offer valuable insights into the role of lncRNAs during the pathogenesis of diabetes.

The matricellular protein CCN5 induces apoptosis in myofibroblasts through SMAD7-mediated inhibition of NFκB.

We previously showed that the matricellular protein CCN5 reverses established cardiac fibrosis (CF) through inducing apoptosis in myofibroblasts (MyoFBs) but not in cardiomyocytes or fibroblasts (FBs). In this study, we set out to elucidate the molecular mechanisms underlying CCN5-mediated selective apoptosis of MyoFBs. We first observed that the apoptotic protein p53 and the anti-apoptotic protein NFκB are simultaneously induced in MyoFBs. When the expression level of p53 was suppressed using a siRNA, CCN5 did not induce apoptosis in MyoFBs. By contrast, when NFκB signaling was inhibited using IKK VII, an IκB inhibitor, MyoFBs underwent apoptosis even in the absence of CCN5. SMAD7 is one of the downstream targets of CCN5 and it was previously shown to potentiate apoptosis in epithelial cells through inhibition of NFκB. In accordance with these reports, when the expression of SMAD7 was suppressed using a siRNA, NFκB signaling was enhanced, and CCN5 did not induce apoptosis. Lastly, we used a luciferase reporter construct to show that CCN5 positively regulated SMAD7 expression at the transcriptional level. Collectively, our data suggest that a delicate balance between the two mutually antagonistic proteins p53 and NFκB is maintained for MyoFBs to survive, and CCN5 tips the balance in favor of the apoptotic protein p53. This study provides insight into the anti-fibrotic activity of CCN5 during the regression of CF.

Single Nucleotide Polymorphisms May Increase the Risk of Aspiration Pneumonia in Post-Stroke Patients with Dysphagia.

This study aimed to evaluate whether genetic polymorphism is associated with an increased risk of infection, specifically post-stroke aspiration pneumonia. Blood samples were obtained from a total of 206 post-stroke participants (males, n = 136; mean age, 63.8 years). Genotyping was performed for catechol-O-methyltransferase (rs4680, rs165599), dopamine receptors (DRD1; rs4532, DRD2; rs1800497, DRD3; rs6280), brain-derived neurotrophic factor (rs6265), apolipoprotein E (rs429358, rs7412), and the interleukin-1 receptor antagonist gene (rs4251961). The subjects were stratified into two groups, aged < 65 (young) and ≥ 65 (elderly). Functional parameters and swallowing outcomes were measured at enrollment and at 3 months post-onset. The primary outcome was the incidence of aspiration pneumonia. Analysis of the association between genetic polymorphisms and aspiration pneumonia history showed that a minor C rs429358 allele was associated with the occurrence of aspiration pneumonia in the young group, both in the additive and the dominant models (odds ratio: 4.53; 95% CI: 1.60−12.84, p = 0.004). In the multivariable analysis, the minor C rs429358 allele increased the risk of post-stroke aspiration pneumonia in young stroke patients by 5.35 (95% CI: 1.64−20.88). In contrast, no such association was observed in the elderly group. Apolipoprotein E polymorphism may affect the risk of post-stroke aspiration pneumonia.