Dementia Assessment Using Mandarin Speech with an Attention-based Speech Recognition Encoder

Dementia diagnosis requires a series of different testing methods, which is complex and time-consuming. Early detection of dementia is crucial as it can prevent further deterioration of the condition. This paper utilizes a speech recognition model to construct a dementia assessment system tailored for Mandarin speakers during the picture description task. By training an attention-based speech recognition model on voice data closely resembling real-world scenarios, we have significantly enhanced the model's recognition capabilities. Subsequently, we extracted the encoder from the speech recognition model and added a linear layer for dementia assessment. We collected Mandarin speech data from 99 subjects and acquired their clinical assessments from a local hospital. We achieved an accuracy of 92.04% in Alzheimer's disease detection and a mean absolute error of 9% in clinical dementia rating score prediction.Comment: submitted to IEEE ICASSP 202

Association Between Net Vertebral Artery Flow Volume and Non-AF Stroke: A Retrospective 2-Year Analysis

Objectives: Association between net vertebral artery flow volume (NVAFV) and stroke types remains unclear. We hypothesize NVAFV is low in patients with posterior circulation infarction (PCI) and an ideal cut-off value for discriminating PCI from anterior circulation infarction (ACI) and controls may be present.Materials and Methods: As study candidates, we retrospectively enrolled hospitalized patients with first-time non-AF stroke within 2-years period. Consecutive non-AF, non-stroke subjects were enrolled as the control group. We compared NVAFV values among the PCI, ACI, and control groups.Results: Overall, 866 candidates—213, 418, and 235 candidates in the PCI, ACI, and control groups, respectively—were enrolled. NVAFV (mean ± SD) values were 134.8 ± 52.7, 152.3 ± 59.2, and 172.0 ± 54.7 mL/min in the PCI, ACI, and control groups, respectively. Statistics revealed significant difference (p < 0.001) among three groups. To use NVAFV as a diagnostic parameter, the AUC of any two groups should be between 0.58 and 0.69. Most (93.6%) of the controls had NVAFV above 100 mL/min. The odds ratio of any non-AF stroke is 3.48 if the NVAFV is below 100 mL/min.Conclusions: NVAFV is lowest in non-AF PCI group. Low NVAFV is associated with both non-AF ACI and PCI. No ideal cut-off value is available to discriminate PCI from other two conditions. We agree that an NVAFV of 100 mL/min is the lower limit of a normal value. Any value below 100 mL/min indicates high stroke risk and implies diffuse cerebral atherosclerosis and impaired cerebral perfusion

Association between plasma levels of hyaluronic acid and functional outcome in acute stroke patients

BACKGROUND: Activation of hyaluronic acid (HA) and associated enzyme synthesis has been demonstrated in experimental stroke animal models. Our study aimed to investigate the plasma levels of HA in acute stroke patients and the associations between HA levels and functional outcome. METHODS: This was a multicenter case–control study. Acute stroke patients and age- and sex-matched non-stroke controls were recruited. Plasma levels of HA in acute stroke patients were determined at <48 hours and at 48 to 72 hours after stroke onset by standard ELISA. Favorable functional outcome was defined as modified Rankin scale ≤2 at 3 months after stroke. RESULTS: The study included 206 acute stroke patients, including 43 who had intracerebral hemorrhage and 163 who had ischemic stroke, and 159 controls. The plasma levels of HA in the acute stroke patients were significantly higher than those in the controls (219.7 ± 203.4 ng/ml for <48 hours and 343.1 ± 710.3 ng/ml for 48 to 72 hours versus 170.4 ± 127.9 ng/ml in the controls; both P < 0.05). For intracerebral hemorrhage patients, HA ≤500 ng/ml (<48 hours) was an independent favorable outcome predictor (P = 0.016). For ischemic stroke patients, an inverted U-shaped association between plasma HA (48 to 72 hours) and outcome was noted, indicating that ischemic stroke patients with too high or too low plasma HA levels tended to have an unfavorable outcome. CONCLUSION: HA plasma level was elevated in patients with acute stroke, and can predict 3-month functional outcome, particularly for patients with intracerebral hemorrhage

Reduction of Monocyte Chemoattractant Protein-1 and Interleukin-8 Levels by Ticlopidine in TNF-α Stimulated Human Umbilical Vein Endothelial Cells

Atherosclerosis and its associated complications represent major causes of morbidity and mortality in the industrialized or Western countries. Monocyte chemoattractant protein-1 (MCP-1) is critical for the initiating and developing of atherosclerotic lesions. Interleukin-8 (IL-8), a CXC chemokine, stimulates neutrophil chemotaxis. Ticlopidine is one of the antiplatelet drugs used to prevent thrombus formation relevant to the pathophysiology of atherothrombosis. In this study, we found that ticlopidine dose-dependently decreased the mRNA and protein levels of TNF-α-stimulated MCP-1, IL-8, and vascular cell adhesion molecule-1 (VCAM-1) in human umbilical vein endothelial cells (HUVECs). Ticlopidine declined U937 cells adhesion and chemotaxis as compared to TNF-α stimulated alone. Furthermore, the inhibitory effects were neither due to decreased HUVEC viability, nor through NF-kB inhibition. These results suggest that ticlopidine decreased TNF-α induced MCP-1, IL-8, and VCAM-1 levels in HUVECs, and monocyte adhesion. Therefore, the data provide additional therapeutic machinery of ticlopidine in treatment and prevention of atherosclerosis

Association Between Acid-Sensing Ion Channel 3 Gene Variants and Balance Impairment in People With Mild Traumatic Brain Injury

Introduction: Dizziness and balance impairment are common symptoms of mild traumatic brain injury (mTBI). Acid-sensing ion channel 3 (ASIC3) is expressed in the vestibular and proprioceptive systems and associated with balance functions. However, whether the genetic variants of ASIC3 are associated with people who suffer dizziness and balance impairment after mTBI remained unknown.Materials and methods: A total of 200 people with mTBI and 109 non-mTBI controls were recruited. Dizziness, balance functions, and the ability to perform daily activities were assessed by Dizziness Handicap Inventory (DHI), and objective balance functions were investigated by the postural stability test. Three diseases-related genetic variants of ASIC3 were determined through polymerase chain reaction and followed by restriction fragment length polymorphism. The Student's t-test and Mann-Whitney U-test were used for normal and abnormal distributed data, respectively. The regression was applied to adjust gender and age. The normality of continuous data was evaluated by Shapiro-Wilk test.Results: In the mTBI people, the rs2288645-A allele carriers exhibited a significantly worse physical domain DHI score (A-allele carriers: 11.39 ± 8.42, non-A carriers: 8.76 ± 7.87, p = 0.03). The rs4148855-GTC deletion carriers an exhibited significantly worse overall postural stability (GTC deletion carriers: 0.53 ± 0.33, non-carriers: 0.46 ± 0.20, p = 0.03). In the controls, rs2288646-A allele carriers were significant worse in the medial-to-lateral postural stability (A-allele carriers: 0.31 ± 0.17, non-A carriers: 0.21 ± 0.10, p = 0.01).Conclusion: The present study demonstrated that ASIC3 genetic variants were associated with certain aspects of balance functions and dizziness questionnaires in people of mTBI and non-mTBI. It provides a possible evidence that ASIC3 could be a new target for the management of the balancing disorders. However, further investigations are warranted to elucidate the underlying mechanisms and clinical significance

Association between genetic variant on chromosome 12p13 and stroke survival and recurrence: a one year prospective study in Taiwan

<p>Abstract</p> <p>Background</p> <p>The association between ischemic stroke and 2 single nucleotide polymorphisms (SNPs) on chromosome 12p13, rs12425791 and rs11833579 appears inconsistent across different samples. These SNPs are close to the ninjurin2 gene which may alter the risk of stroke by affecting brain response to ischemic injury. The purpose of this study was to investigate the association between these two SNPs and ischemic stroke risk, as well as prognostic outcomes in a Taiwanese sample.</p> <p>Methods</p> <p>We examined the relations of these two SNPs to the odds of new-onset ischemic stroke, ischemic stroke subtypes, and to the one year risk of stroke-related death or recurrent stroke following initial stroke in a case-control study. A total of 765 consecutive patients who had first-ever ischemic stroke were compared to 977 stroke-free, age-matched controls. SNPs were genotyped by Taqman fluorescent allelic discrimination assay. The association between ischemic stroke and SNPs were analyzed by multivariate logistic regression. Cox proportional hazard model was used to assess the effect of individual SNPs on stroke-related mortality or recurrent stroke.</p> <p>Results</p> <p>There was no significant association between SNP rs12425791 and rs11833579 and ischemic stroke after multiple testing corrections. However, the marginal significant association was observed between SNP rs12425791 and large artery atherosclerosis under recessive model (OR, 2.30; 95%CI, 1.22-4.34; q-value = 0.062). Among the 765 ischemic stroke patients, 59 died or developed a recurrent stroke. After adjustment for age, sex, vascular risk factors and baseline stroke severity, Cox proportional hazard analysis indicated that the hazard ratios were 2.76 (95%CI, 1.34-5.68; q-value, 0.02) and 2.15 (95%CI, 1.15-4.02; q-value, 0.03) for individuals with homozygous variant allele of rs12425791 and rs11833579, respectively.</p> <p>Conclusions</p> <p>This is a precedent study that found genetic variants of rs12425791 and rs11833579 on chromosome 12p13 are independent predictors of stroke-related mortality or stroke recurrence in patients with incident ischemic stroke in Taiwan. Further study is needed to explore the details of the physiological function and the molecular mechanisms underlying the association of this genetic locus with ischemic stroke.</p

Editorial: Risk Factors and Outcome Predicating Biomarker of Neurodegenerative Diseases.

Neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS) are major public health issues in the aging population. The central nervous system undergoes considerable degeneration for years before the onset of cardinal neurodegenerative symptoms such as resting tremors in PD (1). Failure to identify highly disease-correlated risk factors or biomarkers delays the initiation of neuroprotective treatment; several clinical trials on disease modification in neurodegenerative disorders have failed because of this. The lack of reliable outcome-predicting biomarkers hinders the development of disease modification approaches (2). Epidemiological studies have presented significant risk factors for and biomarkers of neurodegenerative diseases that can be detected before diagnosis, such as mild cognitive impairment (MCI) for AD (3, 4) and rapid eye movement sleep behavioral disorder (RBD) for PD (5). Vascular risk factors accelerate AD progression (6); diabetes is associated with rapid deterioration in PD (7). However, this knowledge does not facilitate robust prediction of neurodegenerative diseases and outcomes or early initiation of neuroprotective treatment in clinical trials. In this special issue, we have gathered eight original articles regarding biomarkers of neurodegenerative diseases. A review article explores the role of neuroimaging in neurodegenerative diseases. Articles in this special issue address three topics: clinical disease biomarkers for neurodegenerative diseases, biomarkers from animal models of neurodegenerative diseases, and biomarkers as therapeutic indicators

Current and Potential Pharmacologic Therapies for Traumatic Brain Injury

The present article reviewed the pharmacologic therapies of traumatic brain injury (TBI), including current and potential treatments. Pharmacologic therapies are an essential part of TBI care, and several agents have well-established effects in TBI care. In the acute phase, tranexamic acid, antiepileptics, hyperosmolar agents, and anesthetics are the mainstay of pharmacotherapy, which have proven efficacies. In the post-acute phase, SSRIs, SNRIs, antipsychotics, zolpidem and amantadine, as well as other drugs, have been used to manage neuropsychological problems, while muscle relaxants and botulinum toxin have been used to manage spasticity. In addition, increasing numbers of pre-clinical and clinical studies of pharmaceutical agents, including potential neuroprotective nutrients and natural therapies, are being carried out. In the present article, we classify the treatments into established and potential agents based on the level of clinical evidence and standard of practice. It is expected that many of the potential medicines under investigation will eventually be accepted as standard practice in the care of TBI patients

Endothelial Dysfunction in Neurodegenerative Diseases

The cerebral vascular system stringently regulates cerebral blood flow (CBF). The components of the blood&ndash;brain barrier (BBB) protect the brain from pathogenic infections and harmful substances, efflux waste, and exchange substances; however, diseases develop in cases of blood vessel injuries and BBB dysregulation. Vascular pathology is concurrent with the mechanisms underlying aging, Alzheimer&rsquo;s disease (AD), and vascular dementia (VaD), which suggests its involvement in these mechanisms. Therefore, in the present study, we reviewed the role of vascular dysfunction in aging and neurodegenerative diseases, particularly AD and VaD. During the development of the aforementioned diseases, changes occur in the cerebral blood vessel morphology and local cells, which, in turn, alter CBF, fluid dynamics, and vascular integrity. Chronic vascular inflammation and blood vessel dysregulation further exacerbate vascular dysfunction. Multitudinous pathogenic processes affect the cerebrovascular system, whose dysfunction causes cognitive impairment. Knowledge regarding the pathophysiology of vascular dysfunction in neurodegenerative diseases and the underlying molecular mechanisms may lead to the discovery of clinically relevant vascular biomarkers, which may facilitate vascular imaging for disease prevention and treatment