Displaying publications 1 - 20 of 25 in total

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  1. Duffin E, Bland AR, Schaefer A, de Kamps M
    Front Neurosci, 2014;8:30.
    PMID: 24600342 DOI: 10.3389/fnins.2014.00030
    Computational models of learning have proved largely successful in characterizing potential mechanisms which allow humans to make decisions in uncertain and volatile contexts. We report here findings that extend existing knowledge and show that a modified reinforcement learning model, which has separate parameters according to whether the previous trial gave a reward or a punishment, can provide the best fit to human behavior in decision making under uncertainty. More specifically, we examined the fit of our modified reinforcement learning model to human behavioral data in a probabilistic two-alternative decision making task with rule reversals. Our results demonstrate that this model predicted human behavior better than a series of other models based on reinforcement learning or Bayesian reasoning. Unlike the Bayesian models, our modified reinforcement learning model does not include any representation of rule switches. When our task is considered purely as a machine learning task, to gain as many rewards as possible without trying to describe human behavior, the performance of modified reinforcement learning and Bayesian methods is similar. Others have used various computational models to describe human behavior in similar tasks, however, we are not aware of any who have compared Bayesian reasoning with reinforcement learning modified to differentiate rewards and punishments.
  2. Abd Hamid AI, Gall C, Speck O, Antal A, Sabel BA
    Front Neurosci, 2015;9:391.
    PMID: 26578858 DOI: 10.3389/fnins.2015.00391
    Cognitive and neurological dysfunctions can severely impact a patient's daily activities. In addition to medical treatment, non-invasive transcranial alternating current stimulation (tACS) has been proposed as a therapeutic technique to improve the functional state of the brain. Although during the last years tACS was applied in numerous studies to improve motor, somatosensory, visual and higher order cognitive functions, our knowledge is still limited regarding the mechanisms as to which type of ACS can affect cortical functions and altered neuronal oscillations seem to be the key mechanism. Because alternating current send pulses to the brain at predetermined frequencies, the online- and after-effects of ACS strongly depend on the stimulation parameters so that "optimal" ACS paradigms could be achieved. This is of interest not only for neuroscience research but also for clinical practice. In this study, we summarize recent findings on ACS-effects under both normal conditions and in brain diseases.
  3. Ilmie MU, Jaafar H, Mansor SM, Abdullah JM
    Front Neurosci, 2015;9:189.
    PMID: 26136645 DOI: 10.3389/fnins.2015.00189
    Mitragyna speciosa Korth, or better known as ketum, has long been used by traditional folk around Southeast Asia to prevent fatigue from working under hot tropical weather and as a replacement of opium, which can then cause addiction. To date, no findings have been reported of the toxic effect of ketum subchronically (28 days). Hence, the aim of this study was to investigate the toxicity of subchronic effect of standardized methanolic extract of ketum (SMEMS) in Sprague-Dawley rats. Rats were orally administered with 100, 200, and 500 mg/kg of SMEMS for 28 days. Body weights were recorded daily. They were terminated at day 28 to obtain data for hematology, biochemistry, and histopathology of the brain, liver, kidney, lung, heart, sciatic nerve, and spinal cord. The SMEMS affected body weight compared to control group. Biochemistry findings showed that liver and kidney were affected with the abnormal values in AST, creatinine, globulin, glucose, total protein, and urea. However, SMEMS produced toxic effect more to liver, kidney, and lung than other organs as observed histopathologically. The results suggested subchronic exposure of ketum is toxic to the physiology of the animals.
  4. Prasad P, Ogawa S, Parhar IS
    Front Neurosci, 2015;9:195.
    PMID: 26097446 DOI: 10.3389/fnins.2015.00195
    The neuroendocrine mechanism regulates reproduction through the hypothalamo-pituitary-gonadal (HPG) axis which is evolutionarily conserved in vertebrates. The HPG axis is regulated by a variety of internal as well as external factors. Serotonin, a monoamine neurotransmitter, is involved in a wide range of reproductive functions. In mammals, serotonin regulates sexual behaviors, gonadotropin release and gonadotropin-release hormone (GnRH) secretion. However, the serotonin system in teleost may also play unique role in the control of reproduction as the mechanism of reproductive control in teleosts is not always the same as in the mammalian models. In fish, the serotonin system is also regulated by natural environmental factors as well as chemical substances. In particular, selective serotonin reuptake inhibitors (SSRIs) are commonly detected as pharmaceutical contaminants in the natural environment. Those factors may influence fish reproductive functions via the serotonin system. This review summarizes the functional significance of serotonin in the teleosts reproduction.
  5. Chung CH, Bretherton B, Zainalabidin S, Deuchars SA, Deuchars J, Mahadi MK
    Front Neurosci, 2020;14:906.
    PMID: 33013299 DOI: 10.3389/fnins.2020.00906
    Background: Myocardial infarction (MI) reperfusion therapy causes paradoxical cardiac complications. Following restoration of blood flow to infarcted regions, a multitude of inflammatory cells are recruited to the site of injury for tissue repair. Continual progression of cardiac inflammatory responses does, however, lead to adverse cardiac remodeling, inevitably causing heart failure.

    Main Body: Increasing evidence of the cardioprotective effects of both invasive and non-invasive vagal nerve stimulation (VNS) suggests that these may be feasible methods to treat myocardial ischemia/reperfusion injury via anti-inflammatory regulation. The mechanisms through which auricular VNS controls inflammation are yet to be explored. In this review, we discuss the potential of autonomic nervous system modulation, particularly via the parasympathetic branch, in ameliorating MI. Novel insights are provided about the activation of the cholinergic anti-inflammatory pathway on cardiac macrophages. Acetylcholine binding to the α7 nicotinic acetylcholine receptor (α7nAChR) expressed on macrophages polarizes the pro-inflammatory into anti-inflammatory subtypes. Activation of the α7nAChR stimulates the signal transducer and activator of transcription 3 (STAT3) signaling pathway. This inhibits the secretion of pro-inflammatory cytokines, limiting ischemic injury in the myocardium and initiating efficient reparative mechanisms. We highlight recent developments in the controversial auricular vagal neuro-circuitry and how they may relate to activation of the cholinergic anti-inflammatory pathway.

    Conclusion: Emerging published data suggest that auricular VNS is an inexpensive healthcare modality, mediating the dynamic balance between pro- and anti-inflammatory responses in cardiac macrophages and ameliorating cardiac ischemia/reperfusion injury.

  6. Haider HF, Bojić T, Ribeiro SF, Paço J, Hall DA, Szczepek AJ
    Front Neurosci, 2018;12:866.
    PMID: 30538616 DOI: 10.3389/fnins.2018.00866
    Tinnitus is the conscious perception of a sound without a corresponding external acoustic stimulus, usually described as a phantom perception. One of the major challenges for tinnitus research is to understand the pathophysiological mechanisms triggering and maintaining the symptoms, especially for subjective chronic tinnitus. Our objective was to synthesize the published literature in order to provide a comprehensive update on theoretical and experimental advances and to identify further research and clinical directions. We performed literature searches in three electronic databases, complemented by scanning reference lists from relevant reviews in our included records, citation searching of the included articles using Web of Science, and manual searching of the last 6 months of principal otology journals. One-hundred and thirty-two records were included in the review and the information related to peripheral and central mechanisms of tinnitus pathophysiology was collected in order to update on theories and models. A narrative synthesis examined the main themes arising from this information. Tinnitus pathophysiology is complex and multifactorial, involving the auditory and non-auditory systems. Recent theories assume the necessary involvement of extra-auditory brain regions for tinnitus to reach consciousness. Tinnitus engages multiple active dynamic and overlapping networks. We conclude that advancing knowledge concerning the origin and maintenance of specific tinnitus subtypes origin and maintenance mechanisms is of paramount importance for identifying adequate treatment.
  7. Edvall NK, Gunan E, Genitsaridi E, Lazar A, Mehraei G, Billing M, et al.
    Front Neurosci, 2019;13:879.
    PMID: 31548840 DOI: 10.3389/fnins.2019.00879
    There is increasing evidence of associations between the presence of temporomandibular joint (TMJ) disorders and tinnitus. It has been recently proposed that tinnitus patients with TMJ complaints could constitute a subtype, meaning a subgroup of tinnitus patients responsive to specific treatments. Tinnitus patients with TMJ complaints are often young women with somatosensory features of their tinnitus. Here, we investigate the socio-economic factors, phenotypic characteristics and psychological variables of tinnitus subjects from the Swedish Tinnitus Outreach Project, with (n = 486) or without (n = 1,996) TMJ complaints. The prevalence of TMJ complaints was greater in tinnitus subjects with severe tinnitus (36%) when compared to those with any tinnitus (19%), strongly indicating the contribution of TMJ problems to the severity of tinnitus. Comparing subgroups with or without TMJ complaints in the whole sample, differences were found regarding a large number of socioeconomic, phenotypic, and psychological characteristics. Subjects with TMJ complaints were more often women, more often reported stress as the cause of tinnitus, were more severely affected by tinnitus, scored worse in measures of psychological well-being and life quality, and were more often affected by problems tolerating sounds, headache, vertigo/dizziness, and neck pain. In addition, they more often reported pulsating and tonal tinnitus, somatic modulation of tinnitus, and aggravation of tinnitus by loud sounds and stress. When focusing the analysis in subjects with tinnitus as a big problem using the Tinnitus Functional Index cut-off ≥ 48, or with severe tinnitus according to the Tinnitus Handicap Inventory cut-off ≥ 58, the impact of somatosensory modulations and stress on tinnitus were greater in subjects with TMJ complaints in comparison to those without. In light of these results, we hypothesize that stress could contribute to the co-occurrence of TMJ problems and tinnitus and also to the development of severe tinnitus. Our study supports the need of involving dental care and stress management in the holistic treatment of patients with severe tinnitus.
  8. Nies YH, Mohamad Najib NH, Lim WL, Kamaruzzaman MA, Yahaya MF, Teoh SL
    Front Neurosci, 2021;15:660379.
    PMID: 33994934 DOI: 10.3389/fnins.2021.660379
    Parkinson's disease (PD) is a severely debilitating neurodegenerative disease, affecting the motor system, leading to resting tremor, cogwheel rigidity, bradykinesia, walking and gait difficulties, and postural instability. The severe loss of dopaminergic neurons in the substantia nigra pars compacta causes striatal dopamine deficiency and the presence of Lewy bodies indicates a pathological hallmark of PD. Although the current treatment of PD aims to preserve dopaminergic neurons or to replace dopamine depletion in the brain, it is notable that complete recovery from the disease is yet to be achieved. Given the complexity and multisystem effects of PD, the underlying mechanisms of PD pathogenesis are yet to be elucidated. The advancement of medical technologies has given some insights in understanding the mechanism and potential treatment of PD with a special interest in the role of microRNAs (miRNAs) to unravel the pathophysiology of PD. In PD patients, it was found that striatal brain tissue and dopaminergic neurons from the substantia nigra demonstrated dysregulated miRNAs expression profiles. Hence, dysregulation of miRNAs may contribute to the pathogenesis of PD through modulation of PD-associated gene and protein expression. This review will discuss recent findings on PD-associated miRNAs dysregulation, from the regulation of PD-associated genes, dopaminergic neuron survival, α-synuclein-induced inflammation and circulating miRNAs. The next section of this review also provides an update on the potential uses of miRNAs as diagnostic biomarkers and therapeutic tools for PD.
  9. Kawashima T, Ahmed WM, Nagino K, Ubuka T, Tsutsui K
    Front Neurosci, 2016;10:296.
    PMID: 27445667 DOI: 10.3389/fnins.2016.00296
    Most of the currently used toxicity assays for environmental chemicals use acute or chronic systemic or reproductive toxicity endpoints rather than neurobehavioral endpoints. In addition, the current standard approaches to assess reproductive toxicity are time-consuming. Therefore, with increasing numbers of chemicals being developed with potentially harmful neurobehavioral effects in higher vertebrates, including humans, more efficient means of assessing neuro- and reproductive toxicity are required. Here we discuss the use of a Galliformes-based avian test battery in which developmental toxicity is assessed by means of a combination of chemical exposure during early embryonic development using an embryo culture system followed by analyses after hatching of sociosexual behaviors such as aggression and mating and of visual memory via filial imprinting. This Galliformes-based avian test battery shows promise as a sophisticated means not only of assessing chemical toxicity in avian species but also of assessing the risks posed to higher vertebrates, including humans, which are markedly sensitive to nervous or neuroendocrine system dysfunction.
  10. Jasni F, Hamzaid NA, Mohd Syah NE, Chung TY, Abu Osman NA
    Front Neurosci, 2017;11:230.
    PMID: 28487630 DOI: 10.3389/fnins.2017.00230
    The walking mechanism of a prosthetic leg user is a tightly coordinated movement of several joints and limb segments. The interaction among the voluntary and mechanical joints and segments requires particular biomechanical insight. This study aims to analyze the inter-relationship between amputees' voluntary and mechanical coupled leg joints variables using cyclograms. From this analysis, the critical gait parameters in each gait phase were determined and analyzed if they contribute to a better powered prosthetic knee control design. To develop the cyclogram model, 20 healthy able-bodied subjects and 25 prosthesis and orthosis users (10 transtibial amputees, 5 transfemoral amputees, and 10 different pathological profiles of orthosis users) walked at their comfortable speed in a 3D motion analysis lab setting. The gait parameters (i.e., angle, moment and power for the ankle, knee and hip joints) were coupled to form 36 cyclograms relationship. The model was validated by quantifying the gait disparities of all the pathological walking by analyzing each cyclograms pairs using feed-forward neural network with backpropagation. Subsequently, the cyclogram pairs that contributed to the highest gait disparity of each gait phase were manipulated by replacing it with normal values and re-analyzed. The manipulated cyclograms relationship that showed highest improvement in terms of gait disparity calculation suggested that they are the most dominant parameters in powered-knee control. In case of transfemoral amputee walking, it was identified using this approach that at each gait sub-phase, the knee variables most responsible for closest to normal walking were: knee power during loading response and mid-stance, knee moment and knee angle during terminal stance phase, knee angle and knee power during pre-swing, knee angle at initial swing, and knee power at terminal swing. No variable was dominant during mid-swing phase implying natural pendulum effect of the lower limb between the initial and terminal swing phases. The outcome of this cyclogram adoption approach proposed an insight into the method of determining the causal effect of manipulating a particular joint's mechanical properties toward the joint behavior in an amputee's gait by determining the curve closeness, C, of the modified cyclogram curve to the normal conventional curve, to enable quantitative judgment of the effect of changing a particular parameter in the prosthetic leg gait.
  11. Paudel YN, Shaikh MF, Chakraborti A, Kumari Y, Aledo-Serrano Á, Aleksovska K, et al.
    Front Neurosci, 2018;12:628.
    PMID: 30271319 DOI: 10.3389/fnins.2018.00628
    High mobility group box protein 1 (HMGB1) is a ubiquitous nuclear protein released by glia and neurons upon inflammasome activation and activates receptor for advanced glycation end products (RAGE) and toll-like receptor (TLR) 4 on the target cells. HMGB1/TLR4 axis is a key initiator of neuroinflammation. In recent days, more attention has been paid to HMGB1 due to its contribution in traumatic brain injury (TBI), neuroinflammatory conditions, epileptogenesis, and cognitive impairments and has emerged as a novel target for those conditions. Nevertheless, HMGB1 has not been portrayed as a common prognostic biomarker for these HMGB1 mediated pathologies. The current review discusses the contribution of HMGB1/TLR4/RAGE signaling in several brain injury, neuroinflammation mediated disorders, epileptogenesis and cognitive dysfunctions and in the light of available evidence, argued the possibilities of HMGB1 as a common viable biomarker of the above mentioned neurological dysfunctions. Furthermore, the review also addresses the result of preclinical studies focused on HMGB1 targeted therapy by the HMGB1 antagonist in several ranges of HMGB1 mediated conditions and noted an encouraging result. These findings suggest HMGB1 as a potential candidate to be a common biomarker of TBI, neuroinflammation, epileptogenesis, and cognitive dysfunctions which can be used for early prediction and progression of those neurological diseases. Future study should explore toward the translational implication of HMGB1 which can open the windows of opportunities for the development of innovative therapeutics that could prevent several associated HMGB1 mediated pathologies discussed herein.
  12. Yong SJ, Tong T, Chew J, Lim WL
    Front Neurosci, 2019;13:1361.
    PMID: 32009871 DOI: 10.3389/fnins.2019.01361
    The accumulating knowledge of the host-microbiota interplay gives rise to the microbiota-gut-brain (MGB) axis. The MGB axis depicts the interkingdom communication between the gut microbiota and the brain. This communication process involves the endocrine, immune and neurotransmitters systems. Dysfunction of these systems, along with the presence of gut dysbiosis, have been detected among clinically depressed patients. This implicates the involvement of a maladaptive MGB axis in the pathophysiology of depression. Depression refers to symptoms that characterize major depressive disorder (MDD), a mood disorder with a disease burden that rivals that of heart diseases. The use of probiotics to treat depression has gained attention in recent years, as evidenced by increasing numbers of animal and human studies that have supported the antidepressive efficacy of probiotics. Physiological changes observed in these studies allow for the elucidation of probiotics antidepressive mechanisms, which ultimately aim to restore proper functioning of the MGB axis. However, the understanding of mechanisms does not yet complete the endeavor in applying probiotics to treat MDD. Other challenges remain which include the heterogeneous nature of both the gut microbiota composition and depressive symptoms in the clinical setting. Nevertheless, probiotics offer some advantages over standard pharmaceutical antidepressants, in terms of residual symptoms, side effects and stigma involved. This review outlines antidepressive mechanisms of probiotics based on the currently available literature and discusses therapeutic potentials of probiotics for depression.
  13. Bhuvanendran S, Hanapi NA, Ahemad N, Othman I, Yusof SR, Shaikh MF
    Front Neurosci, 2019;13:495.
    PMID: 31156375 DOI: 10.3389/fnins.2019.00495
    Embelin is well-known in ethnomedicine and reported to have central nervous system activities. However, there is no report on blood-brain barrier (BBB) permeability of embelin. Here the BBB permeability of embelin was evaluated using in vitro primary porcine brain endothelial cell (PBEC) model of the BBB. Embelin was also evaluated for acetylcholinesterase (AChE) inhibitory activity and docking prediction for interaction with AChE and amyloid beta (Aβ) binding sites. Embelin was found to be non-toxic to the PBECs and did not disturb the PBEC barrier function. The PBECs showed restrictive tight junctions with average transendothelial electrical resistance of 365.37 ± 113.00 Ω.cm2, for monolayers used for permeability assays. Permeability assays were conducted from apical-to-basolateral direction (blood-to-brain side). Embelin showed apparent permeability (Papp) value of 35.46 ± 20.33 × 10-6 cm/s with 85.53% recovery. In vitro AChE inhibitory assay demonstrated that embelin could inhibit the enzyme. Molecular docking study showed that embelin binds well to active site of AChE with CDOCKER interaction energy of -65.75 kcal/mol which correlates with the in vitro results. Docking of embelin with Aβ peptides also revealed the promising binding with low CDOCKER interaction energy. Thus, findings from this study indicate that embelin could be a suitable molecule to be further developed as therapeutic molecule to treat neurological disorders particularly Alzheimer's disease.
  14. Higuchi Y, Soga T, Parhar IS
    Front Neurosci, 2017;11:604.
    PMID: 29163009 DOI: 10.3389/fnins.2017.00604
    Social stress has a high impact on many biological systems in the brain, including serotonergic (5-HT) system-a major drug target in the current treatment for depression. Hyperactivity of hypothalamic-pituitary-adrenal (HPA) axis and monoamine oxidase A (MAO-A) are well-known stress responses, which are involved in the central 5-HT system. Although, many MAO-A inhibitors have been developed and used in the therapeutics of depression, effective management of depression by modulating the activity of MAO-A has not been achieved. Identifying the molecular pathways that regulate the activity of MAO-A in the brain is crucial for developing new drug targets for precise control of MAO-A activity. Over the last few decades, several regulatory pathways of MAO-A consisting of Kruppel like factor 11 (KLF11), Sirtuin1, Ring finger protein in neural stem cells (RINES), and Cell division cycle associated 7-like protein (R1) have been identified, and the influence of social stress on these regulatory factors evaluated. This review explores various aspects of these pathways to expand our understanding of the roles of the HPA axis and MAO-A regulatory pathways during social stress. The first part of this review introduces some components of the HPA axis, explains how stress affects them and how they interact with the 5-HT system in the brain. The second part summarizes the novel regulatory pathways of MAO-A, which have high potential as novel therapeutic targets for depression.
  15. Samat NA, Abdul Murad NA, Mohamad K, Abdul Razak MR, Mohamed Ibrahim N
    Front Neurosci, 2017;11:712.
    PMID: 29326545 DOI: 10.3389/fnins.2017.00712
    Background: Cognitive impairment is prevalent in Parkinson's disease (PD), affecting 15-20% of patients at diagnosis. α-synuclein expression and genetic polymorphisms of Apolipoprotein E (ApoE) have been associated with the presence of cognitive impairment in PD although data have been inconsistent. Objectives: To determine the prevalence of cognitive impairment in patients with PD using Montreal Cognitive Assessment (MoCA), Comprehensive Trail Making Test (CTMT) and Parkinson's disease-cognitive rating scale (PDCRS), and its association with plasma α-synuclein and ApoE genetic polymorphisms. Methods: This was across-sectional study involving 46 PD patients. Patients were evaluated using Montreal cognitive assessment test (MoCA), and detailed neuropsychological tests. The Parkinson's disease cognitive rating scale (PDCRS) was used for cognitive function and comprehensive trail making test (CTMT) for executive function. Blood was drawn for plasma α-synuclein measurements and ApoE genetic analysis. ApoE polymorphism was detected using MutaGELAPoE from ImmunDiagnostik. Plasma α-synuclein was detected using the ELISA Technique (USCN Life Science Inc.) according to the standard protocol. Results: Based on MoCA, 26 (56.5%) patients had mild cognitive impairment (PD-MCI) and 20 (43.5%) had normal cognition (PD-NC). Based on the PDCRS, 18 (39.1%) had normal cognition (PDCRS-NC), 17 (37%) had mild cognitive impairment (PDCRS-MCI), and 11 (23.9%) had dementia (PDCRS-PDD). In the PDCRS-MCI group, 5 (25%) patients were from PD-NC group and all PDCRS-PDD patients were from PD-MCI group. CTMT scores were significantly different between patients with MCI and normal cognition on MoCA (p = 0.003). Twenty one patients (72.4%) with executive dysfunction were from the PD-MCI group; 17 (77.3%) with severe executive dysfunction and 4 (57.1%) had mild to moderate executive dysfunction. There were no differences in the plasma α-synuclein concentration between the presence or types of cognitive impairment based on MoCA, PDCRS, and CTMT. TheApoEe4 allele carrier frequency was significantly higher in patients with executive dysfunction (p = 0.014). Conclusion: MCI was prevalent in our PD population. PDCRS appeared to be more discriminatory in detecting MCI and PDD than MoCA. Plasma α-synuclein level was not associated with presence nor type of cognitive impairment, but the ApoEe4 allele carrier status was significantly associated with executive dysfunction in PD.
  16. Zhao S, Lin H, Chi A, Gao Y
    Front Neurosci, 2023;17:986368.
    PMID: 36743803 DOI: 10.3389/fnins.2023.986368
    INTRODUCTION: Various approaches have been used to explore different aspects of the regulation of brain activity by acute exercise, but few studies have been conducted on the effects of acute exercise fatigue on large-scale brain functional networks. Therefore, the present study aimed to explore the effects of acute exercise fatigue on resting-state electroencephalogram (EEG) microstates and large-scale brain network rhythm energy.

    METHODS: The Bruce protocol was used as the experimental exercise model with a self-controlled experimental design. Thirty males performed incremental load exercise tests on treadmill until exhaustion. EEG signal acquisition was completed before and after exercise. EEG microstates and resting-state cortical rhythm techniques were used to analyze the EEG signal.

    RESULTS: The microstate results showed that the duration, occurrence, and contribution of Microstate C were significantly higher after exhaustive exercise (p's < 0.01). There was a significantly lower contribution of Microstate D (p < 0.05), a significant increase in transition probabilities between Microstate A and C (p < 0.05), and a significant decrease in transition probabilities between Microstate B and D (p < 0.05). The results of EEG rhythm energy on the large-scale brain network showed that the energy in the high-frequency β band was significantly higher in the visual network (p < 0.05).

    DISCUSSION: Our results suggest that frequently Microstate C associated with the convexity network are important for the organism to respond to internal and external information stimuli and thus regulate motor behavior in time to protect organism integrity. The decreases in Microstate D parameters, associated with the attentional network, are an important neural mechanism explaining the decrease in attention-related cognitive or behavioral performance due to acute exercise fatigue. The high energy in the high-frequency β band on the visual network can be explained in the sense of the neural efficiency hypothesis, which indicates a decrease in neural efficiency.

  17. Chen Y, Wang H, Zhang D, Zhang L, Tao L
    Front Neurosci, 2023;17:1272834.
    PMID: 37822349 DOI: 10.3389/fnins.2023.1272834
    INTRODUCTION: Diagnosing Alzheimer's disease (AD) lesions via visual examination of Electroencephalography (EEG) signals poses a considerable challenge. This has prompted the exploration of deep learning techniques, such as Convolutional Neural Networks (CNNs) and Visual Transformers (ViTs), for AD prediction. However, the classification performance of CNN-based methods has often been deemed inadequate. This is primarily attributed to CNNs struggling with extracting meaningful lesion signals from the complex and noisy EEG data.

    METHODS: In contrast, ViTs have demonstrated proficiency in capturing global signal patterns. In light of these observations, we propose a novel approach to enhance AD risk assessment. Our proposition involves a hybrid architecture, merging the strengths of CNNs and ViTs to compensate for their respective feature extraction limitations. Our proposed Dual-Branch Feature Fusion Network (DBN) leverages both CNN and ViT components to acquire texture features and global semantic information from EEG signals. These elements are pivotal in capturing dynamic electrical signal changes in the cerebral cortex. Additionally, we introduce Spatial Attention (SA) and Channel Attention (CA) blocks within the network architecture. These attention mechanisms bolster the model's capacity to discern abnormal EEG signal patterns from the amalgamated features. To make well-informed predictions, we employ a two-factor decision-making mechanism. Specifically, we conduct correlation analysis on predicted EEG signals from the same subject to establish consistency.

    RESULTS: This is then combined with results from the Clinical Neuropsychological Scale (MMSE) assessment to comprehensively evaluate the subject's susceptibility to AD. Our experimental validation on the publicly available OpenNeuro database underscores the efficacy of our approach. Notably, our proposed method attains an impressive 80.23% classification accuracy in distinguishing between AD, Frontotemporal dementia (FTD), and Normal Control (NC) subjects.

    DISCUSSION: This outcome outperforms prevailing state-of-the-art methodologies in EEG-based AD prediction. Furthermore, our methodology enables the visualization of salient regions within pathological images, providing invaluable insights for interpreting and analyzing AD predictions.

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