Displaying publications 1 - 20 of 52 in total

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  1. Waran V, Vairavan N, Sia SF, Abdullah B
    J. Neurosurg., 2009 Dec;111(6):1127-30.
    PMID: 19408977 DOI: 10.3171/2009.4.JNS081506
    The authors describe a newly developed expandable cannula to enable a more efficient use of an endoscope in removing intraparenchymal spontaneous hypertensive intracerebral hematomas. The cannula is introduced like a conventional brain cannula, using neuronavigation techniques to reach the targeted hematoma accurately, and, once deployed, conventional microsurgical techniques are used under direct endoscopic visualization. This method was used in 6 patients, and, based on the results of intraoperative intracranial pressure monitoring and postoperative CT scanning, the authors were able to achieve good hematoma removal. They found that by using the expandable cannula, efficient endoscopic surgery in the brain parenchyma was possible.
    Matched MeSH terms: Brain/physiopathology
  2. Ay B, Yildirim O, Talo M, Baloglu UB, Aydin G, Puthankattil SD, et al.
    J Med Syst, 2019 May 28;43(7):205.
    PMID: 31139932 DOI: 10.1007/s10916-019-1345-y
    Depression affects large number of people across the world today and it is considered as the global problem. It is a mood disorder which can be detected using electroencephalogram (EEG) signals. The manual detection of depression by analyzing the EEG signals requires lot of experience, tedious and time consuming. Hence, a fully automated depression diagnosis system developed using EEG signals will help the clinicians. Therefore, we propose a deep hybrid model developed using convolutional neural network (CNN) and long-short term memory (LSTM) architectures to detect depression using EEG signals. In the deep model, temporal properties of the signals are learned with CNN layers and the sequence learning process is provided through the LSTM layers. In this work, we have used EEG signals obtained from left and right hemispheres of the brain. Our work has provided 99.12% and 97.66% classification accuracies for the right and left hemisphere EEG signals respectively. Hence, we can conclude that the developed CNN-LSTM model is accurate and fast in detecting the depression using EEG signals. It can be employed in psychiatry wards of the hospitals to detect the depression using EEG signals accurately and thus aid the psychiatrists.
    Matched MeSH terms: Brain/physiopathology*
  3. Narayanan SN, Jetti R, Kesari KK, Kumar RS, Nayak SB, Bhat PG
    Environ Sci Pollut Res Int, 2019 Oct;26(30):30693-30710.
    PMID: 31463749 DOI: 10.1007/s11356-019-06278-5
    The primary objective of mobile phone technology is to achieve communication with any person at any place and time. In the modern era, it is impossible to ignore the usefulness of mobile phone technology in cases of emergency as many lives have been saved. However, the biological effects they may have on humans and other animals have been largely ignored and not been evaluated comprehensively. One of the reasons for this is the speedy uncontrollable growth of this technology which has surpassed our researching ability. Initiated with the first generation, the mobile telephony currently reaches to its fifth generation without being screened extensively for any biological effects that they may have on humans or on other animals. Mounting evidences suggest possible non-thermal biological effects of radiofrequency electromagnetic radiation (RF-EMR) on brain and behavior. Behavioral studies have particularly concentrated on the effects of RF-EMR on learning, memory, anxiety, and locomotion. The literature analysis on behavioral effects of RF-EMR demonstrates complex picture with conflicting observations. Nonetheless, numerous reports suggest a possible behavioral effect of RF-EMR. The scientific findings about this issue are presented in the current review. The possible neural and molecular mechanisms for the behavioral effects have been proposed in the light of available evidences from the literature.
    Matched MeSH terms: Brain/physiopathology
  4. Smith ES, Smith DR, Eyring C, Braileanu M, Smith-Connor KS, Ei Tan Y, et al.
    Neurobiol Learn Mem, 2019 Nov;165:106962.
    PMID: 30502397 DOI: 10.1016/j.nlm.2018.11.007
    Rett Syndrome (RTT) is a genetic disorder that is caused by mutations in the x-linked gene coding for methyl-CpG-biding-protein 2 (MECP2) and that mainly affects females. Male and female transgenic mouse models of RTT have been studied extensively, and we have learned a great deal regarding RTT neuropathology and how MeCP2 deficiency may be influencing brain function and maturation. In this manuscript we review what is known concerning structural and coinciding functional and behavioral deficits in RTT and in mouse models of MeCP2 deficiency. We also introduce our own corroborating data regarding behavioral phenotype and morphological alterations in volume of the cortex and striatum and the density of neurons, aberrations in experience-dependent plasticity within the barrel cortex and the impact of MeCP2 loss on glial structure. We conclude that regional structural changes in genetic models of RTT show great similarity to the alterations in brain structure of patients with RTT. These region-specific modifications often coincide with phenotype onset and contribute to larger issues of circuit connectivity, progression, and severity. Although the alterations seen in mouse models of RTT appear to be primarily due to cell-autonomous effects, there are also non-cell autonomous mechanisms including those caused by MeCP2-deficient glia that negatively impact healthy neuronal function. Collectively, this body of work has provided a solid foundation on which to continue to build our understanding of the role of MeCP2 on neuronal and glial structure and function, its greater impact on neural development, and potential new therapeutic avenues.
    Matched MeSH terms: Brain/physiopathology
  5. Sakharkar MK, Kashmir Singh SK, Rajamanickam K, Mohamed Essa M, Yang J, Chidambaram SB
    PLoS One, 2019;14(9):e0220995.
    PMID: 31487305 DOI: 10.1371/journal.pone.0220995
    Parkinson's disease (PD) is an irreversible and incurable multigenic neurodegenerative disorder. It involves progressive loss of mid brain dopaminergic neurons in the substantia nigra pars compacta (SN). We compared brain gene expression profiles with those from the peripheral blood cells of a separate sample of PD patients to identify disease-associated genes. Here, we demonstrate the use of gene expression profiling of brain and blood for detecting valid targets and identifying early PD biomarkers. Implementing this systematic approach, we discovered putative PD risk genes in brain, delineated biological processes and molecular functions that may be particularly disrupted in PD and also identified several putative PD biomarkers in blood. 20 of the differentially expressed genes in SN were also found to be differentially expressed in the blood. Further application of this methodology to other brain regions and neurological disorders should facilitate the discovery of highly reliable and reproducible candidate risk genes and biomarkers for PD. The identification of valid peripheral biomarkers for PD may ultimately facilitate early identification, intervention, and prevention efforts as well.
    Matched MeSH terms: Brain/physiopathology
  6. Lee PF, Kan DPX, Croarkin P, Phang CK, Doruk D
    J Clin Neurosci, 2018 Jan;47:315-322.
    PMID: 29066239 DOI: 10.1016/j.jocn.2017.09.030
    BACKGROUND: There is an unmet need for practical and reliable biomarkers for mood disorders in young adults. Identifying the brain activity associated with the early signs of depressive disorders could have important diagnostic and therapeutic implications. In this study we sought to investigate the EEG characteristics in young adults with newly identified depressive symptoms.

    METHODS: Based on the initial screening, a total of 100 participants (n = 50 euthymic, n = 50 depressive) underwent 32-channel EEG acquisition. Simple logistic regression and C-statistic were used to explore if EEG power could be used to discriminate between the groups. The strongest EEG predictors of mood using multivariate logistic regression models.

    RESULTS: Simple logistic regression analysis with subsequent C-statistics revealed that only high-alpha and beta power originating from the left central cortex (C3) have a reliable discriminative value (ROC curve >0.7 (70%)) for differentiating the depressive group from the euthymic group. Multivariate regression analysis showed that the single most significant predictor of group (depressive vs. euthymic) is the high-alpha power over C3 (p = 0.03).

    CONCLUSION: The present findings suggest that EEG is a useful tool in the identification of neurophysiological correlates of depressive symptoms in young adults with no previous psychiatric history.

    SIGNIFICANCE: Our results could guide future studies investigating the early neurophysiological changes and surrogate outcomes in depression.

    Matched MeSH terms: Brain/physiopathology*
  7. Gururaj A, Sztriha L, Hertecant J, Eapen V
    J Psychosom Res, 2006 Sep;61(3):343-7.
    PMID: 16938512
    This study aimed to determine the clinical, electroencephalographic, and radiological factors associated with medically intractable seizures in children in the Al Ain Medical District in the United Arab Emirates.
    Matched MeSH terms: Brain/physiopathology
  8. Harun MSR, Marsh V, Elsaied NA, Webb KF, Elsheikha HM
    Brain Res, 2020 11 01;1746:147002.
    PMID: 32592740 DOI: 10.1016/j.brainres.2020.147002
    Toxoplasma gondii can cause parasitic encephalitis, a life-threatening infection that predominately occurs in immunocompromised individuals. T. gondii has the ability to invade the brain, but the mechanisms by which this parasite crosses the blood-brain-barrier (BBB) remain incompletely understood. The present study reports the changes associated with infection and replication of T. gondii within human brain microvascular endothelial cells (BMECs) in vitro. Our results indicated that exposure to T. gondii had an adverse impact on the function and integrity of the BMECs - through induction of cell cycle arrest, disruption of the BMEC barrier integrity, reduction of cellular viability and vitality, depolarization of the mitochondrial membrane potential, increase of the DNA fragmentation, and alteration of the expression of immune response and tight junction genes. The calcium channel/P-glycoprotein transporter inhibitor verapamil was effective in inhibiting T. gondii crossing the BMECs in a dose-dependent manner. The present study showed that T. gondii can compromise several functions of BMECs and demonstrated the ability of verapamil to inhibit T. gondii crossing of the BMECs in vitro.
    Matched MeSH terms: Brain/physiopathology
  9. Salim MA, van der Veen FM, van Dongen JD, Franken IH
    Biol Psychol, 2015 Sep;110:50-8.
    PMID: 26188154 DOI: 10.1016/j.biopsycho.2015.07.001
    Psychopathy has been associated with behavioral adaptation deficits, which might be associated with problems in feedback and reward processing. In the present study, we examined the relation between psychopathic traits and reward processing in a passive gambling task. A total of 39 male participants who scored high (HP) and 39 male participants who scored low (LP) on the Triarchic Psychopathy Measure (TriPM), total score were tested. Feedback-related Event-Related Potentials (ERPs; i.e., P2, FRN, and P3) on predicted and unpredicted rewards and reward omissions were compared between both groups. It was found that in HP individuals, the P2 was enhanced for predicted rewards and reward omissions, but not for unpredicted stimuli. Moreover, HP individuals as compared to the LP individuals demonstrated a generally reduced P3 amplitude. The FRN amplitude, however, did not differ between the two groups. In addition, HP individuals showed enhanced reward sensitivity on the self-report level. Taken together, these findings suggest that HP individuals show enhanced sensitivity to early and reduced sensitivity to later markers of processing reinforcement learning signals, which points in the direction of compromised behavioral adaptation.
    Matched MeSH terms: Brain/physiopathology*
  10. Wang QM, Cui H, Han SJ, Black-Schaffer R, Volz MS, Lee YT, et al.
    Neurosci Lett, 2014 May 21;569:6-11.
    PMID: 24631567 DOI: 10.1016/j.neulet.2014.03.011
    Noninvasive transcranial direct current stimulation (tDCS) and methylphenidate (MP) are associated with motor recovery after stroke. Based on the potentially complementary mechanisms of these interventions, we examined whether there is an interactive effect between MP and tDCS. In this preliminary study, we randomized subacute stroke subjects to receive tDCS alone, MP alone or combination of tDCS and MP. A blinded rater measured safety, hand function, and cortical excitability before and after treatment. None of the treatments caused any major or severe adverse effects or induced significant differences in cortical excitability. Analysis of variance of gain score, as measured by Purdue pegboard test, showed a significant between-group difference (F(2,6)=12.167, p=0.008). Post hoc analysis showed that the combination treatment effected greater Purdue pegboard gain scores than tDCS alone (p=0.017) or MP alone (p=0.01). Our preliminary data with nine subjects shows an interesting dissociation between motor function improvement and lack of motor corticospinal plasticity changes as indexed by transcranial magnetic stimulation in subacute stroke subjects.
    Matched MeSH terms: Brain/physiopathology
  11. Motlagh F, Ibrahim F, Menke JM, Rashid R, Seghatoleslam T, Habil H
    J Neurosci Res, 2016 Apr;94(4):297-309.
    PMID: 26748947 DOI: 10.1002/jnr.23703
    Neuroelectrophysiological properties have been used in human heroin addiction studies. These studies vary in their approach, experimental conditions, paradigms, and outcomes. However, it is essential to integrate previous findings and experimental methods for a better demonstration of current issues and challenges in designing such studies. This Review examines methodologies and experimental conditions of neuroelectrophysiological research among heroin addicts during withdrawal, abstinence, and methadone maintenance treatment and presents the findings. The results show decrements in attentional processing and dysfunctions in brain response inhibition as well as brain activity abnormalities induced by chronic heroin abuse. Chronic heroin addiction causes increased β and α2 power activity, latency of P300 and P600, and diminished P300 and P600 amplitude. Findings confirm that electroencephalography (EEG) band power and coherence are associated with craving indices and heroin abuse history. First symptoms of withdrawal can be seen in high-frequency EEG bands, and the severity of these symptoms is associated with brain functional connectivity. EEG spectral changes and event-related potential (ERP) properties have been shown to be associated with abstinence length and tend to normalize within 3-6 months of abstinence. From the conflicting criteria and confounding effects in neuroelectrophysiological studies, the authors suggest a comprehensive longitudinal study with a multimethod approach for monitoring EEG and ERP attributes of heroin addicts from early stages of withdrawal until long-term abstinence to control the confounding effects, such as nicotine abuse and other comorbid and premorbid conditions.
    Matched MeSH terms: Brain/physiopathology*
  12. Motlagh F, Ibrahim F, Rashid R, Seghatoleslam T, Habil H
    J Neurosci Res, 2017 08;95(8):1633-1646.
    PMID: 27862172 DOI: 10.1002/jnr.23988
    This study aims to introduce a new approach of a comprehensive paradigm to evaluate brain electrophysiological properties among addicts. Electroencephalographic spectral power as well as amplitudes and latencies of mismatch negativity (MMN), P300, and P600 components were evaluated among 19 male heroin addicts and 19 healthy nonsmoker subjects using a paradigm consisting of three subparadigms, namely (1) digit span Wechsler test, (2) auditory oddball, and (3) visual cue-reactivity oddball paradigms. Task 1 provided auditory P300 and P600 in association with working memory. Task 2 provided auditory P300 as well as small and large deviant MMN event-related potential (ERPs). Finally, task 3 provided visual cue-reactivity P300. Results show that beta power was higher among heroin addicts while delta, theta, and alpha powers were decreased compared with healthy subjects. ERP analysis confirmed the decline of brain-evoked potential amplitudes when compared with healthy subjects, thus indicating a broad neurobiological vulnerability of preattentive and attentional processing including attentional deficits and compromise of discrimination abilities. The prolonged latency of ERPs reflects poor cognitive capacity in the engagement of attention and memory resources. On the other hand, an increase of attention towards the heroin-related stimuli could be concluded from the increase of P300 in the cue-reactivity condition among heroin addicts. Findings suggest that applying this paradigm in addiction studies benefits comprehensive evaluation of neuroelectrophysiological activity among addicts, which can promote a better understanding of drugs' effects on the brain as well as define new neuroelectrophysiological characteristics of addiction properties. © 2016 Wiley Periodicals, Inc.
    Matched MeSH terms: Brain/physiopathology*
  13. Motlagh F, Ibrahim F, Rashid R, Shafiabady N, Seghatoleslam T, Habil H
    Psychopharmacology (Berl), 2018 Nov;235(11):3273-3288.
    PMID: 30310960 DOI: 10.1007/s00213-018-5035-0
    Methadone as the most prevalent opioid substitution medication has been shown to influence the neurophysiological functions among heroin addicts. However, there is no firm conclusion on acute neuroelectrophysiological changes among methadone-treated subjects as well as the effectiveness of methadone in restoring brain electrical abnormalities among heroin addicts. This study aims to investigate the acute and short-term effects of methadone administration on the brain's electrophysiological properties before and after daily methadone intake over 10 weeks of treatment among heroin addicts. EEG spectral analysis and single-trial event-related potential (ERP) measurements were used to investigate possible alterations in the brain's electrical activities, as well as the cognitive attributes associated with MMN and P3. The results confirmed abnormal brain activities predominantly in the beta band and diminished information processing ability including lower amplitude and prolonged latency of cognitive responses among heroin addicts compared to healthy controls. In addition, the alteration of EEG activities in the frontal and central regions was found to be associated with the withdrawal symptoms of drug users. Certain brain regions were found to be influenced significantly by methadone intake; acute effects of methadone induction appeared to be associative to its dosage. The findings suggest that methadone administration affects cognitive performance and activates the cortical neuronal networks, resulting in cognitive responses enhancement which may be influential in reorganizing cognitive dysfunctions among heroin addicts. This study also supports the notion that the brain's oscillation powers and ERPs can be utilized as neurophysiological indices for assessing the addiction treatment traits.
    Matched MeSH terms: Brain/physiopathology
  14. Magalingam KB, Radhakrishnan A, Ping NS, Haleagrahara N
    Biomed Res Int, 2018;2018:3740461.
    PMID: 29707568 DOI: 10.1155/2018/3740461
    Neurodegenerative diseases are hereditary or sporadic conditions that result in the progressive loss of the structure and function of neurons as well as neuronal death. Although a range of diseases lie under this umbrella term, Alzheimer's disease (AD) and Parkinson's disease (PD) are the most common neurodegenerative diseases that affect a large population around the globe. Alzheimer's disease is characterized by the abnormal accumulation of extracellular amyloid-β plaques and intraneuronal neurofibrillary tangles in brain regions and manifests as a type of dementia in aged individuals that results in memory loss, multiple cognitive abnormalities, and intellectual disabilities that interfere with quality of life. Since the discovery of AD, a wealth of new information has emerged that delineates the causes, mechanisms of disease, and potential therapeutic agents, but an effective remedy to cure the diseases has not been identified yet. This could be because of the complexity of the disease process, as it involves various contributing factors that include environmental factors and genetic predispositions. This review summarizes the current understanding on neurodegenerative mechanisms that lead to the emergence of the pathology of AD.
    Matched MeSH terms: Brain/physiopathology*
  15. Hazalin NAMN, Liao P, Hassan Z
    Behav Brain Res, 2020 09 01;393:112781.
    PMID: 32619565 DOI: 10.1016/j.bbr.2020.112781
    Chronic cerebral hypoperfusion (CCH) been well characterized as a common pathological status contributing to neurodegenerative diseases such as Alzheimer's disease and vascular dementia. CCH is an important factor that leads to cognitive impairment, but the underlying neurobiological mechanism is poorly understood and no effective treatment is available. Recently, transient receptor potential melastatin 4 (TRPM4) cation channel has been identified as an important molecular element in focal cerebral ischemia. Over activation of the channel is a major molecular mechanism of oncotic cell death. However, the role of TRPM4 in CCH that propagates global brain hypoxia have not been explored. Therefore, the present study is designed to investigate the effect of TRPM4 inhibition on the cognitive functions of the rats following CCH via permanent bilateral occlusion of common carotid arteries (PBOCCA) model. In this model, treatment with siRNA suppressed TRPM4 expression at both the mRNA and protein levels and improved cognitive deficits of the CCH rats without affecting their motor function. Furthermore, treatment with siRNA rescued the LTP impairment in CCH-induced rats. Consistent with the restored of LTP, western blot analysis revealed that siRNA treatment prevented the reduction of synaptic proteins, including calcium/calmodulin-dependent kinase II alpha (CaMKIIα) and brain-derived neurotrophic factor (BDNF) in brain regions of CCH rats. The present findings provide a novel role of TRPM4 in restricting cognitive functions in CCH and suggest inhibiting TRPM4 may represent a promising therapeutic strategy in targeting ion channels to prevent the progression of cognitive deficits induced by ischemia.
    Matched MeSH terms: Brain/physiopathology
  16. Tiang N, Ahad MA, Murugaiyah V, Hassan Z
    J Pharm Pharmacol, 2020 Nov;72(11):1629-1644.
    PMID: 32743849 DOI: 10.1111/jphp.13345
    OBJECTIVES: Xanthones isolated from the pericarp of Garcinia mangostana has been reported to exhibit neuroprotective effect.

    METHODS: In this study, the effect of xanthone-enriched fraction of Garcinia mangostana (XEFGM) and α-mangostin (α-MG) were investigated on cognitive functions of the chronic cerebral hypoperfusion (CCH) rats.

    KEY FINDINGS: HPLC analysis revealed that XEFGM contained 55.84% of α-MG. Acute oral administration of XEFGM (25, 50 and 100 mg/kg) and α-MG (25 and 50 mg/kg) before locomotor activity and Morris water maze (MWM) tests showed no significant difference between the groups for locomotor activity.

    CONCLUSIONS: However, α-MG (50 mg/kg) and XEFGM (100 mg/kg) reversed the cognitive impairment induced by CCH in MWM test. α-MG (50 mg/kg) was further tested upon sub-acute 14-day treatment in CCH rats. Cognitive improvement was shown in MWM test but not in long-term potentiation (LTP). BDNF but not CaMKII was found to be down-regulated in CCH rats; however, both parameters were not affected by α-MG. In conclusion, α-MG ameliorated learning and memory deficits in both acute and sub-acute treatments in CCH rats by improving the spatial learning but not hippocampal LTP. Hence, α-MG may be a promising lead compound for CCH-associated neurodegenerative diseases, including vascular dementia and Alzheimer's disease.

    Matched MeSH terms: Brain/physiopathology
  17. Husain SF, Yu R, Tang TB, Tam WW, Tran B, Quek TT, et al.
    Sci Rep, 2020 06 16;10(1):9740.
    PMID: 32546704 DOI: 10.1038/s41598-020-66784-2
    Reduced haemodynamic response in the frontotemporal cortices of patients with major depressive disorder (MDD) has been demonstrated using functional near-infrared spectroscopy (fNIRS). Most notably, changes in cortical oxy-haemoglobin during a Japanese phonetic fluency task can differentiate psychiatric patients from healthy controls (HC). However, this paradigm has not been validated in the English language. Therefore, the present work aimed to distinguish patients with MDD from HCs, using haemodynamic response measured during an English letter fluency task. One hundred and five HCs and 105 patients with MDD took part in this study. NIRS signals during the verbal fluency task (VFT) was acquired using a 52-channel system, and changes in oxy-haemoglobin in the frontal and temporal regions were quantified. Depression severity, psychosocial functioning, pharmacotherapy and psychiatric history were noted. Patients with MDD had smaller changes in oxy-haemoglobin in the frontal and temporal cortices than HCs. In both regions of interest, oxy-haemoglobin was not associated with any of the clinical variables studied. 75.2% and 76.5% of patients with MDD were correctly classified using frontal and temporal region oxy-haemoglobin, respectively. Haemodynamic response measured by fNIRS during an English letter fluency task is a promising biomarker for MDD.
    Matched MeSH terms: Brain/physiopathology
  18. Asaduzzaman K, Reaz MB, Mohd-Yasin F, Sim KS, Hussain MS
    Adv Exp Med Biol, 2010;680:593-9.
    PMID: 20865544 DOI: 10.1007/978-1-4419-5913-3_65
    Electroencephalogram (EEG) serves as an extremely valuable tool for clinicians and researchers to study the activity of the brain in a non-invasive manner. It has long been used for the diagnosis of various central nervous system disorders like seizures, epilepsy, and brain damage and for categorizing sleep stages in patients. The artifacts caused by various factors such as Electrooculogram (EOG), eye blink, and Electromyogram (EMG) in EEG signal increases the difficulty in analyzing them. Discrete wavelet transform has been applied in this research for removing noise from the EEG signal. The effectiveness of the noise removal is quantitatively measured using Root Mean Square (RMS) Difference. This paper reports on the effectiveness of wavelet transform applied to the EEG signal as a means of removing noise to retrieve important information related to both healthy and epileptic patients. Wavelet-based noise removal on the EEG signal of both healthy and epileptic subjects was performed using four discrete wavelet functions. With the appropriate choice of the wavelet function (WF), it is possible to remove noise effectively to analyze EEG significantly. Result of this study shows that WF Daubechies 8 (db8) provides the best noise removal from the raw EEG signal of healthy patients, while WF orthogonal Meyer does the same for epileptic patients. This algorithm is intended for FPGA implementation of portable biomedical equipments to detect different brain state in different circumstances.
    Matched MeSH terms: Brain/physiopathology
  19. Sase T, Kitajo K
    PLoS Comput Biol, 2021 04;17(4):e1008929.
    PMID: 33861737 DOI: 10.1371/journal.pcbi.1008929
    Metastability in the brain is thought to be a mechanism involved in the dynamic organization of cognitive and behavioral functions across multiple spatiotemporal scales. However, it is not clear how such organization is realized in underlying neural oscillations in a high-dimensional state space. It was shown that macroscopic oscillations often form phase-phase coupling (PPC) and phase-amplitude coupling (PAC), which result in synchronization and amplitude modulation, respectively, even without external stimuli. These oscillations can also make spontaneous transitions across synchronous states at rest. Using resting-state electroencephalographic signals and the autism-spectrum quotient scores acquired from healthy humans, we show experimental evidence that the PAC combined with PPC allows amplitude modulation to be transient, and that the metastable dynamics with this transient modulation is associated with autistic-like traits. In individuals with a longer attention span, such dynamics tended to show fewer transitions between states by forming delta-alpha PAC. We identified these states as two-dimensional metastable states that could share consistent patterns across individuals. Our findings suggest that the human brain dynamically organizes inter-individual differences in a hierarchy of macroscopic oscillations with multiple timescales by utilizing metastability.
    Matched MeSH terms: Brain/physiopathology*
  20. Siddiqui A, Shah Z, Jahan RN, Othman I, Kumari Y
    Biomed Pharmacother, 2021 Dec;144:112250.
    PMID: 34607104 DOI: 10.1016/j.biopha.2021.112250
    The resin/gum of Boswellia species belonging to the family of Burseraceae is a naturally occurring mixture of bioactive compounds, which was traditionally used as a folk medicine to treat conditions like chronic inflammation. Several research studies have also explored its' therapeutic potential against multiple neurodegenerative diseases such as Alzheimer's disease (AD). The main chemical constituents of this gum include boswellic acids (BAs) like 3-O-acetyl-11-keto-β boswellic acid (AKBA) that possess potent anti-inflammatory and neuroprotective properties in AD. It is also involved in inhibiting the acetylcholinesterase (AChE) activity in the cholinergic pathway and improve choline levels as well as its binding with nicotinic receptors to produce anti-inflammatory effects. Multiple shreds of evidence have demonstrated that BAs modulate key molecular targets and signalling pathways like 5-lipoxygenase/cyclooxygenase, Nrf2, NF-kB, cholinergic, amyloid-beta (Aβ), and neurofibrillary tangles formation (NFTs) that are involved in AD progression. The present review focuses on the possible mechanistic therapeutic role of BAs in modulating the 5-LOX/COX pathway in arachidonic acid metabolism, activating Nrf2 through binding of ARE, inhibiting NF-kB and AChE activity. In addition, an inhibition of amyloid plaques (Aβ) and neurofibrillary tangles (NFTs) induced neurotoxicity and neuroinflammation in AD by BAs is also discussed in this review. We have also highlighted that BAs possess beneficial effects in AD by targeting multiple molecular pathways and makes it an emerging drug candidate for treating neurodegenerative diseases.
    Matched MeSH terms: Brain/physiopathology
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