Displaying publications 1 - 20 of 28 in total

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  1. Ahad MA, Chear NJ, Keat LG, Has ATC, Murugaiyah V, Hassan Z
    Ageing Res Rev, 2023 Aug;89:101990.
    PMID: 37343678 DOI: 10.1016/j.arr.2023.101990
    Research employing a bio-enhanced fraction of Clitoria ternatea (CT) to treat cognitive decline in the animal model has not yet been found. This study aimed to determine the neuroprotective effect of CT root bioactive fraction (CTRF) in chronic cerebral hypoperfusion (CCH) rat model. CTRF and its major compound, clitorienolactones A (CLA), were obtained using column chromatography. A validated HPLC-UV method was employed for the standardization of CTRF. CCH rats were given orally either vehicle or fraction (10, 20 and 40 mg/kg). Behavioural and hippocampal neuroplasticity studies were conducted following 4 weeks post-surgery. The brain hippocampus was extracted for proteins and neurotransmitters analyses. HPLC analysis showed that CTRF contained 25% (w/w) of CLA. All tested doses of CTRF and CLA (10 mg/kg) significantly restored cognitive deficits and reversed the inhibition of neuroplasticity by CCH. However, only CTRF (40 mg/kg) and CLA (10 mg/kg) significantly reversed the elevation of amyloid-beta plaque. Subsequently, treatment with CTRF (40 mg/kg) and CLA (10 mg/kg) alleviated the downregulation of molecular synaptic signalling proteins levels caused by CCH. The neurotransmitters level was restored following treatment of CTRF and CLA. Our finding suggested that CTRF improves memory and neuroplasticity in CCH rats which was mainly contributed by CLA.
    Matched MeSH terms: Neuronal Plasticity
  2. Babu MGR, Kadavigere R, Koteshwara P, Sathian B, Rai KS
    Sci Rep, 2020 09 30;10(1):16177.
    PMID: 32999361 DOI: 10.1038/s41598-020-73221-x
    Studies provide evidence that practicing meditation enhances neural plasticity in reward processing areas of brain. No studies till date, provide evidence of such changes in Rajyoga meditation (RM) practitioners. The present study aimed to identify grey matter volume (GMV) changes in reward processing areas of brain and its association with happiness scores in RM practitioners compared to non-meditators. Structural MRI of selected participants matched for age, gender and handedness (n = 40/group) were analyzed using voxel-based morphometric method and Oxford Happiness Questionnaire (OHQ) scores were correlated. Significant increase in OHQ happiness scores were observed in RM practitioners compared to non-meditators. Whereas, a trend towards significance was observed in more experienced RM practitioners, on correlating OHQ scores with hours of meditation experience. Additionally, in RM practitioners, higher GMV were observed in reward processing centers-right superior frontal gyrus, left inferior orbitofrontal cortex (OFC) and bilateral precuneus. Multiple regression analysis showed significant association between OHQ scores of RM practitioners and reward processing regions right superior frontal gyrus, left middle OFC, right insula and left anterior cingulate cortex. Further, with increasing hours of RM practice, a significant positive association was observed in bilateral ventral pallidum. These findings indicate that RM practice enhances GMV in reward processing regions associated with happiness.
    Matched MeSH terms: Neuronal Plasticity/physiology*
  3. Cacha LA, Poznanski RR
    J Integr Neurosci, 2011 Dec;10(4):423-37.
    PMID: 22262534
    In earlier models, synaptic plasticity forms the basis for cellular signaling underlying learning and memory. However, synaptic computation of learning and memory in the brain remains controversial. In this paper, we discuss ways in which synaptic plasticity remodels subcellular networks by deflecting trajectories in neuronal state-space as regulating patterns for the synthesis of dynamic continuity that form cognitive networks of associable representations through endogenous dendritic coding to consolidate memory.
    Matched MeSH terms: Neuronal Plasticity/physiology*
  4. Chan HH, Leong YQ, Voon SM, Pan ML, Leong CO, Lim CL, et al.
    Rep Biochem Mol Biol, 2021 Jan;9(4):417-425.
    PMID: 33969135 DOI: 10.52547/rbmb.9.4.417
    Background: Alzheimer's disease (AD) is a neurodegenerative disorder that causes cognitive dysfunction. Previous studies have suggested that amyloid plaques, mainly comprising of amyloid-beta peptides, play a pivotal role in AD pathophysiology. This study focuses on the evaluation of the effects of amyloid precursor protein (APP) overexpression on NF-κB, Rho-GTPase and Bcl-2 mediated pro-apoptotic pathways in neuronal cells.

    Methods: A lentiviral transduction system was used to generate SH-SY5Y cells overexpressing APP. Immunoblotting was conducted to determine expression levels of NF-κB, Rho-GTPase, and Bcl-2 family proteins in the APP overexpressed cells.

    Results: In the NF-κB signaling pathway, APP-overexpressing SH-SY5Y cells showed that there was a reduction of p-NF-κB (p< 0.05) and IKKα. Subsequently, there was upregulation of protein expression of NF-Κb, IKKβ and IκBα. On the other hand, protein expression of RhoC (p< 0.05) and Rac1/2/3 was upregulated as compared to the control group. Meanwhile, a decrease in RhoA, Cdc42 (p< 0.05) and p-Rac1/cdc42 protein levels was observed in the APP-overexpressed group. Lastly, in the pro-apoptotic pathway, the expression of Bcl-2, Bid, Bok and Puma (p< 0.05) was up regulated in the APP-overexpressed group. Downregulation of Bad and Bim expression was observed in the APP-overexpressed as compared to the control group, and Bax expression remained unchanged in the APP-overexpressed group.

    Conclusion: APP overexpression regulated signaling in the NF-κB, Rho-GTPase and Bcl-2 family pathways in neuronal cells, suggesting that these are involved in promoting neuronal survival and modulating synaptic plasticity in AD. However, further studies are essential to elucidate the APP-mediated mechanism of action.

    Matched MeSH terms: Neuronal Plasticity
  5. Conlon B, Hamilton C, Meade E, Leong SL, O Connor C, Langguth B, et al.
    Sci Rep, 2022 Jun 30;12(1):10845.
    PMID: 35773272 DOI: 10.1038/s41598-022-13875-x
    More than 10% of the population suffers from tinnitus, which is a phantom auditory condition that is coded within the brain. A new neuromodulation approach to treat tinnitus has emerged that combines sound with electrical stimulation of somatosensory pathways, supported by multiple animal studies demonstrating that bimodal stimulation can elicit extensive neural plasticity within the auditory brain. More recently, in a large-scale clinical trial, bimodal neuromodulation combining sound and tongue stimulation drove significant reductions in tinnitus symptom severity during the first 6 weeks of treatment, followed by diminishing improvements during the second 6 weeks of treatment. The primary objective of the large-scale randomized and double-blinded study presented in this paper was to determine if background wideband noise as used in the previous clinical trial was necessary for bimodal treatment efficacy. An additional objective was to determine if adjusting the parameter settings after 6 weeks of treatment could overcome treatment habituation effects observed in the previous study. The primary endpoint at 6-weeks involved within-arm and between-arm comparisons for two treatment arms with different bimodal neuromodulation settings based on two widely used and validated outcome instruments, Tinnitus Handicap Inventory and Tinnitus Functional Index. Both treatment arms exhibited a statistically significant reduction in tinnitus symptoms during the first 6-weeks, which was further reduced significantly during the second 6-weeks by changing the parameter settings (Cohen's d effect size for full treatment period per arm and outcome measure ranged from - 0.7 to - 1.4). There were no significant differences between arms, in which tongue stimulation combined with only pure tones and without background wideband noise was sufficient to reduce tinnitus symptoms. These therapeutic effects were sustained up to 12 months after the treatment ended. The study included two additional exploratory arms, including one arm that presented only sound stimuli during the first 6 weeks of treatment and bimodal stimulation in the second 6 weeks of treatment. This arm revealed the criticality of combining tongue stimulation with sound for treatment efficacy. Overall, there were no treatment-related serious adverse events and a high compliance rate (83.8%) with 70.3% of participants indicating benefit. The discovery that adjusting stimulation parameters overcomes previously observed treatment habituation can be used to drive greater therapeutic effects and opens up new opportunities for optimizing stimuli and enhancing clinical outcomes for tinnitus patients with bimodal neuromodulation.
    Matched MeSH terms: Neuronal Plasticity/physiology
  6. Effendy MA, Yunusa S, Mat NH, Has ATC, Müller CP, Hassan Z
    Behav Brain Res, 2023 Feb 13;438:114169.
    PMID: 36273648 DOI: 10.1016/j.bbr.2022.114169
    Mitragynine, an indole alkaloid from the plant Mitragyna speciosa (Kratom), has been reported to modify hippocampal synaptic transmission. However, the role of glutamatergic neurotransmission modulating synaptic plasticity in mitragynine-induced synaptic changes is still unknown. Here, we determined the role of AMPA- and NMDA glutamate receptors in mitragynine-induced synaptic plasticity in the hippocampus. Male Sprague Dawley rats received either vehicle or mitragynine (10 mg/kg), with or without the AMPA receptor antagonist, NBQX (3 mg/kg), or the NMDA receptor antagonist, MK-801 (0.2 mg/kg). Field excitatory postsynaptic potentials (fEPSP) during baseline, paired-pulse facilitation (PPF) and long-term potentiation (LTP) were recorded in-vivo in the hippocampal CA1 area of anaesthetised rats. Basal synaptic transmission and LTP were significantly impaired after mitragynine, NBQX, and MK-801 alone, without an effect on PPF. Combined effects suggest a weak functional AMPA- as well as NMDA receptor antagonist action of mitragynine.
    Matched MeSH terms: Neuronal Plasticity
  7. Hanani Abdul Manan, Zamzuri Idris, Jafri Malin Abdullah, Mohammed Faruque Reza, Hazim Omar
    MyJurnal
    Neuroplasticity has been subjected to a great deal of research in the last century. Recently, significant emphasis has been
    placed on the global effect of localized plastic changes throughout the central nervous system, and on how these changes
    integrate in a pathological context. The present study aimed to demonstrate the functional cortical reorganization before
    and after surgery using magnetoencephalography (MEG) in a participant with brain tumor. Results of Visual Evoked
    Magnetic Field (VEF) based on functional MEG study revealed significantly different of MEG N100 waveforms before and
    after surgery. Larger and additional new locations for visual activation areas after the surgery were found suggesting
    neuroplasticity. The present study highlight a physiological plasticity in a teenage brain and the alterations regarding
    neural plasticity and network remodeling described in pathological contexts in higher-order visual association areas.
    Matched MeSH terms: Neuronal Plasticity
  8. Hashim NA, Abd Razak NA, Gholizadeh H, Abu Osman NA
    JMIR Serious Games, 2021 Feb 04;9(1):e17017.
    PMID: 33538698 DOI: 10.2196/17017
    BACKGROUND: Brain plasticity is an important factor in prosthesis usage. This plasticity helps with brain adaptation to learn new movement and coordination patterns needed to control a prosthetic hand. It can be achieved through repetitive muscle training that is usually very exhausting and often results in considerable reduction in patient motivation. Previous studies have shown that a playful concept in rehabilitation can increase patient engagement and perseverance.

    OBJECTIVE: This study investigated whether the inclusion of video games in the upper limb amputee rehabilitation protocol could have a beneficial impact for muscle preparation, coordination, and patient motivation among individuals who have undergone transradial upper limb amputation.

    METHODS: Ten participants, including five amputee participants and five able-bodied participants, were enrolled in 10 1-hour sessions within a 4-week rehabilitation program. In order to investigate the effects of the rehabilitation protocol used in this study, virtual reality box and block tests and electromyography (EMG) assessments were performed. Maximum voluntary contraction was measured before, immediately after, and 2 days after interacting with four different EMG-controlled video games. Participant motivation was assessed with the Intrinsic Motivation Inventory (IMI) questionnaire and user evaluation survey.

    RESULTS: Survey analysis showed that muscle strength and coordination increased at the end of training for all the participants. The results of Pearson correlation analysis indicated that there was a significant positive association between the training period and the box and block test score (r8=0.95, P

    Matched MeSH terms: Neuronal Plasticity
  9. Khairuddin S, Ngo FY, Lim WL, Aquili L, Khan NA, Fung ML, et al.
    J Clin Med, 2020 Oct 12;9(10).
    PMID: 33053848 DOI: 10.3390/jcm9103260
    Major depression contributes significantly to the global disability burden. Since the first clinical study of deep brain stimulation (DBS), over 406 patients with depression have now undergone this neuromodulation therapy, and 30 animal studies have investigated the efficacy of subgenual cingulate DBS for depression. In this review, we aim to provide a comprehensive overview of the progress of DBS of the subcallosal cingulate in humans and the medial prefrontal cortex, its rodent homolog. For preclinical animal studies, we discuss the various antidepressant-like behaviors induced by medial prefrontal cortex DBS and examine the possible mechanisms including neuroplasticity-dependent/independent cellular and molecular changes. Interestingly, the response rate of subcallosal cingulate Deep brain stimulation marks a milestone in the treatment of depression. DBS among patients with treatment-resistant depression was estimated to be approximately 54% across clinical studies. Although some studies showed its stimulation efficacy was limited, it still holds great promise as a therapy for patients with treatment-resistant depression. Overall, further research is still needed, including more credible clinical research, preclinical mechanistic studies, precise selection of patients, and customized electrical stimulation paradigms.
    Matched MeSH terms: Neuronal Plasticity
  10. Konuri A, Bhat KMR, Rai KS, Gourishetti K, Phaneendra M YS
    Anat Sci Int, 2021 Mar;96(2):197-211.
    PMID: 32944877 DOI: 10.1007/s12565-020-00574-8
    Cognitive impairment due to natural or surgical menopause is always associated with estrogen deficiency leading to reduced brain-derived neurotrophic factor (BDNF). Reduced BDNF levels in menopause affect neuronal maturation, survival, axonal and dendritic arborization and the maintenance of dendritic spine density. Conventional long-term estrogen replacement therapy reported causing the risk of venous thromboembolism and breast cancer. To overcome these undesirable effects, phytoestrogens have been used in menopause-induced condition without the risk of side effects. Therefore, the aim of the present study was to investigate the effect of dietary supplementation of fenugreek seed extract (FG) either alone or in combination with choline-DHA on BDNF and dendritic arborization of pyramidal neurons in CA1 and CA3 regions of the hippocampus in ovariectomized rats. Female Wistar rats of 9-10 months old were divided into six groups as normal control (NC); ovariectomy (OVX); OVX + FG; OVX + choline-DHA; OVX + FG + choline-DHA; and OVX + estradiol. All the groups, except NC, were ovariectomized. After 2 weeks of ovariectomy, dietary supplementation was initiated for a period of 30 days. After supplementation, behavioral studies, BDNF levels and dendritic arborization were estimated. Ovariectomized (OVX) rats showed reduced BDNF levels, dendritic branching points and dendritic intersections of pyramidal neurons in CA1 and CA3 regions of the hippocampus. OVX rats supplemented with FG with choline-DHA showed significantly improved BDNF levels, dendritic branching points and dendritic intersections. These results are demonstrating that FG with choline-DHA supplementation can be an alternative for estrogen replacement therapy to modulate menopause-induced learning and memory deficits.
    Matched MeSH terms: Neuronal Plasticity/drug effects*
  11. Li P, Huang W, Chen Y, Aslam MS, Cheng W, Huang Y, et al.
    Neural Plast, 2023;2023:1474841.
    PMID: 37179843 DOI: 10.1155/2023/1474841
    PURPOSE: To explore the therapeutic efficiency of acupuncture and the related molecular mechanism of neural plasticity in depression.

    METHODS: Chronic unpredictable mild stress- (CUMS-) induced rats were established for the depression animal model. There were a total of four rat groups, including the control group, the CUMS group, the CUMS+acupuncture group, and the CUMS+fluoxetine group. The acupuncture group and the fluoxetine group were given a 3-week treatment after the modeling intervention. The researcher performed the open-field, elevated plus maze, and sucrose preference tests to evaluate depressive behaviors. The number of nerve cells, dendrites' length, and the prefrontal cortex's spine density were detected using Golgi staining. The prefrontal cortex expression, such as BDNF, PSD95, SYN, and PKMZ protein, was detected using the western blot and RT-PCR.

    RESULTS: Acupuncture could alleviate depressive-like behaviors and promote the recovery of the neural plasticity functions in the prefrontal cortex, showing the increasing cell numbers, prolonging the length of the dendrites, and enhancing the spine density. The neural plasticity-related proteins in the prefrontal cortex, including BDNF, PSD95, SYN, and PKMZ, were all downregulated in the CUMS-induced group; however, these effects could be partly reversed after being treated by acupuncture and fluoxetine (P < 0.05).

    CONCLUSION: Acupuncture can ameliorate depressive-like behaviors by promoting the recovery of neural plasticity functions and neural plasticity-related protein upregulation in the prefrontal cortex of CUMS-induced depressed rats. Our study provides new insights into the antidepressant approach, and further studies are warranted to elucidate the mechanisms of acupuncture involved in depression treatment.

    Matched MeSH terms: Neuronal Plasticity/physiology
  12. Lu GL, Lee MT, Chiou LC
    Addict Biol, 2019 11;24(6):1153-1166.
    PMID: 30276922 DOI: 10.1111/adb.12672
    Orexins (also called hypocretins) are implicated in reward and addiction, but little is known about their role(s) in the association between hippocampal synaptic plasticity and drug preference. Previously, we found that exogenous orexin via OX1 and OX2 receptors can impair low frequency stimulation-induced depotentiation, i.e. restoring potentiation of excitatory synaptic transmission (re-potentiation) in mouse hippocampal slices. Here, we found this re-potentiation in hippocampal slices from mice that had acquired conditioned place preference (CPP) to cocaine. Both 10 and 20 mg/kg of cocaine induced similar magnitudes of CPP in mice and re-potentiation in their hippocampal slices, but differed in their susceptibility to TCS1102, a dual (OX1 and OX2 ) orexin receptor antagonist. TCS1102 significantly attenuated CPP and hippocampal re-potentiation induced by cocaine at 10 mg/kg but not at 20 mg/kg. Nonetheless, SCH23390, an antagonist of dopamine D1-like receptors (D1-likeRs), inhibited the effects induced by both doses of cocaine. SKF38393, a D1-likeR-selective agonist, also induced hippocampal re-potentiation in vitro. Interestingly, this effect was attenuated by TCS1102. Conversely, SCH23390 prevented orexin A-induced hippocampal re-potentiation. These results suggest that endogenous orexins are released in mice during cocaine-CPP acquisition, which sustains potentiated hippocampal transmission via OX1 /OX2 receptors and may contribute to the addiction memory of cocaine. This effect of endogenous orexins, however, may be substituted by dopamine that may dominate hippocampal re-potentiation and CPP via D1-likeRs when the reinforcing effect of cocaine is high.
    Matched MeSH terms: Neuronal Plasticity*
  13. Mijanur Rahman M, Gan SH, Khalil MI
    PMID: 24876885 DOI: 10.1155/2014/958721
    Honey is the only insect-derived natural product with therapeutic, traditional, spiritual, nutritional, cosmetic, and industrial value. In addition to having excellent nutritional value, honey is a good source of physiologically active natural compounds, such as polyphenols. Unfortunately, there are very few current research projects investigating the nootropic and neuropharmacological effects of honey, and these are still in their early stages. Raw honey possesses nootropic effects, such as memory-enhancing effects, as well as neuropharmacological activities, such as anxiolytic, antinociceptive, anticonvulsant, and antidepressant activities. Research suggests that the polyphenol constituents of honey can quench biological reactive oxygen species and counter oxidative stress while restoring the cellular antioxidant defense system. Honey polyphenols are also directly involved in apoptotic activities while attenuating microglia-induced neuroinflammation. Honey polyphenols are useful in improving memory deficits and can act at the molecular level. Therefore, the ultimate biochemical impact of honey on specific neurodegenerative diseases, apoptosis, necrosis, neuroinflammation, synaptic plasticity, and behavior-modulating neural circuitry should be evaluated with appropriate mechanistic approaches using biochemical and molecular tools.
    Matched MeSH terms: Neuronal Plasticity
  14. Mohamed RMP, Kumar J, Yap E, Mohamed IN, Sidi H, Adam RL, et al.
    Curr Drug Targets, 2019;20(2):158-165.
    PMID: 28641520 DOI: 10.2174/1389450118666170622092824
    Memories associated with substance use disorders, or substance-associated cues increase the likelihood of craving and relapse during abstinence. There is a growing consensus that manipulation of synaptic plasticity may reduce the strength of substance abuse-related memories. On the biological front, there are new insights that suggest memories associated with substance use disorder may follow unique neurobiological pathways that render them more accessible to pharmacological intervention. In parallel to this, research in neurochemistry has identified several potential candidate molecules that could influence the formation and maintenance of long-term memory. Drugs that target these molecules (blebbistatin, isradipine and zeta inhibitory peptide) have shown promise at the preclinical stage. In this review, we shall provide an overview of the evolving understanding on the biochemical mechanisms involved in memory formation and expound on the premise that substance use disorder is a learning disorder.
    Matched MeSH terms: Neuronal Plasticity/drug effects
  15. Mohandas Rao KG, Muddanna Rao S, Gurumadhva Rao S
    Evid Based Complement Alternat Med, 2006 Sep;3(3):349-57.
    PMID: 16951719
    Centella asiatica (CeA) is a creeping plant growing in damp places in India and other Asian countries. The leaves of CeA are used for memory enhancement in the Ayurvedic system of medicine, an alternative system of medicine in India. In this study, we have investigated the effect during the rat growth spurt period of CeA fresh leaf extract treatment on the dendritic morphology of hippocampal CA3 neurons, one of the regions of the brain concerned with learning and memory. Neonatal rat pups (7 days old) were fed with 2, 4 or 6 ml kg(-1) body weight of fresh leaf extract of CeA for 2, 4 or 6 weeks. After the treatment period the rats were killed, their brains were removed and the hippocampal neurons were impregnated with silver nitrate (Golgi staining). Hippocampal CA3 neurons were traced using a camera lucida, and dendritic branching points (a measure of dendritic arborization) and intersections (a measure of dendritic length) were quantified. These data were compared with data for age-matched control rats. The results showed a significant increase in the dendritic length (intersections) and dendritic branching points along the length of both apical and basal dendrites in rats treated with 4 and 6 ml kg(-1) body weight per day of CeA for longer periods of time (i.e. 4 and 6 weeks). We conclude that the constituents/active principles present in CeA fresh leaf extract have a neuronal dendritic growth stimulating property; hence, the extract can be used for enhancing neuronal dendrites in stress and neurodegenerative and memory disorders.
    Matched MeSH terms: Neuronal Plasticity
  16. Muslimov IA, Tuzhilin A, Tang TH, Wong RK, Bianchi R, Tiedge H
    J. Cell Biol., 2014 May 26;205(4):493-510.
    PMID: 24841565 DOI: 10.1083/jcb.201310045
    A key determinant of neuronal functionality and plasticity is the targeted delivery of select ribonucleic acids (RNAs) to synaptodendritic sites of protein synthesis. In this paper, we ask how dendritic RNA transport can be regulated in a manner that is informed by the cell's activity status. We describe a molecular mechanism in which inducible interactions of noncanonical RNA motif structures with targeting factor heterogeneous nuclear ribonucleoprotein (hnRNP) A2 form the basis for activity-dependent dendritic RNA targeting. High-affinity interactions between hnRNP A2 and conditional GA-type RNA targeting motifs are critically dependent on elevated Ca(2+) levels in a narrow concentration range. Dendritic transport of messenger RNAs that carry such GA motifs is inducible by influx of Ca(2+) through voltage-dependent calcium channels upon β-adrenergic receptor activation. The combined data establish a functional correspondence between Ca(2+)-dependent RNA-protein interactions and activity-inducible RNA transport in dendrites. They also indicate a role of genomic retroposition in the phylogenetic development of RNA targeting competence.
    Matched MeSH terms: Neuronal Plasticity/genetics*
  17. Noh NA
    Malays J Med Sci, 2016 Jul;23(4):5-16.
    PMID: 27660540 MyJurnal DOI: 10.21315/mjms2016.23.4.2
    Transcranial magnetic stimulation (TMS) is a non-invasive, non-pharmacological technique that is able to modulate cortical activity beyond the stimulation period. The residual aftereffects are akin to the plasticity mechanism of the brain and suggest the potential use of TMS for therapy. For years, TMS has been shown to transiently improve symptoms of neuropsychiatric disorders, but the underlying neural correlates remain elusive. Recently, there is evidence that altered connectivity of brain network dynamics is the mechanism underlying symptoms of various neuropsychiatric illnesses. By combining TMS and electroencephalography (EEG), the functional connectivity patterns among brain regions, and the causal link between function or behaviour and a specific brain region can be determined. Nonetheless, the brain network connectivity are highly complex and involve the dynamics interplay among multitude of brain regions. In this review article, we present previous TMS-EEG co-registration studies, which explore the functional connectivity patterns of human cerebral cortex. We argue the possibilities of neural correlates of long-term potentiation/depression (LTP-/LTD)-like mechanisms of synaptic plasticity that drive the TMS aftereffects as shown by the dissociation between EEG and motor evoked potentials (MEP) cortical output. Here, we also explore alternative explanations that drive the EEG oscillatory modulations post TMS. The precise knowledge of the neurophysiological mechanisms underlying TMS will help characterise disturbances in oscillatory patterns, and the altered functional connectivity in neuropsychiatric illnesses.
    Matched MeSH terms: Neuronal Plasticity
  18. Pati S, Muthuraju S, Hadi RA, Huat TJ, Singh S, Maletic-Savatic M, et al.
    Curr Stem Cell Res Ther, 2016;11(2):149-57.
    PMID: 26763886
    Traumatic brain injury (TBI) imposes horrendous neurophysiological alterations leading to most devastating forms of neuro-disability. Which includes impaired cognition, distorted locomotors activity and psychosomatic disability in both youths and adults. Emerging evidence from recent studies has identified mesenchymal stem cells (MSCs) as one of the promising category of stem cells having excellent neuroregenerative capability in TBI victims. Some of the clinical and animal studies reported that MSCs transplantation could cure neuronal damage as well as improve cognitive and locomotors behaviors in TBI. However, mechanism behind their broad spectrum neuroregenerative potential in TBI has not been reviewed yet. Therefore, in the present article, we present a comprehensive data on the important attributes of MSCs, such as neurotransdifferentiation, neuroprotection, axonal repair and plasticity, maintenance of blood-brain integrity, reduction of reactive oxygen species (ROS) and immunomodulation. We have reviewed in detail the crucial neurogenic capabilities of MSCs in vivo and provided consolidated knowledge regarding their cellular remodeling in TBI for future therapeutic implications.
    Matched MeSH terms: Neuronal Plasticity/genetics
  19. Rahayu UB, Wibowo S, Setyopranoto I, Hibatullah Romli M
    NeuroRehabilitation, 2020;47(4):463-470.
    PMID: 33164953 DOI: 10.3233/NRE-203210
    BACKGROUND: Brain injuries such as strokes cause damage and death of the neuron cells. Physiotherapy interventions help to improve patient's performance and ability. However, this is only theorized but the impact of the physiotherapy intervention on brain plasticity is not known.

    OBJECTIVE: The present study aimed to investigate the effect of physiotherapy interventions on brain neuroplasticity by evaluating the brain plasticity regeneration, balance and functional ability.

    METHODS: A randomized controlled trial was conducted with 64 stroke patients from three hospitals in the Surakarta region, Indonesia. Control groups (n = 32) received conventional physiotherapy and intervention groups (n = 32) received neurorestoration protocol, which both lasted for seven days. Efficacy of the interventions were measured on brain-derived neurotropic factor serum analysis, Berg Balance Scale and Barthel Index, respectively.

    RESULTS: Both groups showed improvements in all parameters but only balance and functional performance had a statistically significant outcome.

    CONCLUSION: Neurorestoration protocol that combined several established physiotherapy interventions was effective in improving balance and functional ability of stroke patients in only a seven days period.

    Matched MeSH terms: Neuronal Plasticity/physiology*
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