Displaying publications 181 - 200 of 206 in total

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  1. Fulltext Brain Beta-Catenin Signalling During Stress and Depression
    Teo CH, Soga T, Parhar IS
    Neurosignals, 2018 02 22;26(1):31-42.
    PMID: 29490303 DOI: 10.1159/000487764
    Beta-catenin is a protein with dual functions in the cell, playing a role in both adhesion between cells as well as gene transcription via the canonical Wnt signalling pathway. In the canonical Wnt signalling pathway, beta-catenin again plays multiple roles. In the embryonic stage, the regulation of beta-catenin levels activates genes that govern cell proliferation and differentiation. In an adult organism, beta-catenin continues to regulate the cell cycle - as a result over-expression of beta-catenin may lead to cancer. In the brain, dysfunctions in Wnt signalling related to beta-catenin levels may also cause various pathological conditions like Alzheimer's disease, Parkinson's disease, and depression. Beta-catenin can be influenced by stressful conditions and increases in glucocorticoid levels. In addition, beta-catenin can be regulated by neurotransmitters such as serotonin and dopamine. Fluctuations in beta-catenin in brain regions under duress have been associated with depressive-like behaviours. It is theorized that the change in behaviour can be attributed to the regulation of Dicer by beta-catenin. Dicer, a protein that produces micro-RNAs in the cell, is a target gene for beta-catenin. Amongst the micro-RNA that it produces are those involved in stress resilience. In this way, beta-catenin has taken its place in the well-studied biochemistry of stress and depression, and future research into this interesting protein may yet yield fruitful results in that field.
    Matched MeSH terms: Alzheimer Disease
  2. Neuropharmacological potentials of β-carboline alkaloids for neuropsychiatric disorders
    Ayipo YO, Mordi MN, Mustapha M, Damodaran T
    Eur J Pharmacol, 2021 Feb 15;893:173837.
    PMID: 33359647 DOI: 10.1016/j.ejphar.2020.173837
    Neuropsychiatric disorders are diseases of the central nervous system (CNS) which are characterised by complex pathomechanisms that including homeostatic failure, malfunction, atrophy, pathology remodelling and reactivity anomaly of the neuronal system where treatment options remain challenging. β-Carboline (βC) alkaloids are scaffolds of structurally diverse tricyclic pyrido[3,4-b]indole alkaloid with vast occurrence in nature. Their unique structural features which favour interactions with enzymes and protein receptor targets account for their potent neuropharmacological properties. However, our current understanding of their biological mechanisms for these beneficial effects, especially for neuropsychiatric disorders is sparse. Therefore, we present a comprehensive review of the scientific progress in the last two decades on the prospective pharmacology and physiology of the βC alkaloids in the treatment of some neuropsychiatric conditions such as depression, anxiety, Alzheimer's disease, Parkinson's disease, brain tumour, essential tremor, epilepsy and seizure, licking behaviour, dystonia, agnosia, spasm, positive ingestive response as demonstrated in non-clinical models. The current evidence supports that βC alkaloids offer potential therapeutic agents against most of these disorders and amenable for further drug design.
    Matched MeSH terms: Alzheimer Disease
  3. The effects of polyphenols-rich tropical fruit juice on cognitive function and metabolomics profile - a randomized controlled trial in middle-aged women
    Rosli H, Shahar S, Rajab NF, Che Din N, Haron H
    Nutr Neurosci, 2021 Mar 05.
    PMID: 33666540 DOI: 10.1080/1028415X.2021.1880312
    Objectives: Polyphenols, particularly anthocyanins, have received attention in improving health issues during old age, including decline in cognitive function and other health parameters. We aimed to determine the effects of polyphenols-rich tropical fruit TP 3-in-1™ juice towards improving cognitive function, oxidative stress and metabolomics profiles among middle-aged women.Methods: This clinical trial involved 31 subjects with signs of poor cognitive function, as assessed using the Rey Auditory Verbal Learning Test (RAVLT). They were randomized to receive either TP 3-in-1™ juice (n = 16) or placebo (n = 15). Study subjects consumed 500 ml of beverages for three times per day, three days per week, for a period of ten weeks. Juice supplementation provided 9135 mg GAE of total phenolic content and 194.1 mg cyanidin-3-glucoside of total anthocyanin monomer.Results: There was a significant interaction effects on RAVLT immediate recall (p 
    Matched MeSH terms: Alzheimer Disease
  4. Fulltext Effects of Amyloid Precursor Protein Overexpression on NF-κB, Rho-GTPase and Pro-Apoptosis Bcl-2 Pathways in Neuronal Cells
    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: Alzheimer Disease
  5. Thioredoxin-albumin fusion protein prevents copper enhanced zinc-induced neurotoxicity via its antioxidative activity
    Tanaka KI, Shimoda M, Chuang VTG, Nishida K, Kawahara M, Ishida T, et al.
    Int J Pharm, 2018 Jan 15;535(1-2):140-147.
    PMID: 29122608 DOI: 10.1016/j.ijpharm.2017.11.012
    Zinc (Zn) is a co-factor for a vast number of enzymes, and functions as a regulator for immune mechanism and protein synthesis. However, excessive Zn release induced in pathological situations such as stroke or transient global ischemia is toxic. Previously, we demonstrated that the interaction of Zn and copper (Cu) is involved in the pathogenesis of Alzheimer's disease and vascular dementia. Furthermore, oxidative stress has been shown to play a significant role in the pathogenesis of various metal ions induced neuronal death. Thioredoxin-Albumin fusion (HSA-Trx) is a derivative of thioredoxin (Trx), an antioxidative protein, with improved plasma retention and stability of Trx. In this study, we examined the effect of HSA-Trx on Cu2+/Zn2+-induced neurotoxicity. Firstly, HSA-Trx was found to clearly suppress Cu2+/Zn2+-induced neuronal cell death in mouse hypothalamic neuronal cells (GT1-7 cells). Moreover, HSA-Trx markedly suppressed Cu2+/Zn2+-induced ROS production and the expression of oxidative stress related genes, such as heme oxygenase-1. In contrast, HSA-Trx did not affect the intracellular levels of both Cu2+ and Zn2+ after Cu2+/Zn2+ treatment. Finally, HSA-Trx was found to significantly suppress endoplasmic reticulum (ER) stress response induced by Cu2+/Zn2+ treatment in a dose dependent manner. These results suggest that HSA-Trx counteracted Cu2+/Zn2+-induced neurotoxicity by suppressing the production of ROS via interfering the related gene expressions, in addition to the highly possible radical scavenging activity of the fusion protein. Based on these findings, HSA-Trx has great potential as a promising therapeutic agent for the treatment of refractory neurological diseases.
    Matched MeSH terms: Alzheimer Disease
  6. Fulltext Lipid Peroxidation in Chronic Cerebral HypoperfusionInduced Neurodegeneration in Rats
    Anil Kumar, S., Saif, S.A., Oothuman, P., Mustafa, M.I.A.
    International Medical Journal Malaysia, 2011;10(2):3-6.
    MyJurnal
    Introduction: Reduced cerebral blood fl ow is associated with neurodegenerative disorders and dementia, in particular. Experimental evidence has demonstrated the initiating role of chronic cerebral hypoperfusion in neuronal damage to the hippocampus, the cerebral cortex, the white matter areas and the visual system. Permanent, bilateral occlusion of the common carotid arteries of rats (two vessel occlusion - 2VO) has been introduced for the reproduction of chronic cerebral hypoperfusion as it occurs in Alzheimer’s disease and human aging. Increased generation of free radicals through lipid peroxidation can damage neuronal cell membrane. Markers of lipid peroxidation have been found to be elevated in brain tissues and body fl uids in neurodegenerative diseases, including Alzheimer’s disease, Parkinson disease and amyotrophic lateral sclerosis. Materials and Methods: Malondialdehyde (MDA), fi nal product of lipid peroxidation, was estimated by thiobarbituric acid-reactive substances (TBARS) assay kit at eight weeks after induction of 2VO in the rats and control group. Results: Our study revealed a highly signifi cant (p
    Matched MeSH terms: Alzheimer Disease
  7. Fulltext Charles Bonnet syndrome: a precursor to Alzheimer disease
    Janaki, V., Rosdinom, R., Hatta, S.
    Medicine & Health, 2015;10(2):146-150.
    MyJurnal
    This case report highlights Charles Bonnet Syndrome as a precursor to the development of major neurocognitive disorder due to Alzheimer’s disease in the elderly with visual impairment and the possible differential diagnoses that could be considered. We report a case of an elderly lady with no known previous medical illness, who presented for the first time to the psychiatric clinic with complex visual hallucinations consisting of well-formed images of people and inanimate objects of long standing duration of 18 months. About a year later, there was emergence of cognitive impairment which progressed gradually accompanied by other psychotic symptoms such as auditory hallucinations and persecutory delusions. There were no affective or obsessional symptoms. She had poor insight towards her illness. Ophthalmological examination revealed significant reduction in bilateral visual acuity. Otherwise, physical examination was unremarkable. She received inpatient treatment with Rivastigmine patch 4.6 mg/24 hours and Zydis 10 mg noctre. Her cognitive impairment and psychotic symptoms gradually improved over a period of 2 weeks upon commencing treatment and on subsequent follow-ups at outpatient clinic. She had also gained some insight into her illness. Charles Bonnet syndrome could be a possible precipitating factor and precursor to the development of major neurocognitive disorder due to Alzheimer’s disease in the elderly with visual impairment which is often overlooked or misdiagnosed and hence under reported.
    Study site: Psychiatric clinic, Pusat Perubatan Universiti Kebangsaan Malaysia (PPUKM), Kuala Lumpur, Malaysia
    Matched MeSH terms: Alzheimer Disease
  8. Fulltext Development of clinical pathway for Mild Cognitive Impairment and Dementia to quantify cost of age-related cognitive disorders in Malaysia
    Syed Mohamed Aljunid, Namaitijiang Maimaiti, Zafar Ahmed, Amrizal Muhammad Nur, Norashidah Mohamed Nor, Normazwana Ismail, et al.
    Malaysian Journal of Public Health Medicine, 2014;14(3):0-0.
    MyJurnal
    As the Malaysian population ages, the burden of age-related cognitive disorders such as dementia and Alzheimer’s disease will increase concomitantly. This is one of the sub-study under a research project titled by quantify the cost of age-related cognitive impairment in Malaysia, which was undertaken to develop a clinical pathway for Mild Cognitive Impairment (MCI) and Dementia. The clinical pathway (CP) will be used to support the costing studies of MCI and Dementia. An expert group discussion (EGD) was conducted among selected experts from six (6) government hospitals from different states of Malaysia, Ministry of Health, and United Nations University, International Institute for Global Health, UKM and UPM. The expert group includes psychiatrist specialists and public health medicine specialists. A total of 15 participants took part in the EGD. The group was presented with the different approach in managing MCI and Dementia. Finally, the group came to the consensus agreement on the most appropriate and efficient ways of managing the two conditions. In the EGD, an operational definition for MCI and Dementia was agreed upon and a pathway was developed for the usual practice in the Malaysian health system. A typical case used, as a reference is a 60-year-old patient referred to a memory clinic with complaint of “forgetfulness”. After three outpatient visits in the clinic, the diagnosis of MCI and Dementia could be clinically established. The clinical pathways covered all active clinical and non-clinical management of the patient over a period of one year. The experts identified the additional resources required to manage these patients for the whole spectrum of lifetime based on the expected life expectancy. The Clinical pathway (CP) for MCI and Dementia was successfully developed in EGD with strong support from practitioners in the health system. The findings will help the researchers to identify all-important clinical activities and interventions that will be included in the costing study.
    Matched MeSH terms: Alzheimer Disease
  9. Melatonin receptors: distribution in mammalian brain and their respective putative functions
    Ng KY, Leong MK, Liang H, Paxinos G
    Brain Struct Funct, 2017 Sep;222(7):2921-2939.
    PMID: 28478550 DOI: 10.1007/s00429-017-1439-6
    Melatonin, through its different receptors, has pleiotropic functions in mammalian brain. Melatonin is secreted mainly by the pineal gland and exerts its effects via receptor-mediated and non-receptor-mediated actions. With recent advancement in neuroanatomical mapping, we may now understand better the localizations of the two G protein-coupled melatonin receptors MT1 and MT2. The abundance of these melatonin receptors in respective brain regions suggests that receptor-mediated actions of melatonin might play crucial roles in the functions of central nervous system. Hence, this review aims to summarize the distribution of melatonin receptors in the brain and to discuss the putative functions of melatonin in the retina, cerebral cortex, reticular thalamic nucleus, habenula, hypothalamus, pituitary gland, periaqueductal gray, dorsal raphe nucleus, midbrain and cerebellum. Studies on melatonin receptors in the brain are important because cumulative evidence has pointed out that melatonin receptors not only play important physiological roles in sleep, anxiety, pain and circadian rhythm, but might also be involved in the pathogenesis of a number of neurodegenerative diseases including Alzheimer's disease, Parkinson's disease and Huntington's disease.
    Matched MeSH terms: Alzheimer Disease
  10. Therapeutic potential of combined viral transduction and CRISPR/Cas9 gene editing in treating neurodegenerative diseases
    Kuruvilla J, Sasmita AO, Ling APK
    Neurol Sci, 2018 Nov;39(11):1827-1835.
    PMID: 30076486 DOI: 10.1007/s10072-018-3521-0
    BACKGROUND AND PURPOSE: The central nervous system (CNS) faces unique difficulties in attaining permanent therapy for neurodegenerative disorder (ND). Genomic level forms of therapy have garnered interest in the recent decade, with the novel CRISPR/Cas9 gene editing tool continuing to be explored due to its efficiency, safety, and adaptability to varying conditions. With the aid of viral vectors as transport vectors, the gene editing tool has produced promising in vitro and in vivo findings in study models. Thus, this review focuses on the recent advancements and update of CRISPR/Cas9 to combat neurodegenerative diseases.

    METHODS: Articles detailing potential applications of CRISPR/Cas9 in neurodegenerative settings were retrieved from PubMed and Google Scholar with the keywords "CRISPR," "gene editing," and "neurodegenerative diseases." Relevant information was collected and critically reviewed.

    RESULTS: The utility of CRISPR/Cas9 coupled with viral transduction ranges from the disruption of amyloid precursor protein (APP) production at a genomic level in Alzheimer's disease (AD) to the deletion of varying exon portions of the Dmd gene in Duchenne muscular dystrophy (DMD) which would increase dystrophin expression. This usage of CRISPR/Cas9 also extends to experimentally ameliorate the neurodegenerative effects caused by viral infections.

    CONCLUSION: The CRISPR/Cas9 gene editing tool is a powerful arsenal in the field of gene therapy and molecular medicine; hence, more research should be called to focus on the ample potential this tool has to offer in the field of neurodegenerative diseases.

    Matched MeSH terms: Alzheimer Disease
  11. Fulltext Ethanolic Extract of Orthosiphon stamineus Improves Memory in Scopolamine-Induced Amnesia Model
    Retinasamy T, Shaikh MF, Kumari Y, Othman I
    Front Pharmacol, 2019;10:1216.
    PMID: 31736744 DOI: 10.3389/fphar.2019.01216
    Alzheimer's disease (AD) is a chronic neurodegenerative brain disease which is characterized by impairment in cognitive functioning. Orthosiphon stamineus (OS) Benth. (Lamiaceae) is a medicinal plant found around Southeast Asia that has been employed as treatments for various diseases. OS extract contains many active compounds that have been shown to possess various pharmacological properties whereby in vitro studies have demonstrated neuroprotective as well as cholinesterase inhibitory effects. This study, therefore aimed at determining whether this Malaysian plant derived flavonoid can reverse scopolamine induced learning and memory dysfunction in the novel object recognition (NOR) test and the elevated plus maze (EPM) test. In the present study, rats were treated once daily with OS 50 mg/kg, 100 mg/kg, 200 mg/kg and donepezil 1 mg/kg via oral dosing and were given intraperitoneal (ip) injection of scopolamine 1 mg/kg daily to induce cognitive deficits. Rats were subjected to behavioral analysis to assess learning and memory functions and hippocampal tissues were extracted for gene expression and immunohistochemistry studies. All the three doses demonstrated improved scopolamine-induced impairment by showing shortened transfer latency as well as the higher inflexion ratio when compared to the negative control group. OS extract also exhibited memory-enhancing activity against chronic scopolamine-induced memory deficits in the long-term memory novel object recognition performance as indicated by an increase in the recognition index. OS extract was observed to have modulated the mRNA expression of CREB1, BDNF, and TRKB genes and pretreatment with OS extract were observed to have increased the immature neurons against hippocampal neurogenesis suppressed by scopolamine, which was confirmed by the DCX-positive stained cells. These research findings suggest that the OS ethanolic extract demonstrated an improving effect on memory and hence could serve as a potential therapeutic target for the treatment of neurodegenerative diseases like AD.
    Matched MeSH terms: Alzheimer Disease
  12. Protective effect of daidzein against streptozotocin-induced Alzheimer's disease via improving cognitive dysfunction and oxidative stress in rat model
    Wei J, Yang F, Gong C, Shi X, Wang G
    J Biochem Mol Toxicol, 2019 Jun;33(6):e22319.
    PMID: 30897277 DOI: 10.1002/jbt.22319
    Oxidative stress is performing an essential role in developing Alzheimer's disease (AD), and age-related disorder and other neurodegenerative diseases. In existing research, we have aimed at investigating the daidzein (4',7-dihydroxyisoflavone) effect (10 and 20 mg/kg of body weight), as a free radical scavenger and antioxidant in streptozotocin (STZ) infused AD in rat model. Daidzein treatment led to significant improvement in intracerebroventricular-streptozotocin (ICV-STZ)-induced memory and learning impairments that was evaluated by Morris water maze test and spontaneous locomotor activity. It significantly restored the alterations in malondialdehyde, catalase, superoxide dismutase, and reduced glutathione levels. In addition, histopathological observations in cerebral cortex and hippocampal areas confirmed the neuroprotective effect of daidzein. These outcomes provide experimental proof showing preventive effect of daidzein on memory, learning dysfunction and oxidative stress in case of ICV-STZ rats. In conclusion, daidzein offers a potential treatment module for various neurodegenerative disorders with regard to mental deficits like AD.
    Matched MeSH terms: Alzheimer Disease
  13. Fulltext Predisposition to Alzheimer's and Age-Related Brain Pathologies by PM2.5 Exposure: Perspective on the Roles of Oxidative Stress and TRPM2 Channel
    Wang L, Wei LY, Ding R, Feng Y, Li D, Li C, et al.
    Front Physiol, 2020;11:155.
    PMID: 32174842 DOI: 10.3389/fphys.2020.00155
    Accumulating epidemiological evidence supports that chronic exposure to ambient fine particular matters of <2.5 μm (PM2.5) predisposes both children and adults to Alzheimer's disease (AD) and age-related brain damage leading to dementia. There is also experimental evidence to show that PM2.5 exposure results in early onset of AD-related pathologies in transgenic AD mice and development of AD-related and age-related brain pathologies in healthy rodents. Studies have also documented that PM2.5 exposure causes AD-linked molecular and cellular alterations, such as mitochondrial dysfunction, synaptic deficits, impaired neurite growth, neuronal cell death, glial cell activation, neuroinflammation, and neurovascular dysfunction, in addition to elevated levels of amyloid β (Aβ) and tau phosphorylation. Oxidative stress and the oxidative stress-sensitive TRPM2 channel play important roles in mediating multiple molecular and cellular alterations that underpin AD-related cognitive dysfunction. Documented evidence suggests critical engagement of oxidative stress and TRPM2 channel activation in various PM2.5-induced cellular effects. Here we discuss recent studies that favor causative relationships of PM2.5 exposure to increased AD prevalence and AD- and age-related pathologies, and raise the perspective on the roles of oxidative stress and the TRPM2 channel in mediating PM2.5-induced predisposition to AD and age-related brain damage.
    Matched MeSH terms: Alzheimer Disease
  14. Fulltext Knowledge on Alzheimer's Disease among Public Hospitals and Health Clinics Pharmacists in the State of Selangor, Malaysia
    Mat Nuri TH, Hong YH, Ming LC, Mohd Joffry S, Othman MF, Neoh CF
    Front Pharmacol, 2017;8:739.
    PMID: 29123479 DOI: 10.3389/fphar.2017.00739
    The prevalence of Alzheimer's disease (AD) has increased with the fast growing of aging population, thereby posing great challenges to provision of care for AD patients. Pharmacists play a vital role in the management of AD; this includes recognizing early symptoms of AD, providing medication counseling to AD patients and their caretakers, and identifying potential adverse drug reactions. A comprehensive understanding of the disease progression, as well as the pharmacological therapy, is essential to provide effective care to AD patients. The level of knowledge about AD among the pharmacists, however, remains unknown. Hence, this study aimed to assess the knowledge on AD among the pharmacists in public hospitals and health clinics and its correlates. A clear picture of the characteristics associated with different levels of knowledge could facilitate the targeted re-training of pharmacists. The 30-item validated Alzheimer disease knowledge scale (ADKS) tool was pilot-tested and used in this cross-sectional study. All pharmacists, from nine public hospitals and seven public health clinics in the State of Selangor, Malaysia, were invited to participate in this cross-sectional survey. The ADKS score was computed and compared across demographics characteristics. A total of 445 pharmacists responded to the survey. These pharmacists had a moderate overall score in ADKS; nevertheless, high scores were recorded in the domains of treatment management and care giving. No difference in AD knowledge was found among pharmacists worked in public hospitals and health clinics, except for the domain of care giving (p = 0.033). Ethnicity and age group were independent predictors of ADKS score in the current study. The pharmacists in the current study had moderate AD knowledge. On-going education and training programme on AD, in particular the domains other than treatment management and care giving, should be provided to the pharmacists to ensure delivery of quality care to AD patients.
    Study site: Klinik Kesihatan, Hospitals, Selangor, Malaysia
    Matched MeSH terms: Alzheimer Disease
  15. Fulltext Germinated Brown Rice Alters Aβ(1-42) Aggregation and Modulates Alzheimer's Disease-Related Genes in Differentiated Human SH-SY5Y Cells
    Azmi NH, Ismail M, Ismail N, Imam MU, Alitheen NB, Abdullah MA
    Evid Based Complement Alternat Med, 2015;2015:153684.
    PMID: 26858770 DOI: 10.1155/2015/153684
    The pathogenesis of Alzheimer's disease involves complex etiological factors, of which the deposition of beta-amyloid (Aβ) protein and oxidative stress have been strongly implicated. We explored the effects of H2O2, which is a precursor for highly reactive hydroxyl radicals, on neurotoxicity and genes related to AD on neuronal cells. Candidate bioactive compounds responsible for the effects were quantified using HPLC-DAD. Additionally, the effects of germinated brown rice (GBR) on the morphology of Aβ(1-42) were assessed by Transmission Electron Microscopy and its regulatory effects on gene expressions were explored. The results showed that GBR extract had several phenolic compounds and γ-oryzanol and altered the structure of Aβ(1-42) suggesting an antiamyloidogenic effect. GBR was also able to attenuate the oxidative effects of H2O2 as implied by reduced LDH release and intracellular ROS generation. Furthermore, gene expression analyses showed that the neuroprotective effects of GBR were partly mediated through transcriptional regulation of multiple genes including Presenilins, APP, BACE1, BACE2, ADAM10, Neprilysin, and LRP1. Our findings showed that GBR exhibited neuroprotective properties via transcriptional regulation of APP metabolism with potential impact on Aβ aggregation. These findings can have important implications for the management of neurodegenerative diseases like AD and are worth exploring further.
    Matched MeSH terms: Alzheimer Disease
  16. Fulltext Ginger (Zingiber officinale Roscoe) in the Prevention of Ageing and Degenerative Diseases: Review of Current Evidence
    Mohd Sahardi NFN, Makpol S
    Evid Based Complement Alternat Med, 2019;2019:5054395.
    PMID: 31531114 DOI: 10.1155/2019/5054395
    Currently, the age of the population is increasing as a result of increased life expectancy. Ageing is defined as the progressive loss of physiological integrity, which can be characterized by functional impairment and high vulnerability to various types of diseases, such as diabetes, hypertension, Alzheimer's disease (AD), Parkinson's disease (PD), and atherosclerosis. Numerous studies have reported that the presence of oxidative stress and inflammation contributes to the development of these diseases. In general, oxidative stress could induce proinflammatory cytokines and reduce cellular antioxidant capacity. Increased oxidative stress levels beyond the production of antioxidant agents cause oxidative damage to biological molecules, including DNA, protein, and carbohydrates, which affects normal cell signalling, cell growth, differentiation, and apoptosis and leads to disease pathogenesis. Since oxidative stress and inflammation contribute to these diseases, ginger (Zingiber officinale Roscoe) is one of the potential herbs that can be used to reduce the level of oxidative stress and inflammation. Ginger consists of two major active components, 6-gingerol and 6-shogaol, which are essential for preventing oxidative stress and inflammation. Thus, this paper will review the effects of ginger on ageing and degenerative diseases, including AD, PD, type 2 diabetes mellitus (DM), hypertension, and osteoarthritis.
    Matched MeSH terms: Alzheimer Disease
  17. Fulltext Vitamin E-Mediated Modulation of Glutamate Receptor Expression in an Oxidative Stress Model of Neural Cells Derived from Embryonic Stem Cell Cultures
    Abd Jalil A, Khaza'ai H, Nordin N, Mansor N, Zaulkffali AS
    Evid Based Complement Alternat Med, 2017;2017:6048936.
    PMID: 29348770 DOI: 10.1155/2017/6048936
    Glutamate is the primary excitatory neurotransmitter in the central nervous system. Excessive concentrations of glutamate in the brain can be excitotoxic and cause oxidative stress, which is associated with Alzheimer's disease. In the present study, the effects of vitamin E in the form of tocotrienol-rich fraction (TRF) and alpha-tocopherol (α-TCP) in modulating the glutamate receptor and neuron injury markers in an in vitro model of oxidative stress in neural-derived embryonic stem (ES) cell cultures were elucidated. A transgenic mouse ES cell line (46C) was differentiated into a neural lineage in vitro via induction with retinoic acid. These cells were then subjected to oxidative stress with a significantly high concentration of glutamate. Measurement of reactive oxygen species (ROS) was performed after inducing glutamate excitotoxicity, and recovery from this toxicity in response to vitamin E was determined. The gene expression levels of glutamate receptors and neuron-specific enolase were elucidated using real-time PCR. The results reveal that neural cells derived from 46C cells and subjected to oxidative stress exhibit downregulation of NMDA, kainate receptor, and NSE after posttreatment with different concentrations of TRF and α-TCP, a sign of neurorecovery. Treatment of either TRF or α-TCP reduced the levels of ROS in neural cells subjected to glutamate-induced oxidative stress; these results indicated that vitamin E is a potent antioxidant.
    Matched MeSH terms: Alzheimer Disease
  18. Fulltext Effect of Edible Bird's Nest Extract on Lipopolysaccharide-Induced Impairment of Learning and Memory in Wistar Rats
    Careena S, Sani D, Tan SN, Lim CW, Hassan S, Norhafizah M, et al.
    Evid Based Complement Alternat Med, 2018;2018:9318789.
    PMID: 30186358 DOI: 10.1155/2018/9318789
    Cognitive disability is a common feature associated with a variety of neurological conditions including Alzheimer's Disease (AD), Parkinson's Disease (PD), brain injury, and stroke. Emerging evidence has demonstrated that neuroinflammation plays an important role in the development of cognitive impairment. Current available therapies are relatively ineffective in treating or preventing cognitive disabilities, thus representing an important, unfulfilled medical need. Hence, developing potential treatment is one of the major areas of research interest. Edible bird's nests (EBN) are nests formed by swiftlet's saliva containing sialic acid, which is believed to improve brain function. This present study was embarked upon to evaluate the learning and memory enhancing potential effect of EBN by using Morris water maze test in a Wistar rat model of LPS-induced neuroinflammation. LPS elicited cognitive impairment in the rats by significantly increasing the escape latency while decreasing the number of entries in the probe trial, which are coupled with increased production of proinflammatory cytokines (TNF-α, IL-1β, and IL-6) and oxidative markers (ROS and TBARS) in the hippocampus. Treatment with EBN (125 mg/kg, 250 mg/kg, and 500 mg/kg; p.o.) effectively reversed the effect of LPS on escape latency and probe trial and, in addition, inhibited the LPS-induced upregulation of proinflammatory cytokines and oxidative markers. These findings are suggestive that there is existence of neuroprotective effect contained inside the edible bird's nest.
    Matched MeSH terms: Alzheimer Disease
  19. Fulltext Recent updates in the treatment of neurodegenerative disorders using natural compounds
    Rasool M, Malik A, Qureshi MS, Manan A, Pushparaj PN, Asif M, et al.
    Evid Based Complement Alternat Med, 2014;2014:979730.
    PMID: 24864161 DOI: 10.1155/2014/979730
    Neurodegenerative diseases are characterized by protein aggregates and inflammation as well as oxidative stress in the central nervous system (CNS). Multiple biological processes are linked to neurodegenerative diseases such as depletion or insufficient synthesis of neurotransmitters, oxidative stress, abnormal ubiquitination. Furthermore, damaging of blood brain barrier (BBB) in the CNS also leads to various CNS-related diseases. Even though synthetic drugs are used for the management of Alzheimer's disease, Parkinson's disease, autism, and many other chronic illnesses, they are not without side effects. The attentions of researchers have been inclined towards the phytochemicals, many of which have minimal side effects. Phytochemicals are promising therapeutic agents because many phytochemicals have anti-inflammatory, antioxidative as well as anticholinesterase activities. Various drugs of either synthetic or natural origin applied in the treatment of brain disorders need to cross the BBB before they can be used. This paper covers various researches related to phytochemicals used in the management of neurodegenerative disorders.
    Matched MeSH terms: Alzheimer Disease
  20. Fulltext Prevalence of Poor Mental Health and Cognitive Status among Middle-Aged Adults and Its Predictors in Relation to Polyphenols Intake
    Rosli H, Shahar S, Din NC, Haron H, Rajab NF
    Malays J Med Sci, 2019 May;26(3):72-89.
    PMID: 31303852 MyJurnal DOI: 10.21315/mjms2019.26.3.6
    Background: Decline in mental health and cognitive status starts to show its sign during middle-age and is affected by dietary factors, namely the polyphenols intake. Polyphenols have received attention in improving health issues related to aging, including decline in mental health and cognitive. The aim of this study is to determine the prevalence of poor mental health and cognitive status among middle-aged adults and its predictors in relation to polyphenols intake.

    Methods: Subjects' food intakes were calculated by using dietary history questionnaire and food frequency questionnaire for polyphenols. The subjects' mental health and cognitive status were measured by general health questionnaire-28 (GHQ-28) and Rey's auditory verbal learning test (RAVLT).

    Results: More than 40% of middle-aged adults were identified as having signs of poor mental health. A total of 67.9% of the subjects had poor cognitive status according to RAVLT immediate recall. Hierarchical binary logistic regression indicated that fat intake was associated with somatic symptoms for both men [adjusted odds ratio (AOR) = 1.04; P < 0.05] and women (AOR = 1.06; P < 0.05). Intake of lignan (AOR = 1.071; P < 0.05) was associated with better RAVLT immediate recall among women. Additionally, high cholesterol (AOR = 3.14; P < 0.05) was associated with poor score of RAVLT delayed recall for women.

    Conclusions: Early detection of poor mental health and cognitive is crucial to prevent Alzheimer's disease in old age.

    Matched MeSH terms: Alzheimer Disease
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