Displaying publications 41 - 60 of 111 in total

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  1. Wang Y, Lim YY, He Z, Wong WT, Lai WF
    PMID: 33559482 DOI: 10.1080/10408398.2021.1882381
    The last decide has witnessed a growing research interest in the role of dietary phytochemicals in influencing the gut microbiota. On the other hand, recent evidence reveals that dietary phytochemicals exhibit properties of preventing and tackling symptoms of Alzheimer's disease, which is a neurodegenerative disease that has also been linked with the status of the gut microbiota over the last decade. Till now, little serious discussions, however, have been made to link recent understanding of Alzheimer's disease, dietary phytochemicals and the gut microbiota together and to review the roles played by phytochemicals in gut dysbiosis induced pathologies of Alzheimer's disease. Deciphering these connections can provide insights into the development and future use of dietary phytochemicals as anti-Alzheimer drug candidates. This review aims at presenting latest evidence in the modulating role of phytochemicals in the gut microbiota and its relevance to Alzheimer's disease and summarizing the mechanisms behind the modulative activities. Limitations of current research in this field and potential directions will also be discussed for future research on dietary phytochemicals as anti-Alzheimer agents.
    Matched MeSH terms: Neurodegenerative Diseases
  2. Kartikasalwah A, Lh N
    Biomed Imaging Interv J, 2010 Jan-Mar;6(1):e6.
    PMID: 21611066 MyJurnal DOI: 10.2349/biij.6.1.e6
    Leigh syndrome is a progressive neurodegenerative disorder of childhood. The symmetrical necrotic lesions in the basal ganglia and/or brainstem which appear as hyperintense lesions on T2-weighted MRI is characteristic and one of the essential diagnostic criteria. Recognising this MR imaging pattern in a child with neurological problems should prompt the clinician to investigate for Leigh syndrome. We present here two cases of Leigh syndrome due to different biochemical/genetic defects, and discuss the subtle differences in their MR neuroimaging features.
    Matched MeSH terms: Neurodegenerative Diseases
  3. Singh JC, Kakalij RM, Kshirsagar RP, Kumar BH, Komakula SS, Diwan PV
    Pharm Biol, 2015 May;53(5):630-6.
    PMID: 25472801 DOI: 10.3109/13880209.2014.935866
    Vanillic acid (VA), a flavoring agent used in food and drug products, obtained naturally from the plant Angelica sinensis (Oliv.) Diels (Apiaceae), used in the traditional Chinese medicine. It is reported to possess strong antioxidant, anti-inflammatory, and neuroprotective effects. However, the pharmacological effects on oxidative stress-induced neurodegeneration are not well investigated.
    Matched MeSH terms: Neurodegenerative Diseases/chemically induced; Neurodegenerative Diseases/metabolism; Neurodegenerative Diseases/prevention & control*
  4. Sahak MK, Kabir N, Abbas G, Draman S, Hashim NH, Hasan Adli DS
    PMID: 27022403 DOI: 10.1155/2016/6075679
    The loss of the ability for learning and memory is a prominent feature of dementia, which affects millions of individuals all over the world, due to either neurodegenerative diseases or brain injury. Although a lot of information is known about the pathology involved, treatment remains elusive at best. The Black Seed of Nigella sativa has been historically and religiously used for thousands of years for preventing and treating many different kinds of diseases. This review article looks at Nigella sativa and its potential role in facilitating learning and memory. The possible use of this seed's extract or compounds isolated from it, such as thymoquinone, for treating damaged brain neural tissue is discussed. The evidence presented in this paper appears to be supporting the hypothesis that this plant and/or its bioactive constituents can enhance learning and memory in health and disease in animals and humans.
    Matched MeSH terms: Neurodegenerative Diseases
  5. Singh N, Golime R, Kumar A, Roy T
    Mol Neurobiol, 2025 Jan;62(1):461-474.
    PMID: 38867111 DOI: 10.1007/s12035-024-04294-2
    Acute nerve agent exposure can kill a person within minutes or produce multiple neurotoxic effects and subsequent brain damage with potential long-term adverse outcomes. Recent abuse of nerve-agents on Syrian civilians, during Japan terrorist attacks, and personal assassinations in the UK, and Malaysia indicate their potential threat to world population. Existing nerve agent antidotes offer only incomplete protection especially, if the treatment is delayed. To develop the effective drugs, it is advantageous to elucidate the underlying mechanisms of nerve agent-induced multiple neurological impairments. This study aimed to investigate the molecular basis of neuroinflammation during nerve agent toxicity with focus on inflammasome-associated proteins and neurodegeneration. In rats, NOD-like receptor family pyrin domain containing 3 (NLRP3), and glial fibrillary acidic protein (GFAP) immunoreactivity levels were considerably increased in the hippocampus, piriform cortex, and amygdala areas after single subcutaneous soman exposure (90 µg/kg-1). Western analysis indicated a notable increase in the neuroinflammatory indicator proteins, high mobility group box 1 (HMGB1) and inducible nitric oxide synthase (iNOS) levels. The presence of fluorojade-C-stained degenerating neurons in distinct rat brain areas is indicating the neurodegeneration during nerve agent toxicity. Pre-treatment with galantamine (3 mg/kg, - 30 min) followed by post-treatment of atropine (10 mg/kg, i.m.) and midazolam (5 mg/kg, i.m.), has completely protected animals from death induced by supra-lethal dose of soman (2XLD50) and reduced the neuroinflammatory and neurodegenerative changes. Results highlight that this new prophylactic and therapeutic drug combination might be an effective treatment option for soldiers deployed in conflict areas and first responders dealing with accidental/deliberate release of nerve agents.
    Matched MeSH terms: Neurodegenerative Diseases/chemically induced; Neurodegenerative Diseases/drug therapy; Neurodegenerative Diseases/pathology
  6. Chia KY, Ng KY, Koh RY, Chye SM
    CNS Neurol Disord Drug Targets, 2018;17(9):671-679.
    PMID: 29546836 DOI: 10.2174/1871527317666180315161626
    BACKGROUND & OBJECTIVE: Protein misfolding and aggregation have been considered the common pathological hallmarks for a number of neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD) and Huntington's disease (HD). These abnormal proteins aggregates damage mitochondria and induce oxidative stress, resulting in neuronal cell death. Prolonged neuronal damage activates microglia and astrocytes, development of inflammation reaction and further promotes neurodegeneration. Thus, elimination of abnormal protein aggregates without eliciting any adverse effects are the main treatment strategies. To overcome this, recent studies have deployed single- chain fragment variable antibodies (scFvs) to target the pathological protein aggregates, such as amyloid-beta (Aβ) peptides, α-synuclein (α-syn) and Huntingtin (Htt). To date scFv has been effective at inhibiting abnormal protein aggregates formation in both in vitro and in vivo model system of AD, PD and HD.

    CONCLUSION: Currently active research is still ongoing to improve the scFv gene delivery technology, to further enhance brain penetration, intracellular stability, solubility and efficacy of scFv intrabody.

    Matched MeSH terms: Neurodegenerative Diseases/drug therapy*
  7. Putteeraj M, Lim WL, Teoh SL, Yahaya MF
    Curr Drug Targets, 2018;19(14):1710-1720.
    PMID: 29577854 DOI: 10.2174/1389450119666180326125252
    Brain ischemia is among the leading cause of death with majority of the cases are associated with ischemic strokes. It can occur in two forms of either focal or global ischemia. Neurodegenerative disorder such as Alzheimer and Parkinson diseases is also on the rise worldwide. These disorders have common similarities; i.e. they all affecting the central nervous system with debilitating effect to the patient. In this review, we look into the promising role of flavonoids, a natural bioactive compound found abundant in vegetables, fruits and traditional herbs. Treatment with flavonoids such as curcumin, lycopene, ginsenoside, vitexin and baicalin have shown promising neuroprotective effects against ischemic-induced injury. Besides anticancer, antioxidant and immunomodulation properties, flavonoid also exerts neuroprotective effects by increases neuronal viability, increases tissue perfusion and cerebral blood flow and reduce ischemic-related apoptosis. In addition, flavonoid also exerts anti-amyloidogenic effect and reduces loss of dopaminergic neurons in the brain. These results suggesting flavonoids might be able to serve as a potential therapeutic agent in brain disorders.
    Matched MeSH terms: Neurodegenerative Diseases/drug therapy*
  8. Hossen MS, Ali MY, Jahurul MHA, Abdel-Daim MM, Gan SH, Khalil MI
    Pharmacol Rep, 2017 Dec;69(6):1194-1205.
    PMID: 29128800 DOI: 10.1016/j.pharep.2017.07.002
    Honey contains many active constituents and antioxidants such as polyphenols. Polyphenols are phytochemicals, a generic term for the several thousand plant-based molecules with antioxidant properties. Many in vitro studies in human cell cultures as well as many animal studies confirm the protective effect of polyphenols on a number of diseases such as cardiovascular diseases (CVD), diabetes, cancer, neurodegenerative diseases, pulmonary diseases, liver diseases and so on. Nevertheless, it is challenging to identify the specific biological mechanism underlying individual polyphenols and to determine how polyphenols impact human health. To date, several studies have attempted to elucidate the molecular pathway for specific polyphenols acting against particular diseases. In this review, we report on the various polyphenols present in different types of honey according to their classification, source, and specific functions and discuss several of the honey polyphenols with the most therapeutic potential to exert an effect on the various pathologies of some major diseases including CVD, diabetes, cancer, and neurodegenerative diseases.
    Matched MeSH terms: Neurodegenerative Diseases/prevention & control
  9. Jaafaru MS, Abd Karim NA, Enas ME, Rollin P, Mazzon E, Abdull Razis AF
    Nutrients, 2018 May 08;10(5).
    PMID: 29738500 DOI: 10.3390/nu10050580
    Crucifer vegetables, Brassicaceae and other species of the order Brassicales, e.g., Moringaceae that are commonly consumed as spice and food, have been reported to have potential benefits for the treatment and prevention of several health disorders. Though epidemiologically inconclusive, investigations have shown that consumption of those vegetables may result in reducing and preventing the risks associated with neurodegenerative disease development and may also exert other biological protections in humans. The neuroprotective effects of these vegetables have been ascribed to their secondary metabolites, glucosinolates (GLs), and their related hydrolytic products, isothiocyanates (ITCs) that are largely investigated for their various medicinal effects. Extensive pre-clinical studies have revealed more than a few molecular mechanisms of action elucidating multiple biological effects of GLs hydrolytic products. This review summarizes the most significant and up-to-date in vitro and in vivo neuroprotective actions of sulforaphane (SFN), moringin (MG), phenethyl isothiocyanate (PEITC), 6-(methylsulfinyl) hexyl isothiocyanate (6-MSITC) and erucin (ER) in neurodegenerative diseases.
    Matched MeSH terms: Neurodegenerative Diseases/drug therapy*
  10. Choudhury H, Chellappan DK, Sengupta P, Pandey M, Gorain B
    Curr Pharm Des, 2019;25(26):2808-2827.
    PMID: 31309883 DOI: 10.2174/1381612825666190712181955
    The ubiquitous signaling nucleoside molecule, adenosine is found in different cells of the human body to provide its numerous pharmacological role. The associated actions of endogenous adenosine are largely dependent on conformational change of the widely expressed heterodimeric G-protein-coupled A1, A2A, A2B, and A3 adenosine receptors (ARs). These receptors are well conserved on the surface of specific cells, where potent neuromodulatory properties of this bioactive molecule reflected by its easy passage through the rigid blood-brainbarrier, to simultaneously act on the central nervous system (CNS). The minimal concentration of adenosine in body fluids (30-300 nM) is adequate to exert its neuromodulatory action in the CNS, whereas the modulatory effect of adenosine on ARs is the consequence of several neurodegenerative diseases. Modulatory action concerning the activation of such receptors in the CNS could be facilitated towards neuroprotective action against such CNS disorders. Our aim herein is to discuss briefly pathophysiological roles of adenosine on ARs in the modulation of different CNS disorders, which could be focused towards the identification of potential drug targets in recovering accompanying CNS disorders. Researches with active components with AR modulatory action have been extended and already reached to the bedside of the patients through clinical research in the improvement of CNS disorders. Therefore, this review consist of recent findings in literatures concerning the impact of ARs on diverse CNS disease pathways with the possible relevance to neurodegeneration.
    Matched MeSH terms: Neurodegenerative Diseases/physiopathology*
  11. Lim VKE
    Med J Malaysia, 2000 Sep;55(3):389-97; quiz 398.
    PMID: 11200726
    Over the past two decades there has been numerous new associations between chronic diseases traditionally considered non-infectious with infectious agents. This list of diseases include peptic ulcer, coronary heart disease, neuropsychiatric disorders, haematological disorders and malignancies. These associations have been made possible through improvements in diagnostic tests based on molecular biology techniques. The discovery of these associations is important as it opens up exciting opportunities for the prevention and treatment of many diseases hitherto considered incurable.
    Matched MeSH terms: Neurodegenerative Diseases/microbiology*
  12. Loh KW, Chan CY, Chiu CK, Bin Hasan MS, Kwan MK
    J Orthop Surg (Hong Kong), 2016 08;24(2):273-7.
    PMID: 27574278
    Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke (MELAS) syndrome is a progressive multisystemic neurodegenerative disorder. MELAS syndrome impairs oxidative phosphorylation and predisposes patients to lactic acidosis, particularly under metabolic stress. We report 2 siblings with MELAS-associated idiopathic scoliosis who underwent posterior spinal instrumented fusion with measures taken to minimise anaesthetic and surgical stress, blood loss, and operating time.
    Matched MeSH terms: Neurodegenerative Diseases/complications
  13. Mohamad Najib NH, Yahaya MF, Das S, Teoh SL
    Int J Neurosci, 2023 Dec;133(8):822-833.
    PMID: 34623211 DOI: 10.1080/00207454.2021.1990916
    INTRODUCTION: Parkinson's disease (PD) is the second most common neurodegenerative disease caused by selective degeneration of dopaminergic neurons in the substantia nigra. Metallothionein has been shown to act as a neuroprotectant in various brain injury. Thus, this study aims to identify the effects of full-length human metallothionein 2 peptide (hMT2) in paraquat-induced brain injury in the zebrafish.

    METHODOLOGY: A total of 80 adult zebrafish were divided into 4 groups namely control, paraquat-treated, pre-hMT2-treated, and post-hMT2-treated groups. Fish were treated with paraquat intraperitoneally every 3 days for 15 days. hMT2 were injected intracranially on day 0 (pre-treated group) and day 16 (post-treated group). Fish were sacrificed on day 22 and the brains were collected for qPCR, ELISA and immunohistochemistry analysis.

    RESULTS: qPCR analysis showed that paraquat treatment down-regulated the expression of genes related to dopamine activity and biosynthesis (dat and th1) and neuroprotective agent (bdnf). Paraquat treatment also up-regulated the expression of the mt2, smtb and proinflammatory genes (il-1α, il-1β, tnf-α and cox-2). hMT2 treatment was able to reverse the effects of paraquat. Lipid peroxidation decreased in the paraquat and pre-hMT2-treated groups. However, lipid peroxidation increased in the post-hMT2-treated group. Paraquat treatment also led to a reduction of dopaminergic neurons while their numbers showed an increase following hMT2 treatment.

    CONCLUSION: Paraquat has been identified as one of the pesticides that can cause the death of dopaminergic neurons and affect dopamine biosynthesis. Treatment with exogenous hMT2 could reverse the effects of paraquat in the zebrafish brain.

    Matched MeSH terms: Neurodegenerative Diseases*
  14. Najim N, Bathich Y, Zain MM, Hamzah AS, Shaameri Z
    Molecules, 2010 Dec 17;15(12):9340-53.
    PMID: 21169884 DOI: 10.3390/molecules15129340
    The aim of this study was to investigate the in vitro cellular activity of novel spiroisoxazoline type compounds against normal and cancer cell lines from lung tissue (Hs888Lu), neuron-phenotypic cells (SH-SY5Y), neuroblastoma (SH-SY5Y), human histiocytic lymphoma (U937), lung cancer (A549), and leukaemia (HL-60). Our bioassay program revealed that the spiroisoxazoline type compounds show cytotoxicity only in lymphoma cell lines, which is in contrast with the pyrrolidine precursor of these spiroisoxazoline compounds, where significant cytotoxicity is seen in all normal and cancer cell lines. These data suggest a tumour-specific mechanism of action. In addition these data also show that spiroisoxazoline compounds are non-toxic in the human neuronphenotypic neuroblastoma SH-SY5Y cell line, and furthermore that they might protect cells from neurodegenerative disease.
    Matched MeSH terms: Neurodegenerative Diseases/drug therapy
  15. Wong SW, Kyaw L, Ong LC, Zulfiqar AM
    J Paediatr Child Health, 2011 Apr;47(4):237-9.
    PMID: 20500432 DOI: 10.1111/j.1440-1754.2010.01739.x
    Sturge-Weber syndrome is a neurocutaneous syndrome characterised by facial port wine stain, ipsilateral leptomeningeal angioma and vascular eye abnormalities. We report a rare case of Sturge-Weber syndrome without facial nevus presenting with neonatal seizures.
    Matched MeSH terms: Neurodegenerative Diseases/physiopathology
  16. Mohd Sahardi NFN, Makpol S
    Molecules, 2023 Aug 03;28(15).
    PMID: 37570837 DOI: 10.3390/molecules28155867
    Inflammation or inflamm-aging is a chronic low-grade inflammation that contributes to numerous types of degenerative diseases among the elderly and might be impeded by introducing an anti-inflammatory agent like Moringa oleifera Lam (moringa) and Zingiber officinale Roscoe (ginger). Therefore, this paper aims to review the role of moringa and ginger in suppressing inflamm-aging to prevent degenerative diseases. Various peer-reviewed publications were searched and downloaded using the reputed search engine "Pubmed" and "Google Scholar". These materials were reviewed and tabulated. A comparison between these previous findings was made based on the mechanism of action of moringa and ginger against degenerative diseases, focusing on their anti-inflammatory properties. Many studies have reported the efficacy of moringa and ginger in type 2 diabetes mellitus, neurodegenerative disease, cardiovascular disease, cancer, and kidney disease by reducing inflammatory cytokines activities, mainly of TNF-α and IL-6. They also enhanced the activity of antioxidant enzymes, including catalase, glutathione, and superoxide dismutase. The anti-inflammatory activities can be seen by inhibiting NF-κβ activity. Thus, the anti-inflammatory potential of moringa and ginger in various types of degenerative diseases due to inflamm-aging has been shown in many recent types of research.
    Matched MeSH terms: Neurodegenerative Diseases*
  17. Cheng J, Wang H, Wei S, Mei J, Liu F, Zhang G
    Comput Biol Med, 2024 Mar;170:108000.
    PMID: 38232453 DOI: 10.1016/j.compbiomed.2024.108000
    Alzheimer's disease (AD) is a neurodegenerative disease characterized by various pathological changes. Utilizing multimodal data from Fluorodeoxyglucose positron emission tomography(FDG-PET) and Magnetic Resonance Imaging(MRI) of the brain can offer comprehensive information about the lesions from different perspectives and improve the accuracy of prediction. However, there are significant differences in the feature space of multimodal data. Commonly, the simple concatenation of multimodal features can cause the model to struggle in distinguishing and utilizing the complementary information between different modalities, thus affecting the accuracy of predictions. Therefore, we propose an AD prediction model based on de-correlation constraint and multi-modal feature interaction. This model consists of the following three parts: (1) The feature extractor employs residual connections and attention mechanisms to capture distinctive lesion features from FDG-PET and MRI data within their respective modalities. (2) The de-correlation constraint function enhances the model's capacity to extract complementary information from different modalities by reducing the feature similarity between them. (3) The mutual attention feature fusion module interacts with the features within and between modalities to enhance the modal-specific features and adaptively adjust the weights of these features based on information from other modalities. The experimental results on ADNI database demonstrate that the proposed model achieves a prediction accuracy of 86.79% for AD, MCI and NC, which is higher than the existing multi-modal AD prediction models.
    Matched MeSH terms: Neurodegenerative Diseases*
  18. Chew ZX, Lim CL, Ng KY, Chye SM, Ling APK, Koh RY
    CNS Neurol Disord Drug Targets, 2023;22(3):329-352.
    PMID: 34970960 DOI: 10.2174/1871527321666211231100255
    Parkinson's disease (PD) is a progressive neurodegenerative disease characterised by reduced dopamine levels in the substantial nigra. This may lead to typical motor features such as bradykinesia, resting tremors and rigid muscles, as well as non-motor symptoms such as neuropsychiatric symptoms, sleep disorders, autonomic dysfunction, and sensory disturbances. Inhibitors of monoamine oxidase B (MAO-B) are used to alleviate symptoms by reducing monoamine oxidase-catalysed degradation of dopamine; hence, preserving functional levels of dopamine. The very first MAO-B inhibitor used therapeutically was selegiline, followed by rasagiline, its indane derivative which has superior efficacy and selectivity. Both inhibitors can be used as monotherapy or in combination with other anti- Parkinson drugs. Safinamide, a reversible MAO-B inhibitor that utilises both dopaminergic and non-dopaminergic mechanisms, was recently approved by the European Medicines Agency (EMA) (2015) and U.S. FDA (2017) as an add-on therapy for patients with mid- or late-stage Parkinson's disease. Furthermore, MAO-B inhibitors were found to be associated with potential neuroprotective and disease modifying effects. However, evidence of their efficacy and role in PD models is scarce and warrants further investigation.
    Matched MeSH terms: Neurodegenerative Diseases*
  19. Pasupuleti VR, Sammugam L, Ramesh N, Gan SH
    Oxid Med Cell Longev, 2017;2017:1259510.
    PMID: 28814983 DOI: 10.1155/2017/1259510
    BACKGROUND: There are several health benefits that honeybee products such as honey, propolis, and royal jelly claim toward various types of diseases in addition to being food.

    SCOPE AND APPROACH: In this paper, the effects of honey, propolis, and royal jelly on different metabolic diseases, cancers, and other diseases have been reviewed. The modes of actions of these products have also been illustrated for purposes of better understanding.

    KEY FINDINGS AND CONCLUSIONS: An overview of honey, propolis, and royal jelly and their biological potentials was highlighted. The potential health benefits of honey, such as microbial inhibition, wound healing, and its effects on other diseases, are described. Propolis has been reported to have various health benefits related to gastrointestinal disorders, allergies, and gynecological, oral, and dermatological problems. Royal jelly is well known for its protective effects on reproductive health, neurodegenerative disorders, wound healing, and aging. Nevertheless, the exact mechanisms of action of honey, propolis, and royal jelly on the abovementioned diseases and activities have not been not fully elucidated, and further research is warranted to explain their exact contributions.

    Matched MeSH terms: Neurodegenerative Diseases/pathology; Neurodegenerative Diseases/prevention & control
  20. Kong YR, Tay KC, Su YX, Wong CK, Tan WN, Khaw KY
    Molecules, 2021 Jan 30;26(3).
    PMID: 33573300 DOI: 10.3390/molecules26030728
    Alkaloids are a class of secondary metabolites that can be derived from plants, fungi and marine sponges. They are widely known as a continuous source of medicine for the management of chronic disease including cancer, diabetes and neurodegenerative diseases. For example, galanthamine and huperzine A are alkaloid derivatives currently being used for the symptomatic management of neurodegenerative disease. The etiology of neurodegenerative diseases is polygenic and multifactorial including but not limited to inflammation, oxidative stress and protein aggregation. Therefore, natural-product-based alkaloids with polypharmacology modulation properties are potentially useful for further drug development or, to a lesser extent, as nutraceuticals to manage neurodegeneration. This review aims to discuss and summarise recent developments in relation to naturally derived alkaloids for neurodegenerative diseases.
    Matched MeSH terms: Neurodegenerative Diseases/drug therapy*; Neurodegenerative Diseases/metabolism
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