Displaying publications 1 - 20 of 48 in total

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  1. Development of the clinical assessment scale in autoimmune encephalitis
    Lim JA, Lee ST, Moon J, Jun JS, Kim TJ, Shin YW, et al.
    Ann Neurol, 2019 03;85(3):352-358.
    PMID: 30675918 DOI: 10.1002/ana.25421
    OBJECTIVE: There is no scale for rating the severity of autoimmune encephalitis (AE). In this study, we aimed to develop a novel scale for rating severity in patients with diverse AE syndromes and to verify the reliability and validity of the developed scale.

    METHODS: The key items were generated by a panel of experts and selected according to content validity ratios. The developed scale was initially applied to 50 patients with AE (development cohort) to evaluate its acceptability, reproducibility, internal consistency, and construct validity. Then, the scale was applied to another independent cohort (validation cohort, n = 38).

    RESULTS: A new scale consisting of 9 items (seizure, memory dysfunction, psychiatric symptoms, consciousness, language problems, dyskinesia/dystonia, gait instability and ataxia, brainstem dysfunction, and weakness) was developed. Each item was assigned a value of up to 3 points. The total score could therefore range from 0 to 27. We named the scale the Clinical Assessment Scale in Autoimmune Encephalitis (CASE). The new scale showed excellent interobserver (intraclass correlation coefficient [ICC] = 0.97) and intraobserver (ICC = 0.96) reliability for total scores, was highly correlated with modified Rankin scale (r = 0.86, p

    Matched MeSH terms: Memory Disorders/etiology; Memory Disorders/physiopathology
  2. Beneficial effects of TQRF and TQ nano- and conventional emulsions on memory deficit, lipid peroxidation, total antioxidant status, antioxidants genes expression and soluble Aβ levels in high fat-cholesterol diet-induced rats
    Ismail N, Ismail M, Azmi NH, Bakar MFA, Yida Z, Stanslas J, et al.
    Chem Biol Interact, 2017 Sep 25;275:61-73.
    PMID: 28734741 DOI: 10.1016/j.cbi.2017.07.014
    The study determined the effect of thymoquinone rich fraction (TQRF) and thymoquinone (TQ) in the forms of nano- and conventional emulsions on learning and memory, lipid peroxidation, total antioxidant status, antioxidants genes expression and soluble β-amyloid (Aβ) levels in rats fed with a high fat-cholesterol diet (HFCD). The TQRF was extracted from Nigella sativa seeds using a supercritical fluid extraction system and prepared into nanoemulsion, which later named as TQRF nanoemulsion (TQRFNE). Meanwhile, TQ was acquired commercially and prepared into thymoquinone nanoemulsion (TQNE). The TQRF and TQ conventional emulsions (CE), named as TQRFCE and TQCE, respectively were studied for comparison. Statin (simvastatin) and non-statin (probucol) cholesterol-lowering agents, and a mild-to-severe Alzheimer's disease drug (donepezil) were served as control drugs. The Sprague Dawley rats were fed with HFCD for 6 months, and treated with the intervention groups via oral gavage daily for the last 3 months. As a result, HFCD-fed rats exhibited hypercholesterolaemia, accompanied by memory deficit, increment of lipid peroxidation and soluble Aβ levels, decrement of total antioxidant status and down-regulation of antioxidants genes expression levels. TQRFNE demonstrated comparable effects to the other intervention groups and control drugs in serum biomarkers as well as in the learning and memory test. Somehow, TQRFNE was more prominent than those intervention groups and control drugs in brain biomarkers concomitant to gene and protein expression levels. Supplementation of TQRFNE into an HFCD thus could ameliorate memory deficit, lipid peroxidation and soluble Aβ levels as well as improving the total antioxidant status and antioxidants genes expression levels.
    Matched MeSH terms: Memory Disorders/drug therapy
  3. Fulltext Protective effect of mangiferin on memory impairment: A systematic review
    Lum PT, Sekar M, Gan SH, Pandy V, Bonam SR
    Saudi J Biol Sci, 2021 Jan;28(1):917-927.
    PMID: 33424383 DOI: 10.1016/j.sjbs.2020.11.037
    Memory impairment (MI) is one of the predominant criteria generally used to identify schizophrenia, dementia and amnesia that are associated with neurodegenerative disorders by evaluating patient's cognitive symptoms. To date, there is no available treatment that can completely mitigate MI. Currently, there is a trend in recent investigations towards symptomatic therapy approaches using a variety of natural compounds. Mangiferin is one of them that have been investigated extensively. Mangiferin is a naturally occurring potent glucoxilxanthone and is mainly isolated from the Mangifera indica (Mango) plant. This review is aimed at providing a comprehensive overview on the efficacy of mangiferin on MI, based on in-vivo animal studies. After screening through articles identified from Scopus and PubMed based on the inclusion and exclusion criteria, a total of 11 articles between 2009 and 2019 were included. The minimum and maximum dose of mangiferin were 10 and 200 mg/kg respectively and administered over the period of 12-154 days. The results of 11 articles showed that mangiferin effectively improved spatial recognition, episodic aversive events, short- and long-term memories primarily occurring via its antioxidant and anti-inflammatory effects. The outcomes of the review revealed that mangiferin improves memory and cognitive impairment in different animal models, indicating that it has potential preventive and therapeutic roles in MI.
    Matched MeSH terms: Memory Disorders
  4. Protective Effect of Natural Products against Huntington's Disease: An Overview of Scientific Evidence and Understanding Their Mechanism of Action
    Lum PT, Sekar M, Gan SH, Bonam SR, Shaikh MF
    ACS Chem Neurosci, 2021 Feb 03;12(3):391-418.
    PMID: 33475334 DOI: 10.1021/acschemneuro.0c00824
    Huntington's disease (HD), a neurodegenerative disease, normally starts in the prime of adult life, followed by a gradual occurrence of characteristic psychiatric disturbances and cognitive and motor dysfunction. To the best of our knowledge, there is no treatment available to completely mitigate the progression of HD. Among various therapeutic approaches, exhaustive literature reports have confirmed the medicinal benefits of natural products in HD experimental models. Building on this information, this review presents a brief overview of the neuroprotective mechanism(s) of natural products against in vitro/in vivo models of HD. Relevant studies were identified from several scientific databases, including PubMed, ScienceDirect, Scopus, and Google Scholar. After screening through literature from 2005 to the present, a total of 14 medicinal plant species and 30 naturally isolated compounds investigated against HD based on either in vitro or in vivo models were included in the present review. Behavioral outcomes in the HD in vivo model showed that natural compounds significantly attenuated 3-nitropropionic acid (3-NP) induced memory loss and motor incoordination. The biochemical alteration has been markedly alleviated with reduced lipid peroxidation, increased endogenous enzymatic antioxidants, reduced acetylcholinesterase activity, and increased mitochondrial energy production. Interestingly, following treatment with certain natural products, 3-NP-induced damage in the striatum was ameliorated, as seen histologically. Overall, natural products afforded varying degrees of neuroprotection in preclinical studies of HD via antioxidant and anti-inflammatory properties, preservation of mitochondrial function, inhibition of apoptosis, and induction of autophagy.
    Matched MeSH terms: Memory Disorders
  5. 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: Memory Disorders
  6. Fulltext Working Memory From the Psychological and Neurosciences Perspectives: A Review
    Chai WJ, Abd Hamid AI, Abdullah JM
    Front Psychol, 2018;9:401.
    PMID: 29636715 DOI: 10.3389/fpsyg.2018.00401
    Since the concept of working memory was introduced over 50 years ago, different schools of thought have offered different definitions for working memory based on the various cognitive domains that it encompasses. The general consensus regarding working memory supports the idea that working memory is extensively involved in goal-directed behaviors in which information must be retained and manipulated to ensure successful task execution. Before the emergence of other competing models, the concept of working memory was described by the multicomponent working memory model proposed by Baddeley and Hitch. In the present article, the authors provide an overview of several working memory-relevant studies in order to harmonize the findings of working memory from the neurosciences and psychological standpoints, especially after citing evidence from past studies of healthy, aging, diseased, and/or lesioned brains. In particular, the theoretical framework behind working memory, in which the related domains that are considered to play a part in different frameworks (such as memory's capacity limit and temporary storage) are presented and discussed. From the neuroscience perspective, it has been established that working memory activates the fronto-parietal brain regions, including the prefrontal, cingulate, and parietal cortices. Recent studies have subsequently implicated the roles of subcortical regions (such as the midbrain and cerebellum) in working memory. Aging also appears to have modulatory effects on working memory; age interactions with emotion, caffeine and hormones appear to affect working memory performances at the neurobiological level. Moreover, working memory deficits are apparent in older individuals, who are susceptible to cognitive deterioration. Another younger population with working memory impairment consists of those with mental, developmental, and/or neurological disorders such as major depressive disorder and others. A less coherent and organized neural pattern has been consistently reported in these disadvantaged groups. Working memory of patients with traumatic brain injury was similarly affected and shown to have unusual neural activity (hyper- or hypoactivation) as a general observation. Decoding the underlying neural mechanisms of working memory helps support the current theoretical understandings concerning working memory, and at the same time provides insights into rehabilitation programs that target working memory impairments from neurophysiological or psychological aspects.
    Matched MeSH terms: Memory Disorders
  7. 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: Memory Disorders
  8. Phyllanthus amarus protects against spatial memory impairment induced by lipopolysaccharide in mice
    Alagan A, Jantan I, Kumolosasi E, Azmi N
    Bioinformation, 2019;15(8):535-541.
    PMID: 31719762 DOI: 10.6026/97320630015535
    Phyllanthus amarus Schumach. and Thonn. is a wide spread medicinal herb with various traditional uses. It is well documented for its antioxidant, anti-inflammatory, and hepatoprotective activities. Therefore, it is of interest to evaluate the 80% ethanol extract of Phyllanthus amarus (PA) on spatial memory using the 8-radial arm maze (8-RAM) in mice after induction of neuro inflammation by lipopolysaccharide (LPS) in a 14- and 28-days treatment study. LC-MS/MS was performed to profile the chemical composition in PA extract. Mice were treated orally with 5% v/v tween 20, PA extract (100, 200 and 400 mg/kg), or ibuprofen (IBF 40 mg/kg) for 14 and 28 days. All groups were challenged with LPS (1 mg/kg) via intraperitoneal (i.p.) injection a day prior to the 8-RAM task except for the negative control group which received an i.p. injection of saline. Data obtained were analyzed with one-way ANOVA followed by post hoc Dunnett's test (comparison of all groups against vehicle control). Analysis of LC-MS/MS data revealed the presence of 16 compounds in the PA extract. Administration of PA extract at 200 and 400 mg/kg for 14 and 28 days significantly (*P<0.05) decreased the working and reference memory errors against LPS-induced spatial memory impairment. The observed protective action is possibly due to the putative antineuroinflammatory effects of PA. In conclusion, PA extract possess neuroprotective effects against spatial memory impairment mediated by LPS.
    Matched MeSH terms: Memory Disorders
  9. Fulltext Neurological effects of honey: current and future prospects
    Mijanur Rahman M, Gan SH, Khalil MI
    Evid Based Complement Alternat Med, 2014;2014:958721.
    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: Memory Disorders
  10. A standardised Andrographis paniculata Burm. Nees aqueous extract prevents Lipopolysaccharide-induced cognitive deficits through suppression of inflammatory cytokines and oxidative stress mediators
    Sani D, Khatab NIO, Kirby BP, Yong A, Hasan S, Basri H, et al.
    J Adv Res, 2019 Mar;16:87-97.
    PMID: 30899592 DOI: 10.1016/j.jare.2018.11.005
    Substantial evidence has shown that most cases of memory impairment are associated with increased neuroinflammation and oxidative stress. In this study, the potential of a standardised Andrographis paniculata aqueous extract (APAE) to reverse neuroinflammation and cognitive impairment induced by lipopolysaccharide (LPS) was examined in vivo. Rats were treated with APAE (50, 100, 200, and 400 mg·kg-1, p.o.) for 7 consecutive days prior to LPS (1 mg·kg-1, i.p.)-induced neuroinflammation and cognitive impairment. Spatial learning and memory were evaluated using the Morris water maze (MWM) test, while neuroinflammation and oxidative stress were assessed through the measurement of specific mediators, namely, tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-1β, superoxide dismutase (SOD), catalase (CAT), antioxidant glutathione (GSH), reactive oxygen species (ROS), and thiobarbituric acid reactive substance (TBARS). Acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) were also evaluated. LPS caused significant memory deficits in the 2-day MWM protocol, whereas pretreatment with standardised APAE dose-dependently improved performance in the MWM test. APAE treatment also blocked the LPS-induced hippocampal increase in the concentration and expression of proinflammatory cytokines (TNF-α, IL-1β, and IL-6) and production of ROS and TBARS and enhanced the activities of AChE and BChE. Furthermore, APAE enhanced the decrease in the levels and expression of hippocampal antioxidant enzymes (SOD and CAT) following LPS-induced neuroinflammation and cognitive deficit. The findings from these studies suggested that standardised APAE improved memory and had potent neuroprotective effects against LPS-induced neurotoxicity.
    Matched MeSH terms: Memory Disorders
  11. Reversal of memory deficits by Coriandrum sativum leaves in mice
    Mani V, Parle M, Ramasamy K, Abdul Majeed AB
    J Sci Food Agric, 2011 Jan 15;91(1):186-92.
    PMID: 20848667 DOI: 10.1002/jsfa.4171
    Coriandrum sativum L., commonly known as coriander and belonging to the family Apiaceae (Umbelliferae), is cultivated throughout the world for its nutritional value. The present study was undertaken to investigate the effects of fresh Coriandrum sativum leaves (CSL) on cognitive functions, total serum cholesterol levels and brain cholinesterase activity in mice. In this study, CSL (5, 10 and 15% w/w of diet) was fed orally with a specially prepared diet for 45 days consecutively to experimental animals. Elevated plus-maze and passive avoidance apparatus served as the exteroceptive behavioral models for testing memory. Diazepam, scopolamine and ageing-induced amnesia served as the interoceptive behavioral models.
    Matched MeSH terms: Memory Disorders/diet therapy*; Memory Disorders/metabolism
  12. Fulltext Neuroprotective effects of 1`δ-1`-acetoxyeugenol acetate on Aβ(25-35) induced cognitive dysfunction in mice
    Jayasingh Chellammal HS, Veerachamy A, Ramachandran D, Gummadi SB, Manan MM, Yellu NR
    Biomed Pharmacother, 2019 Jan;109:1454-1461.
    PMID: 30551397 DOI: 10.1016/j.biopha.2018.10.189
    The progressive accumulation of amyloid beta (Aβ) peptide is neurotoxic and leads to Alzheimer's type dementia. Accumulation of Aβ has been associated with dysfunction of hypothalamic-pituitary-adrenal (HPA) axis and elevated pro-inflammatory cytokines. In this study, we investigated the effect of 1`δ-1`-acetoxyeugenol acetate (DAEA), isolated from Alpinia galanga (L.), on Aβ(25-35) induced neurodegeneration in mice. Mice were treated with three different doses of DAEA (12.5 mg/kg, 25 mg/kg and 50 mg/kg) for 28 days. Aβ(25-35) was injected by intracerebroventricular (i.c.v.) injection on the 15th day of 28 days. Open field, water maze and step-down inhibitory tests were performed on the 27th day to determine the habituation memory, spatial learning, and short- and long-term memory, respectively. Acetylcholinesterase (AChE), Corticosterone, biogenic amines (serotonin and dopamine), tumour necrosis factor-α (TNF-α), and antioxidant parameters such as superoxide dismutase, catalase, glutathione peroxidase and vitamin C were evaluated in brain homogenates after behavioural tests to ascertain the cognitive improvement through neuro-immune-endocrine modulation. The DAEA treatment with 25 mg/kg and 50 mg/kg resulted in significant (p < 0.001) improvement of habituation memory and step-down inhibitory avoidance task. In spatial learning, the cognitive improvement was significantly improved (p < 0.001) by reduction in escape latency. In the biochemical study, the significant (p < 0.001) reduction of AChE indicates the preeminent neuroprotection. Corticosterone and TNF-α were significantly (p < 0.01) reduced and biogenic amines were increased with antioxidant markers, which signify the potential influence of DAEA on neuroprotection. Our investigation revealed that the drug DAEA attenuates stress mediated through the HPA axis and regulates the neuroendocrine and neuroimmune function to improve the cognition. DAEA could be a potential lead candidate for the treatment of neurodegeneration.
    Matched MeSH terms: Memory Disorders/drug therapy; Memory Disorders/metabolism
  13. Fingolimod affects gene expression profile associated with LPS-induced memory impairment
    Omidbakhsh R, Rajabli B, Nasoohi S, Khallaghi B, Mohamed Z, Naidu M, et al.
    Exp Brain Res, 2014 Nov;232(11):3687-96.
    PMID: 25098558 DOI: 10.1007/s00221-014-4052-4
    Lipopolysaccharide is an endotoxin to induce sickness behavior in several animal models to explore the link between immune activation and cognition. Neuroinflammation playing a pivotal role in disease progress is evidently influenced by sphingosine-1-phosphate. As one of the sphingosine analogs in clinical use for multiple sclerosis, fingolimod (FTY720) was shown to substantially affect gene expression profile in the context of AD in our previous experiments. The present study was designed to evaluate the drug efficacy in the context of the mere inflammatory context leading to memory impairment. FTY720 was repeatedly administered for a few days before or after intracerebral lipopolysaccharide (LPS) injection in rats. Animal's brains were then assigned to histological as well as multiplex mRNA assay following memory performance test. Both FTY720 pre-treatment and post-treatment were similarly capable of ameliorating LPS-induced memory impairment as assessed by passive avoidance test. Such amending effects may be partly accountable by the concomitant alterations in transcriptional levels of mitogen-activated protein kinases as well as inflammatory genes determined by QuantiGene Plex analysis. These findings confirming FTY720 application benefits suggest its efficacy may not differ significantly while considered either as a preventive or as a therapeutic approach against neuroinflammation.
    Matched MeSH terms: Memory Disorders/chemically induced*; Memory Disorders/drug therapy; Memory Disorders/metabolism; Memory Disorders/physiopathology
  14. Red flags in patients presenting with headache: clinical indications for neuroimaging
    Sobri M, Lamont AC, Alias NA, Win MN
    Br J Radiol, 2003 Aug;76(908):532-5.
    PMID: 12893694
    Headache is a very common patient complaint but secondary causes for headache are unusual. Neuroimaging is both expensive and has a low yield in this group. Most patients with intracranial pathology have clinical features that would raise a "red flag". Appropriate selection of patients with headache for neuroimaging to look for secondary causes is very important. Red flags act as screening tools to help in identifying those patients presenting with headache who would benefit from prompt neuroimaging, and may increase the yield. The aim of this study is to evaluate clinical features in patients with headache using neuroimaging as a screening tool for intracranial pathology. 20 red flags were defined. A retrospective study of 111 patients was performed and the outcomes were divided into positive and negative. Abnormal neuroimaging was present in 39 patients. Results were analysed using the Logistic Regression model. Sensitivity and specificity of red flags were analysed to establish the cut-off point to predict abnormal neuroimaging and a receiver operating characteristic (ROC) curve plotted to show the sensitivity of the diagnostic test. Three red flag features proved to be statistically significant with the p-value of less than 0.05 on both univariate and multivariate analysis. These were: paralysis; papilloedema; and "drowsiness, confusion, memory impairment and loss of consciousness". In addition, if three or more red flags from the list were present, this showed strong indication of abnormal neuroimaging, from cut-off point of ROC curve (area under the curve =0.76).
    Matched MeSH terms: Memory Disorders/etiology
  15. Supplementation of fenugreek with choline-docosahexaenoic acid attenuates menopause induced memory loss, BDNF and dendritic arborization in ovariectomized rats
    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: Memory Disorders/metabolism
  16. Lingzhi or Reishi Medicinal Mushroom, Ganoderma lucidum (Agaricomycetes) Ameliorates Spatial Learning and Memory Deficits in Rats with Hypercholesterolemia and Alzheimer's Disease
    Rahman MA, Hossain S, Abdullah N, Aminudin N
    Int J Med Mushrooms, 2020;22(1):93-103.
    PMID: 32464001 DOI: 10.1615/IntJMedMushrooms.2020033383
    Hypercholesterolemia has been implicated as one of the pathomechanistic factors of Alzheimer's disease (AD), the most common neurodegenerative disorder affecting memory and learning abilities. In the present study, ameliorative effect of hot water extract (HWE) of mushroom Ganoderma lucidum to the memory and learning related behavioral performance of hypercholesterolemic and AD rats was investigated using Morris water maze (MWM). Male Wistar rats were randomly grouped into control, extract fed control, hypercholesterolemic, extract fed hypercholesterolemic, AD, and extract fed AD groups, each group containing 8 animals. Hypercholesterolemia was induced in rats by adding 1% cholesterol and 1% cholic acid with the basal diet of the respective group. Alzheimer's disease model rats were prepared through infusion of amyloid β(1-42) to the right ventricle. Memory and learning related performance of all the rats was tested for 6 consecutive days that included time taken to reach the submerged platform (sec) and distance traveled (m). G. lucidum HWE fed rats took less time and traveled less distance to find the submerged platform, which indicates the spatial learning and memory related behavioral amelioration of the extract fed rats compared with their non-fed counterparts. Thus, usage of G. lucidum seems promising in withstanding hypercholesterolemia-induced Alzheimer's disease pathogenesis.
    Matched MeSH terms: Memory Disorders/prevention & control*
  17. Fulltext Ascorbic acid protects against restraint stress-induced memory deficits in Wistar rats
    Kumar RS, Narayanan SN, Nayak S
    Clinics (Sao Paulo), 2009;64(12):1211-7.
    PMID: 20037710 DOI: 10.1590/S1807-59322009001200012
    Chronic stress has been shown to cause oxidative damage in the central nervous system. Although stress-induced impairments in learning and memory have been studied extensively, very few studies have investigated possible ways to prevent their ill effects. The present work was designed to study the protective effects of ascorbic acid in memory loss induced by chronic restraint stress.
    Matched MeSH terms: Memory Disorders/prevention & control*
  18. Activation of sphingosine 1-phosphate receptor-1 by SEW2871 improves cognitive function in Alzheimer's disease model rats
    Asle-Rousta M, Oryan S, Ahmadiani A, Rahnema M
    EXCLI J, 2013;12:449-61.
    PMID: 26417237
    Sphingosine-1 phosphate (S1P) is involved in a variety of cellular processes via activation of S1P receptors (S1PRs; S1PR1 to S1PR5) that are highly expressed in the brain. It has been shown that the level of S1P is reduced in the brain of Alzheimer's disease (AD) patients. However, there is no study designed to evaluate the expression of S1PRs in AD brains. The objectives of the present work are (1) to examine the expression of S1PR1-3 in the hippocampus of beta amyloid (Aβ) 1-42 injected rats and (2) to clarify the effects of chronic S1PR1 activation on S1PR1-3 levels, spatial memory deficit and hippocampal damage in AD rats. SEW2871, the S1PR1 selective agonist, repeatedly was injected intraperitoneally during a period of two weeks. Upon Western Blot data bilateral intrahippocampal injection of Aβ1-42 decreased the expression of S1PR1 while increased S1PR2 level and did not affect that of S1PR3. We found that chronic administration of SEW2871 inhibited the reduction of S1PR1 expression and ameliorated spatial memory impairment in the Morris water maze task in rats. In addition, SEW2871 attenuated the Aβ1-42-induced hippocampal neuronal loss according to Nissl staining findings. Data in the current study highlights the importance of S1PR1 signaling pathway deregulation in AD development and suggests that activation of S1PR1 may represent a potential approach for developing new therapeutics to manage memory deficit and apoptosis associated with neurodegenerative disorders such as AD.
    Matched MeSH terms: Memory Disorders
  19. Modulation of the Nitrergic Pathway via Activation of PPAR-γ Contributes to the Neuroprotective Effect of Pioglitazone Against Streptozotocin-Induced Memory Dysfunction
    Prakash A, Kumar A, Ming LC, Mani V, Majeed AB
    J Mol Neurosci, 2015 Jul;56(3):739-50.
    PMID: 25854775 DOI: 10.1007/s12031-015-0508-7
    Alzheimer's disease (AD) is a neurodegenerative disease characterized by impaired memory function and oxidative damage. NO is a major signaling molecule produced in the central nervous system to modulate neurological activity through modulating nitric oxide synthase. Recently, PPAR-γ agonists have shown neuroprotective effects in neurodegenerative disorders. However, there have been only a few studies identifying mechanisms through which cognitive benefits may be exerted. The present study was designed to investigate the possible nitric oxide mechanism in the protective effect of pioglitazone against streptozotocin (STZ)-induced memory dysfunction. Wistar rats were intracerebroventricularly (ICV) injected with STZ. Then rats were treated with pioglitazone, NO modulators [L-arginine and nitro-L-arginine methyl ester (L-NAME)] for 21 days. Behavioral alterations were assessed in between the study period. Animals were sacrificed immediately after behavioral session, and mito-oxidative parameters, TNF-α, IL-6, and caspase-3 activity were measured. STZ-treated rats showed a memory deficit and significantly increased in mito-oxidative damage and inflammatory mediators and apoptosis in the hippocampus. Chronic treatment of pioglitazone significantly improved memory retention and attenuated mito-oxidative damage parameters, inflammatory markers, and apoptosis in STZ-treated rats. However, L-arginine pretreatment with lower dose of pioglitazone has not produced any protective effect as compared to per se. Furthermore, pretreatment of L-NAME significantly potentiated its protective effect, which indicates the involvement of nitric oxide for activation of PPAR-γ action. These results demonstrate that pioglitazone offers protection against STZ-induced memory dysfunction possibly due to its antioxidant, anti-inflammatory, and anti-apoptotic action mediating nitric oxide pathways and, therefore, could have a therapeutic potential in AD.
    Matched MeSH terms: Memory Disorders/drug therapy*; Memory Disorders/etiology; Memory Disorders/metabolism
  20. Lactobacillus fermentum LAB 9-fermented soymilk with enriched isoflavones and antioxidants improved memory in vivo
    Mohamad Fakri E, Lim S, Musa N, Hazizul Hasan M, Adam A, Ramasamy K
    Sains Malaysiana, 2016;45:1289-1297.
    This study examined lactic acid bacteria (LAB)-fermented soymilk for their ability in hydrolyzing glucosides to aglycones
    and corresponding antioxidant capacity and memory enhancing effect. Twelve LAB isolated from Malaysian fermented food
    and milk products were incubated in commercially available soymilk for 48 h. Generally, soymilk supported LAB growth
    and significantly increased (p<0.05) conversion to bioactive aglycone by 2.1-6.5 fold when compared to unfermented
    soymilk. Lactobacillus fermentum LAB 9- fermented soymilk, in particular, was presented with increased total phenolic
    content (+10%) as opposed to unfermented soymilk. Lactobacilli (LAB 10-12)- and pediococci (LAB 5)-fermented soymilk
    elicited maximal DPPH radical-scavenging activity. LAB 1, 7, 8, 9 and 12 exhibited significantly higher (p<0.05) ferrous
    ion chelating activity when compared to control. Interestingly, LAB 9 had significantly improved memory deficit (p<0.05)
    in LPS-challenged mice. LAB-enriched nutritional value of soymilk could be useful against oxidative stress and memory
    deficit.
    Matched MeSH terms: Memory Disorders
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