Displaying publications 1 - 20 of 96 in total

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  1. 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: Mild Cognitive Impairment*
  2. 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: Mild Cognitive Impairment/drug therapy*; Mild Cognitive Impairment/metabolism
  3. Ian E, Gwen CL, Soo CT, Melissa C, Chun-Kai H, Eosu K, et al.
    Asian J Psychiatr, 2016 Aug;22:182-9.
    PMID: 26617385 DOI: 10.1016/j.ajp.2015.10.009
    HIV-associated neurocognitive disorder incurs a significant burden on HIV patients in Asia-Pacific countries; however, the incidence is difficult to estimate due to a lack of local epidemiological data. The impact of neurocognitive impairment in HIV patients is often underestimated due to a lack of education and awareness, and there are consequently gaps in the provision of screening and diagnosis to enable earlier intervention to limit neurocognitive impairment.
    Matched MeSH terms: Mild Cognitive Impairment/diagnosis*; Mild Cognitive Impairment/etiology*; Mild Cognitive Impairment/therapy
  4. Hafandi A, Begg DP, Premaratna SD, Sinclair AJ, Jois M, Weisinger RS
    Comp. Med., 2014 Apr;64(2):106-9.
    PMID: 24674584
    Dietary deficiency of ω3 fatty acid during development leads to impaired cognitive function. However, the effects of multiple generations of ω3 fatty-acid deficiency on cognitive impairment remain unclear. In addition, we sought to test the hypothesis that the cognitive impairments of ω3 fatty-acid-deficient mice are mediated through the arachidonic acid-cyclooxygenase (COX) pathway. To address these issues, C57BL/6J mice were bred for 3 generations and fed diets either deficient (DEF) or sufficient (SUF) in ω3 fatty acids. At postnatal day 21, the F3 offspring remained on the dam's diet or were switched to the opposite diet, creating 4 groups. In addition, 2 groups that remained on the dam's diet were treated with a COX inhibitor. At 19 wk of age, spatial-recognition memory was tested on a Y-maze. Results showed that 16 wk of SUF diet reversed the cognitive impairment of F3 DEF mice. However, 16 wk of ω3 fatty-acid-deficient diet impaired the cognitive performance of the F3 SUF mice, which did not differ from that of the F3 DEF mice. These findings suggest that the cognitive deficits after multigenerational maintenance on ω3 fatty-acid-deficient diet are not any greater than are those after deficiency during a single generation. In addition, treatment with a COX inhibitor prevented spatial-recognition deficits in F3 DEF mice. Therefore, cognitive impairment due to dietary ω3 fatty-acid deficiency appears to be mediated by the arachidonic acid-COX pathway and can be prevented by 16 wk of dietary repletion with ω3 fatty acids or COX inhibition.
    Matched MeSH terms: Mild Cognitive Impairment/drug therapy*; Mild Cognitive Impairment/etiology; Mild Cognitive Impairment/genetics
  5. Mukari SZS, Ishak WS, Maamor N, Wan Hashim WF
    Ann Otol Rhinol Laryngol, 2017 Oct;126(10):697-705.
    PMID: 28845678 DOI: 10.1177/0003489417727547
    OBJECTIVES: Studies in cognitive aging demonstrated inconsistent association between hearing and cognition in older adults. Furthermore, it is still unclear if hearing loss at high frequencies, which is the earliest to be affected, is associated with cognitive functioning. This study aimed to determine the association between global cognitive status and pure tone average (PTA) at 0.5, 1, and 2 kHz (PTA low) and PTA at 4 and 8 kHz (PTA high).

    METHODS: This study involved 307 adults aged 60 years and older. Participants had their hearing and cognition measured using pure tone audiometry and Mini Mental State Examination (MMSE), respectively.

    RESULTS: Pure tone average (low) accounted for significant but minimal amount of variance in measure of MMSE. Multiple regression analyses were also performed on normal and impaired hearing cohorts and cohorts with younger (60-69 years) and older (≥70 years) groups. The results revealed a significant relationship between PTA (low) and MMSE only in the younger age group. In contrast, no significant relationship was found between PTA (high) and cognition in any of the cohorts.

    CONCLUSION: Pure tone average (low) is significantly but minimally related to measure of general cognitive status. Similar relationship is not observed between high-frequency hearing and cognition. Further research using a more comprehensive cognitive test battery is needed to confirm the lack of association between high-frequency hearing and cognition.

    Matched MeSH terms: Mild Cognitive Impairment/diagnosis*
  6. Lee LK, Shahar S, Rajab N, Yusoff NA, Jamal RA, Then SM
    J Nutr Biochem, 2013 May;24(5):803-8.
    PMID: 22898566 DOI: 10.1016/j.jnutbio.2012.04.014
    The present work explores the effect of dietary omega-3 polyunsaturated fatty acids (PUFAs) intake on lipid peroxidation among mild cognitive impairment (MCI) patients. The plasma lipid hydroperoxide (LPO) levels in 67 MCI patients were compared to those of 134 healthy elderly controls. Omega-3 PUFA intake was assessed using an interviewer-administered food frequency questionnaire. Apolipoprotein E genotyping was performed using polymerase chain reaction and restriction enzyme digestion. The association between various confounders and lipid peroxidation was evaluated using regression analysis. The influence of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) intake on LPO level was investigated. The results revealed that LPO levels were significantly higher in the MCI group than in the control group. Inverse correlations were found between DHA and EPA intake and LPO level among the MCI group. LPO levels decreased significantly with increasing DHA and EPA intake. In summary, the findings revealed that DHA and EPA can play a role in alleviating oxidative stress and reducing the risk of neurodegenerative diseases.
    Matched MeSH terms: Mild Cognitive Impairment/metabolism*
  7. Kashyap M, Mulsant BH, Tannenbaum C
    Am J Geriatr Psychiatry, 2015 Mar;23(3):326-9.
    PMID: 25450763 DOI: 10.1016/j.jagp.2014.09.009
    The discriminative ability of serum anticholinergic activity (SAA) to differentiate between older individuals with stable versus deteriorating cognition remains undetermined. We examined the relationship between SAA changes, the presence or absence of a mild neurocognitive disorder, age and anticholinergic medication over a one-year time period.
    Matched MeSH terms: Mild Cognitive Impairment/blood*; Mild Cognitive Impairment/diagnosis*
  8. Asmuje NF, Mat S, Myint PK, Tan MP
    Curr Hypertens Rep, 2022 10;24(10):375-383.
    PMID: 35731334 DOI: 10.1007/s11906-022-01200-w
    PURPOSE OF REVIEW: To conduct a scoping review of articles which have evaluated BPV and cognitive function. Articles with keywords, titles or abstracts containing the terms 'cognitive' OR 'cognition' OR 'dementia' AND 'blood pressure variability' were identified from CINAHL, Medline, PMC and Web of Science.

    RECENT FINDINGS: Methods of acquisition and analysis of BPV and cognitive measurements and their relationship were extracted from selected articles. Of 656 studies identified, 53 articles were selected. Twenty-five evaluated long-term (LTBPV), nine mid-term (MTBPV), 12 short-term (STBPV) and nine very short-term BPV (VSTBPV) with conflicting findings on the relationship between BPV and cognition. Variations existed in devices, period and procedure for acquisition. The studies also utilized a wide range of methods of BPV calculation. Thirteen cognitive assessment tools were used to measure global cognition or domain functions which were influenced by the population of interest. The interpretation of available studies was hence limited by heterogeneity. There is an urgent need for standardization of BPV assessments to streamline research on BPV and cognition. Future studies should also establish whether BPV could be a potential modifiable risk factor for cognitive decline, as well as a marker for treatment response.

    Matched MeSH terms: Mild Cognitive Impairment*
  9. Rosdinom R, Zarina MZ, Zanariah MS, Marhani M, Suzaily W
    Prev Med, 2013;57 Suppl:S67-9.
    PMID: 23313789 DOI: 10.1016/j.ypmed.2012.12.025
    OBJECTIVE: This study aims to determine the relationships between behavioural and psychological symptoms of dementia (BPSD), cognitive impairment and burden of care of patients with dementia.
    METHOD: A cross-sectional, non-randomised study of 65 elderly patients with dementia and their caregivers was conducted over a 3-month period in January 2007 at the memory clinics of Universiti Kebangsaan Malaysia Medical Centre and Hospital Kuala Lumpur. Patients' cognitive functions were assessed with the Mini Mental State Examination (MMSE). Caregivers were interviewed to determine the severity of BPSD and caregiver burden (CB) using the Neuropsychiatric Inventory (NPI) Questionnaire and Zarit Burden Interview (BI) respectively.
    RESULTS: Cognitive impairment did not contribute significantly to CB. Multiple linear regression analysis showed that high BPSD scores contributed 0.27 more in BI score, female patients contributed 0.37 less in BI score and caregivers with higher educational level contribute 0.5 more in BI score.
    CONCLUSION: Patients' BPSD and male gender, but not cognitive impairment, were associated with CB. Even though CB was experienced more among caregivers with better education, all caregivers should be screened to ensure their general well-being.
    KEYWORDS: BPSD; Caregiver burden; Cognitive impairment
    Study site: Memory clinics, Pusat Perubatan Universiti Kebangsaan Malaysia (PPUKM) and Hospital Kuala Lumpur, Kuala Lumpur, Malaysia
    Matched MeSH terms: Mild Cognitive Impairment/psychology*
  10. Mohd Zulkifly MF, Ghazali SE, Che Din N, Singh DK, Subramaniam P
    ScientificWorldJournal, 2016;2016:3456943.
    PMID: 27340686 DOI: 10.1155/2016/3456943
    In this review, we aimed to identify the risk factors that may influence cognitive impairment among stroke survivors, namely, demographic, clinical, psychological, and physical determinants. A search from Medline, Scopus, and ISI Web of Science databases was conducted for papers published from year 2004 to 2015 related to risk factors of cognitive impairment among adult stroke survivors. A total of 1931 articles were retrieved, but only 27 articles met the criteria and were reviewed. In more than half of the articles it was found that demographical variables that include age, education level, and history of stroke were significant risk factors of cognitive impairment among stroke survivors. The review also indicated that diabetes mellitus, hypertension, types of stroke and affected region of brain, and stroke characteristics (e.g., size and location of infarctions) were clinical determinants that affected cognitive status. In addition, the presence of emotional disturbances mainly depressive symptoms showed significant effects on cognition. Independent relationships between cognition and functional impairment were also identified as determinants in a few studies. This review provided information on the possible risk factors of cognitive impairment in stroke survivors. This information may be beneficial in the prevention and management strategy of cognitive impairments among stroke survivors.
    Matched MeSH terms: Mild Cognitive Impairment/etiology*
  11. Kvestad I, Hysing M, Shrestha M, Ulak M, Thorne-Lyman AL, Henjum S, et al.
    Am J Clin Nutr, 2017 05;105(5):1122-1131.
    PMID: 28330909 DOI: 10.3945/ajcn.116.144931
    Background: Poor vitamin B-12 (cobalamin) status is widespread in South Asia. Insufficient vitamin B-12 status has been linked to poor neurodevelopment in young children.Objective: We measured the associations between vitamin B-12 status in infancy (2-12 mo) and the development and cognitive functioning in Nepalese children 5 y later.Design: Vitamin B-12 status was assessed in infancy with the use of plasma cobalamin, total homocysteine (tHcy), and methylmalonic acid (MMA). At 5 y of age, we measured development with the use of the Ages and Stages Questionnaire, 3rd edition (ASQ-3), and cognitive functioning by using the Developmental Neuropsychological Assessment, 2nd edition (NEPSY II), in 320 children. In regression models, we estimated the associations between vitamin B-12 status, including a combined indicator of vitamin B-12 status (3cB12) and scores on the ASQ-3 and NEPSY II subtests.Results: All markers of vitamin B-12 status with the exception of plasma cobalamin were significantly associated with the total ASQ-3 scores in the multiple regression models. A 1-unit increase in the 3cB12 score was associated with an increase in the total ASQ-3 score of 4.88 (95% CI: 2.09, 7.68; P = 0.001). Increases in both plasma tHcy and MMA (indicating poorer status) were associated with a decrease in scores on the NEPSY II affect recognition and geometric puzzle subtests. Each unit increment in 3cB12 scores was associated with increases of 0.82 (95% CI: 0.49, 1.14; P < 0.0005), 0.59 (95% CI: 0.10, 1.09; P = 0.020), and 0.24 (95% CI: 0.02, 0.47; P = 0.035) in the affect recognition, geometric puzzle, and block construction scores, respectively.Conclusions: Vitamin B-12 status in infancy is associated with development and performance on social perception tasks and visuospatial abilities at 5 y of age. The long-term effects of poor vitamin B-12 status in infancy need further investigation in randomized controlled trials.
    Matched MeSH terms: Mild Cognitive Impairment/blood; Mild Cognitive Impairment/etiology*
  12. Meramat A, Rajab NF, Shahar S, Sharif RA
    J Nutr Health Aging, 2017;21(5):539-545.
    PMID: 28448084 DOI: 10.1007/s12603-016-0759-1
    BACKGROUND: A cross sectional study was conducted in a group of 317 subjects older than 60 in Malaysia, aimed to determine risk factors associated with cognitive impairment in older adults, focusing on trace elements and DNA damage.

    METHOD: Cognitive decline was determined by Montreal Cognitive Assessment (MoCA). Oxidative stress markers (malondialdehyde-MDA and superoxide dismutase-SOD) were determined and DNA damage was assayed using Alkaline Comet Assay. Toenail samples were taken and analyzed using ICP-MS to determine trace element levels.

    RESULTS: A total of 62.1 % of subjects had cognitive impairment. Subjects with cognitive impairment had significantly higher levels of MDA and DNA damage as compared to the group with normal cognitive function; MDA (2.07 ± 0.05 nmol/L vs 1.85 ± 0.06 nmol/L) (p<0.05) and DNA damage (% Tail Density, 14.52 ± 0.32 vs 10.31 ± 0.42; Tail Moment, 1.79 ± 0.06 vs 1.28 ± 0.06) (p<0.05 for all parameters). However, the level of SOD among subjects with cognitive impairment (6.67 ± 0.33 u.e/min/mg protein) was lower than the level among those with normal cognitive functions (11.36 ± 0.65 u.e/min/mg protein) (p<0.05). Multiple logistic regression revealed the predictors for cognitive impairment among the subjects were DNA damage (Adjusted odd ratio [OR], 1.37; 95% confidence interval [CI], 1.18-1.59), level of trace elements in toenails namely, lead (OR, 2.471; CI, 1.535-3.980) and copper (OR, 1.275; CI, 1.047-1.552) (p<0.05).

    CONCLUSION: High levels of lead and copper can lead to increase in oxidative stress levels and are associated with DNA damage that eventually could be associated with cognitive decline.

    Matched MeSH terms: Mild Cognitive Impairment/etiology*
  13. Ooi TC, Meramat A, Rajab NF, Shahar S, Ismail IS, Azam AA, et al.
    Nutrients, 2020 Aug 30;12(9).
    PMID: 32872655 DOI: 10.3390/nu12092644
    Intermittent fasting (IF) refers to various dietary regimens that cycle between a period of non-fasting and a period of total fasting. This study aimed to determine the effects of IF on cognitive function among elderly individuals who practice IF who have mild cognitive impairment (MCI). A total of 99 elderly subjects with MCI of Malay ethnicity without any terminal illness were recruited from a larger cohort study, LRGS TUA. The subjects were divided into three groups, comprising those who were regularly practicing IF (r-IF), irregularly practicing IF (i-IF), and non-fasters (n-IF). Upon 36 months of follow-up, more MCI subjects in the r-IF group reverted to successful aging with no cognitive impairment and diseases (24.3%) compared to those in i-IF (14.2%) and n-IF groups (3.7%). The r-IF group's subjects exhibited significant increment in superoxide dismutase (SOD) activity and reduction in body weight, levels of insulin, fasting blood glucose, malondialdehyde (MDA), C-reactive protein (CRP), and DNA damage. Moreover, metabolomics analysis showed that IF may modulate cognitive function via various metabolite pathways, including the synthesis and degradation of ketone bodies, butanoate metabolism, pyruvate metabolism, and glycolysis and gluconeogenesis pathways. Overall, the MCI-afflicted older adults who practiced IF regularly had better cognitive scores and reverted to better cognitive function at 36 months follow-up.
    Matched MeSH terms: Mild Cognitive Impairment/diet therapy*; Mild Cognitive Impairment/metabolism*
  14. Ooi TC, Meramat A, Rajab NF, Shahar S, Sharif R
    J Nutr Health Aging, 2022;26(3):272-281.
    PMID: 35297471 DOI: 10.1007/s12603-022-1757-0
    OBJECTIVES: This study aimed to determine the relationship between oxidative stress, DNA damage, inflammation, and metabolic biomarkers as the mediating factor between Islamic Sunnah intermittent fasting (IF) practice and cognitive function among older adults with mild cognitive impairment (MCI).

    DESIGN: This study was a 36 months prospective cohort study.

    SETTING: Community-dwelling older participants recruited through a stratified random sampling method from four states representing Malaysia's central, north-west, northeast and southern regions.

    PARTICIPANTS: Ninety-nine Malay Muslim older adults (n= 99) aged 60 and above with MCI and no known critical illnesses were included in the current analysis. The participants were divided into regularly practicing IF (r-IF), irregularly practicing IF (i-IF) and not practicing IF (n-IF) groups.

    MEASUREMENTS: Fasting venous blood was collected and used to determine the levels of oxidative stress, DNA damage, inflammatory and metabolic biomarkers. Mini-Mental State Examination, Montreal Cognitive Assessment, Rey Auditory Verbal Learning Test, Digit Span and Digit symbol were used to evaluate the cognitive function. Then, the mediation analysis was conducted using a multistep regression model to determine the mediating role of various biomarkers between IF practice and cognitive function.

    RESULTS: When comparing the r-IF and n-IF groups, higher SOD activity, lower DNA damage (percentage of DNA in tail), lower CRP levels and higher HDL-cholesterol levels established partial mediation while lower insulin levels established complete mediation between IF practice and better cognitive function. Meanwhile, when comparing the r-IF and i-IF groups, higher SOD activity and lower CRP levels completely mediated the effects of IF practice on better cognitive function.

    CONCLUSION: It can be concluded that changes in antioxidant function, DNA damage, inflammation and a limited set of metabolic biomarkers (insulin and HDL cholesterol) may mediate improvements in cognitive function among older participants with MCI who practice Islamic Sunnah IF.

    Matched MeSH terms: Mild Cognitive Impairment*
  15. Paudel YN, Angelopoulou E, Jones NC, O'Brien TJ, Kwan P, Piperi C, et al.
    ACS Chem Neurosci, 2019 10 16;10(10):4199-4212.
    PMID: 31532186 DOI: 10.1021/acschemneuro.9b00460
    Emerging findings point toward an important interconnection between epilepsy and Alzheimer's disease (AD) pathogenesis. Patients with epilepsy (PWE) commonly exhibit cognitive impairment similar to AD patients, who in turn are at a higher risk of developing epilepsy compared to age-matched controls. To date, no disease-modifying treatment strategy is available for either epilepsy or AD, reflecting an immediate need for exploring common molecular targets, which can delineate a possible mechanistic link between epilepsy and AD. This review attempts to disentangle the interconnectivity between epilepsy and AD pathogenesis via the crucial contribution of Tau protein. Tau protein is a microtubule-associated protein (MAP) that has been implicated in the pathophysiology of both epilepsy and AD. Hyperphosphorylation of Tau contributes to the different forms of human epilepsy and inhibition of the same exerted seizure inhibitions and altered disease progression in a range of animal models. Moreover, Tau-protein-mediated therapy has demonstrated promising outcomes in experimental models of AD. In this review, we discuss how Tau-related mechanisms might present a link between the cause of seizures in epilepsy and cognitive disruption in AD. Untangling this interconnection might be instrumental in designing novel therapies that can minimize epileptic seizures and cognitive deficits in patients with epilepsy and AD.
    Matched MeSH terms: Mild Cognitive Impairment/complications; Mild Cognitive Impairment/metabolism*
  16. Choo BKM, Kundap UP, Johan Arief MFB, Kumari Y, Yap JL, Wong CP, et al.
    PMID: 30844417 DOI: 10.1016/j.pnpbp.2019.02.014
    Epilepsy is marked by seizures that are a manifestation of excessive brain activity and is symptomatically treatable by anti-epileptic drugs (AEDs). Unfortunately, the older AEDs have many side effects, with cognitive impairment being a major side effect that affects the daily lives of people with epilepsy. Thus, this study aimed to determine if newer AEDs (Zonisamide, Levetiracetam, Perampanel, Lamotrigine and Valproic Acid) also cause cognitive impairment, using a zebrafish model. Acute seizures were induced in zebrafish using pentylenetetrazol (PTZ) and cognitive function was assessed using the T-maze test of learning and memory. Neurotransmitter and gene expression levels related to epilepsy as well as learning and memory were also studied to provide a better understanding of the underlying processes. Ultimately, impaired cognitive function was seen in AED treated zebrafish, regardless of whether seizures were induced. A highly significant decrease in γ-Aminobutyric Acid (GABA) and glutamate levels was also discovered, although acetylcholine levels were more variable. The gene expression levels of Brain-Derived Neurotrophic Factor (BDNF), Neuropeptide Y (NPY) and Cyclic Adenosine Monophosphate (CAMP) Responsive Element Binding Protein 1 (CREB-1) were not found to be significantly different in AED treated zebrafish. Based on the experimental results, a decrease in brain glutamate levels due to AED treatment appears to be at least one of the major factors behind the observed cognitive impairment in the treated zebrafish.
    Matched MeSH terms: Mild Cognitive Impairment/chemically induced*; Mild Cognitive Impairment/complications
  17. Foong HF, Hamid TA, Ibrahim R, Haron SA, Shahar S
    Aging Ment Health, 2018 Jan;22(1):109-120.
    PMID: 27732054 DOI: 10.1080/13607863.2016.1231172
    OBJECTIVES: The aim of this study was to identify the predictors of elderly's cognitive function based on biopsychosocial and cognitive reserve perspectives.

    METHOD: The study included 2322 community-dwelling elderly in Malaysia, randomly selected through a multi-stage proportional cluster random sampling from Peninsular Malaysia. The elderly were surveyed on socio-demographic information, biomarkers, psychosocial status, disability, and cognitive function. A biopsychosocial model of cognitive function was developed to test variables' predictive power on cognitive function. Statistical analyses were performed using SPSS (version 15.0) in conjunction with Analysis of Moment Structures Graphics (AMOS 7.0).

    RESULTS: The estimated theoretical model fitted the data well. Psychosocial stress and metabolic syndrome (MetS) negatively predicted cognitive function and psychosocial stress appeared as a main predictor. Socio-demographic characteristics, except gender, also had significant effects on cognitive function. However, disability failed to predict cognitive function.

    CONCLUSION: Several factors together may predict cognitive function in the Malaysian elderly population, and the variance accounted for it is large enough to be considered substantial. Key factor associated with the elderly's cognitive function seems to be psychosocial well-being. Thus, psychosocial well-being should be included in the elderly assessment, apart from medical conditions, both in clinical and community setting.

    Matched MeSH terms: Mild Cognitive Impairment/epidemiology*
  18. Foong HF, Hamid TA, Ibrahim R, Haron SA, Shahar S
    Geriatr Gerontol Int, 2017 Nov;17(11):1914-1920.
    PMID: 28188667 DOI: 10.1111/ggi.12993
    AIM: Metabolic syndrome and chronic conditions are significant predictors of cognition; however, few studies have examined how they work together in predicting cognition in old age. Therefore, the present study examines whether a chronic condition mediates the association between metabolic syndrome and cognition. In addition, it discusses the moderating role of sex in the relationships between metabolic syndrome, chronic conditions and cognition.

    METHODS: Secondary analysis was carried out of data from the Malaysian national survey that involved 2322 community residents aged 60 years or older in Peninsular Malaysia. Cognition was measured by the digit symbol substitution test. Metabolic syndrome was assessed by five biomarkers: triglyceride, fasting blood sugar, systolic blood pressure, cholesterol ratio and body mass index. Chronic conditions were assessed by self-reported medical history. The structural equation modeling technique was used to analyze the mediation and moderation tests.

    RESULTS: The number of chronic conditions partially mediated the association between metabolic syndrome and cognition. Men and women did not differ in the relationship between metabolic syndrome and cognition; however, the number of chronic conditions was found to be negatively associated with cognition in older women, but not in men.

    CONCLUSIONS: Metabolic syndrome might increase the likelihood of older adults to suffer from more chronic conditions; these responses might reduce their cognition. To prevent cognitive decline in old age, specific intervention to minimize the number of chronic conditions by reducing their vascular risk factors is warranted, especially among older women. Geriatr Gerontol Int 2017; 17: 1914-1920.

    Matched MeSH terms: Mild Cognitive Impairment/physiopathology*
  19. Abdo Qaid EY, Zulkipli NN, Zakaria R, Ahmad AH, Othman Z, Muthuraju S, et al.
    Int J Neurosci, 2021 May;131(5):482-488.
    PMID: 32202188 DOI: 10.1080/00207454.2020.1746308
    Hypoxia has been associated with cognitive impairment. Many studies have investigated the role of mTOR signalling pathway in cognitive functions but its role in hypoxia-induced cognitive impairment remains controversial. This review aimed to elucidate the role of mTOR in the mechanisms of cognitive impairment that may pave the way towards the mechanistic understanding and therapeutic intervention of hypoxia-induced cognitive impairment. mTORC1 is normally regulated during mild or acute hypoxic exposure giving rise to neuroprotection, whereas it is overactivated during severe or chronic hypoxia giving rise to neuronal cells death. Thus, it is worth exploring the possibility of maintaining normal mTORC1 activity and thereby preventing cognitive impairment during severe or chronic hypoxia.
    Matched MeSH terms: Mild Cognitive Impairment/etiology; Mild Cognitive Impairment/metabolism*; Mild Cognitive Impairment/prevention & control
  20. Guure CB, Ibrahim NA, Adam MB, Said SM
    Biomed Res Int, 2017;2017:9016924.
    PMID: 28271072 DOI: 10.1155/2017/9016924
    The association of physical activity with dementia and its subtypes has remained controversial in the literature and has continued to be a subject of debate among researchers. A systematic review and meta-analysis of longitudinal studies on the relationship between physical activity and the risk of cognitive decline, all-cause dementia, Alzheimer's disease, and vascular dementia among nondemented subjects are considered. A comprehensive literature search in all available databases was conducted up until April 2016. Well-defined inclusion and exclusion criteria were developed with focus on prospective studies ≥ 12 months. The overall sample from all studies is 117410 with the highest follow-up of 28 years. The analyses are performed with both Bayesian parametric and nonparametric models. Our analysis reveals a protective effect for high physical activity on all-cause dementia, odds ratio of 0.79, 95% CI (0.69, 0.88), a higher and better protective effect for Alzheimer's disease, odds ratio of 0.62, 95% CI (0.49, 0.75), cognitive decline odds ratio of 0.67, 95% CI (0.55, 0.78), and a nonprotective effect for vascular dementia of 0.92, 95% CI (0.62, 1.30). Our findings suggest that physical activity is more protective against Alzheimer's disease than it is for all-cause dementia, vascular dementia, and cognitive decline.
    Matched MeSH terms: Mild Cognitive Impairment/physiopathology*
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