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  1. Article ; Online: Simvastatin Attenuates Hippocampal MMP-9 Expression in the Streptozotocin-Induced Cognitive Impairment

    Adeli, Soheila / Zahmatkesh, Maryam / Ansari Dezfouli, Mitra

    Iranian biomedical journal

    2018  Volume 23, Issue 4, Page(s) 262–271

    Abstract: Background: Matrix metalloproteinase-9 (MMP-9) expression has been implicated in molecular mechanisms of neurodegenerative disorders, and its abnormal level has been reported in Alzheimer’s disease (AD). Some protective mechanisms of statins against ... ...

    Abstract Background: Matrix metalloproteinase-9 (MMP-9) expression has been implicated in molecular mechanisms of neurodegenerative disorders, and its abnormal level has been reported in Alzheimer’s disease (AD). Some protective mechanisms of statins against neurodegeneration might be mediated by the inhibition of MMP-9 expression. Here, we investigated the effect of simvastatin on the hippocampal MMP-9 expression in the context of AD.
    Methods: We examined the influence of three-week simvastatin (5 mg/kg) administration on hippocampal MMP-9 expression in a rat model of cognitive decline induced by streptozotocin (STZ). Spatial long-term memory and MMP-9 expression were assessed by Morris water maze (MWM) test and quantitative polymerase chain reaction, respectively.
    Results: The results showed a decline in the learning and memory in STZ group when compared with the control group. The MMP-9 up-regulated (1.41 ± 0.2 vs. 0.980 ± 0.02, p < 0.05), and cresyl violet staining showed hippocampal cell damage in STZ group compared with the control group. Simvastatin prevented the up-regulation of MMP-9 (1.05 ± 0.05 vs. 1.41 ± 0.2, p < 0.05), improved spatial memory impairment and attenuated hippocampal cell damage. Furthermore, we found a negative correlation (r = 0.77) between MMP-9 expression and cognitive function.
    Conclusion: Our findings suggest that the neuroprotective influence of simvastatin in battle to cognitive impairment is mediated in part by the modulation of MMP-9 expression. The reduction of MMP-9 expression in simvastatin-treated animals is in correlation with the improvement of cognitive functions. Understanding the protective mechanism of simvastatin will shed light on more efficient therapeutic modalities in AD.
    MeSH term(s) Animals ; Cell Shape/drug effects ; Cognitive Dysfunction/chemically induced ; Cognitive Dysfunction/drug therapy ; Cognitive Dysfunction/enzymology ; Cognitive Dysfunction/physiopathology ; Gene Expression Regulation, Enzymologic/drug effects ; Hippocampus/drug effects ; Hippocampus/enzymology ; Hippocampus/physiopathology ; Male ; Matrix Metalloproteinase 9/genetics ; Matrix Metalloproteinase 9/metabolism ; Maze Learning/drug effects ; Memory/drug effects ; Motor Activity/drug effects ; Neurons/drug effects ; Neurons/pathology ; Pyramidal Cells/drug effects ; Pyramidal Cells/metabolism ; Rats, Wistar ; Simvastatin/pharmacology ; Simvastatin/therapeutic use ; Streptozocin
    Chemical Substances Streptozocin (5W494URQ81) ; Simvastatin (AGG2FN16EV) ; Matrix Metalloproteinase 9 (EC 3.4.24.35)
    Language English
    Publishing date 2018-09-16
    Publishing country Iran
    Document type Journal Article
    ZDB-ID 2489282-8
    ISSN 2008-823X ; 1028-852X
    ISSN (online) 2008-823X
    ISSN 1028-852X
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Melatonin protective effect against amyloid β-induced neurotoxicity mediated by mitochondrial biogenesis; involvement of hippocampal Sirtuin-1 signaling pathway.

    Ansari Dezfouli, Mitra / Zahmatkesh, Maryam / Farahmandfar, Maryam / Khodagholi, Fariba

    Physiology & behavior

    2019  Volume 204, Page(s) 65–75

    Abstract: Melatonin has a potential therapeutic value in Alzheimer's disease (AD), a disease that is associated with a dramatic decline in memory and cognitive abilities. The aggregation of the amyloid β (Aβ) peptide, a hallmark of AD, deactivates mitochondrial ... ...

    Abstract Melatonin has a potential therapeutic value in Alzheimer's disease (AD), a disease that is associated with a dramatic decline in memory and cognitive abilities. The aggregation of the amyloid β (Aβ) peptide, a hallmark of AD, deactivates mitochondrial biogenesis and antioxidant defenses. Melatonin as an endogenous antioxidant, decreases in plasma and cerebrospinal fluid of AD patients. Even though several experimental studies have demonstrated the melatonin neuroprotection in AD, clinical trials of melatonin therapy have not yet confirmed outstanding results in AD patients. Better understanding of the molecular mechanisms involved in melatonin neuroprotective effects may pave the way for an efficient therapy. Hence, we investigated the involvement of silent information regulator 1 (SIRT1) signaling and mitochondrial biogenesis in melatonin neuroprotection in a rat model of cognitive impairment induced by intra-hippocampal Aβ injection. Animals assigned to melatonin treatment in the presence or absence of SIRT1 inhibitor (EX527), for 14 consecutive days. Spatial working memory and anxiety level were examined with Y-maze and elevated plus maze tests respectively. Hippocampal SIRT1, transcription factor-A mitochondrial (TFAM) and mitochondrial DNA (mtDNA) copy number were measured. We observed a decrease in hippocampal SIRT1, which accompanied with reduction in TFAM and mtDNA copy number in the Aβ-injected rats. Melatonin treatment increased hippocampal SIRT1 and TFAM expression and enhanced mtDNA copy number in the hippocampus. It also improved memory, ameliorated the anxiety, and attenuated hippocampal cell damage in the Aβ-injected animals. These effects were blocked by EX527 administration, suggesting SIRT1 signaling involvement in melatonin neuroprotective effect. This mechanism may introduce a new promising strategy in battle against AD.
    MeSH term(s) Amyloid beta-Peptides/antagonists & inhibitors ; Amyloid beta-Peptides/toxicity ; Animals ; Anxiety/prevention & control ; Anxiety/psychology ; Carbazoles/pharmacology ; Exploratory Behavior/drug effects ; Gene Dosage ; Hippocampus/drug effects ; Male ; Melatonin/pharmacology ; Memory, Short-Term/drug effects ; Motor Activity/drug effects ; Neuroprotective Agents/pharmacology ; Organelle Biogenesis ; Rats ; Rats, Wistar ; Signal Transduction/drug effects ; Sirtuin 1/antagonists & inhibitors ; Sirtuin 1/drug effects ; Transcription Factors/biosynthesis ; Transcription Factors/genetics
    Chemical Substances 6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide ; Amyloid beta-Peptides ; Carbazoles ; Neuroprotective Agents ; Tfam protein, rat ; Transcription Factors ; Sirt1 protein, rat (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-) ; Melatonin (JL5DK93RCL)
    Language English
    Publishing date 2019-02-12
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3907-x
    ISSN 1873-507X ; 0031-9384
    ISSN (online) 1873-507X
    ISSN 0031-9384
    DOI 10.1016/j.physbeh.2019.02.016
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 747: Show issues Location:
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  3. Article: Genetic and epigenetic effects on couple adjustment in context of romantic relationship: A scoping systematic review.

    Khani, Pouria / Ansari Dezfouli, Mitra / Nasri, Farzad / Rahemi, Maryam / Ahmadloo, Salma / Afkhami, Hamed / Saeidi, Farzane / Tereshchenko, Sergey / Bigdeli, Mohammad Reza / Modarressi, Mohammad Hossein

    Frontiers in genetics

    2023  Volume 14, Page(s) 1002048

    Abstract: Introduction: ...

    Abstract Introduction:
    Language English
    Publishing date 2023-01-24
    Publishing country Switzerland
    Document type Systematic Review
    ZDB-ID 2606823-0
    ISSN 1664-8021
    ISSN 1664-8021
    DOI 10.3389/fgene.2023.1002048
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Does hazelnut consumption affect brain health and function against neurodegenerative diseases?

    Talebi, Shadi / Khodagholi, Fariba / Bahaeddin, Zahra / Ansari Dezfouli, Mitra / Zeinaddini-Meymand, Arman / Berchi Kankam, Samuel / Foolad, Forough / Alijaniha, Fatemeh / Fayazi Piranghar, Fatemeh

    Nutritional neuroscience

    2023  , Page(s) 1–17

    Abstract: Introduction: A healthy daily diet and consuming certain nutrients, such as polyphenols, vitamins, and unsaturated fatty acids, may help neuronal health maintenance. Polyphenolic chemicals, which have antioxidant and anti-inflammatory properties, are ... ...

    Abstract Introduction: A healthy daily diet and consuming certain nutrients, such as polyphenols, vitamins, and unsaturated fatty acids, may help neuronal health maintenance. Polyphenolic chemicals, which have antioxidant and anti-inflammatory properties, are involved in the neuroprotective pathway. Because of their nutritional value, nuts have been shown in recent research to be helpful in neuroprotection.
    Objective: Hazelnut is often consumed worldwide in various items, including processed foods, particularly in bakery, chocolate, and confectionery products. This nut is an excellent source of vitamins, amino acids, tocopherols, phytosterols, polyphenols, minerals, and unsaturated fatty acids. Consuming hazelnut may attenuate the risk of neurodegenerative disorders including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis, and Huntington's disease due to its anti-inflammatory and anti-oxidant qualities.
    Results: Many documents introduce hazelnut as an excellent choice to provide neuroprotection against neurodegenerative disorders and there is some direct proof of its neuroprotective effects.
    Discussion: So hazelnut consumption in daily diet may reduce neurodegenerative disease risk and be advantageous in reducing the imposed costs of dealing with neurodegenerative diseases.
    Language English
    Publishing date 2023-12-27
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1447449-9
    ISSN 1476-8305 ; 1028-415X
    ISSN (online) 1476-8305
    ISSN 1028-415X
    DOI 10.1080/1028415X.2023.2296164
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Bonn / Germany

    Z 7024: Show issues

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  5. Article: Melatonin protective effect against amyloid β-induced neurotoxicity mediated by mitochondrial biogenesis; involvement of hippocampal Sirtuin-1 signaling pathway

    Ansari Dezfouli, Mitra / Zahmatkesh, Maryam / Farahmandfar, Maryam / Khodagholi, Fariba

    Physiology & behavior. 2019 May 15, v. 204

    2019  

    Abstract: Melatonin has a potential therapeutic value in Alzheimer's disease (AD), a disease that is associated with a dramatic decline in memory and cognitive abilities. The aggregation of the amyloid β (Aβ) peptide, a hallmark of AD, deactivates mitochondrial ... ...

    Abstract Melatonin has a potential therapeutic value in Alzheimer's disease (AD), a disease that is associated with a dramatic decline in memory and cognitive abilities. The aggregation of the amyloid β (Aβ) peptide, a hallmark of AD, deactivates mitochondrial biogenesis and antioxidant defenses. Melatonin as an endogenous antioxidant, decreases in plasma and cerebrospinal fluid of AD patients. Even though several experimental studies have demonstrated the melatonin neuroprotection in AD, clinical trials of melatonin therapy have not yet confirmed outstanding results in AD patients. Better understanding of the molecular mechanisms involved in melatonin neuroprotective effects may pave the way for an efficient therapy. Hence, we investigated the involvement of silent information regulator 1 (SIRT1) signaling and mitochondrial biogenesis in melatonin neuroprotection in a rat model of cognitive impairment induced by intra-hippocampal Aβ injection. Animals assigned to melatonin treatment in the presence or absence of SIRT1 inhibitor (EX527), for 14 consecutive days. Spatial working memory and anxiety level were examined with Y-maze and elevated plus maze tests respectively. Hippocampal SIRT1, transcription factor-A mitochondrial (TFAM) and mitochondrial DNA (mtDNA) copy number were measured. We observed a decrease in hippocampal SIRT1, which accompanied with reduction in TFAM and mtDNA copy number in the Aβ-injected rats. Melatonin treatment increased hippocampal SIRT1 and TFAM expression and enhanced mtDNA copy number in the hippocampus. It also improved memory, ameliorated the anxiety, and attenuated hippocampal cell damage in the Aβ-injected animals. These effects were blocked by EX527 administration, suggesting SIRT1 signaling involvement in melatonin neuroprotective effect. This mechanism may introduce a new promising strategy in battle against AD.
    Keywords Alzheimer disease ; amyloid ; animal models ; antioxidant activity ; antioxidants ; anxiety ; biogenesis ; cerebrospinal fluid ; clinical trials ; cognition ; cognitive disorders ; hippocampus ; melatonin ; memory ; mitochondria ; mitochondrial DNA ; neuroprotective effect ; neurotoxicity ; patients ; rats ; signal transduction ; therapeutics ; transcription factors
    Language English
    Dates of publication 2019-0515
    Size p. 65-75.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 3907-x
    ISSN 1873-507X ; 0031-9384
    ISSN (online) 1873-507X
    ISSN 0031-9384
    DOI 10.1016/j.physbeh.2019.02.016
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    In stock of ZB MED Bonn / Germany

    Z 74/401: Show issues

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  6. Article ; Online: Characterization of a Rare Mosaicism in Autosomal Translocation of t(5;21) Using Conventional Cytogenetics and FISH Methods

    Omori Sarabi, Sadaf / Karimzad Hagh, Javad / Behrend, Claudia / Mohseni, Seyed Behrooz / Ansari Dezfouli, Mitra / Rashidi, Seyed Khalil / Omrani, Mir Davood

    Iranian biomedical journal

    2019  Volume 24, Issue 1, Page(s) 60–63

    Abstract: Background: Mosaicism of a normal cell population and an unbalanced autosomal chromosome rearrangement is rarely seen. If the abnormal cell line contributes to a minor part of soma, the phenotype is expected to be normal.: Case report: We report a 29- ...

    Abstract Background: Mosaicism of a normal cell population and an unbalanced autosomal chromosome rearrangement is rarely seen. If the abnormal cell line contributes to a minor part of soma, the phenotype is expected to be normal.
    Case report: We report a 29-year-old woman who had balance chromosomal translocation of 46,XX,t(5;21) with a two-year-old affected girl, characterized by mental retardation, dystrophia, hearing impartment, and dysphagia.
    Methods and results: Cytogenetic investigation revealed a low mosaic unbalanced translocation of 46,XX,t(5;21)/ 46,XX, which was confirmed by fluorescence in situ hybridization analysis. Studying 200 metaphases and interphases of peripheral blood sample revealed 70% partial monosomy of 21q22 and partial trisomy of 5q(35.3) and 30% of normal pattern.
    Conclusion: In rare cases such as this study, parents with balanced translocation with no phenotypes may lead to a mosaic unbalanced translocation with abnormal phenotypes in offspring, which underscores the need for prenatal karyotyping and genetics counseling.
    MeSH term(s) Child, Preschool ; Chromosomes, Human, Pair 21/genetics ; Chromosomes, Human, Pair 5/genetics ; Cytogenetics ; Humans ; In Situ Hybridization, Fluorescence ; Karyotyping ; Mosaicism ; Translocation, Genetic/genetics
    Language English
    Publishing date 2019-07-14
    Publishing country Iran
    Document type Case Reports ; Journal Article
    ZDB-ID 2489282-8
    ISSN 2008-823X ; 1028-852X
    ISSN (online) 2008-823X
    ISSN 1028-852X
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6776: Show issues Location:
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  7. Article: Common Genetic Variant in VIT Is Associated with Human Brain Asymmetry.

    Tadayon, Sayed H / Vaziri-Pashkam, Maryam / Kahali, Pegah / Ansari Dezfouli, Mitra / Abbassian, Abdolhossein

    Frontiers in human neuroscience

    2016  Volume 10, Page(s) 236

    Abstract: Brain asymmetry varies across individuals. However, genetic factors contributing to this normal variation are largely unknown. Here we studied variation of cortical surface area asymmetry in a large sample of subjects. We performed principal component ... ...

    Abstract Brain asymmetry varies across individuals. However, genetic factors contributing to this normal variation are largely unknown. Here we studied variation of cortical surface area asymmetry in a large sample of subjects. We performed principal component analysis (PCA) to capture correlated asymmetry variation across cortical regions. We found that caudal and rostral anterior cingulate together account for a substantial part of asymmetry variation among individuals. To find SNPs associated with this subset of brain asymmetry variation we performed a genome-wide association study followed by replication in an independent cohort. We identified one SNP (rs11691187) that had genome-wide significant association (P Combined = 2.40e-08). The rs11691187 is in the first intron of VIT. In a follow-up analysis, we found that VIT gene expression is associated with brain asymmetry in six donors of the Allen Human Brain Atlas. Based on these findings we suggest that VIT contributes to normal brain asymmetry variation. Our results can shed light on disorders associated with altered brain asymmetry.
    Language English
    Publishing date 2016-05-24
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2425477-0
    ISSN 1662-5161
    ISSN 1662-5161
    DOI 10.3389/fnhum.2016.00236
    Database MEDical Literature Analysis and Retrieval System OnLINE

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