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  1. Article ; Online: Baseline serum brain-derived neurotrophic factor association with future cognition in community-dwelling older adults undergoing annual memory screening.

    Keegan, Andrew P / Stough, Con / Paris, Daniel / Luis, Cheryl A / Abdullah, Laila / Ait-Ghezala, Ghania / Chaykin, Jillian / Crawford, Fiona / Mullan, Michael

    Neurological research

    2024  Volume 46, Issue 3, Page(s) 253–260

    Abstract: Objectives: It has been shown that peripheral measures of brain-derived neurotrophic factor (BNDF), an important neurotrophin instrumental to the biology of learning, may contribute to predicting cognitive decline. However, the two primary forms of BDNF, ...

    Abstract Objectives: It has been shown that peripheral measures of brain-derived neurotrophic factor (BNDF), an important neurotrophin instrumental to the biology of learning, may contribute to predicting cognitive decline. However, the two primary forms of BDNF, mature (mBDNF) and pro (proBDNF), and how they contribute to cognition longitudinally has not been well studied.
    Methods: Eighty-two older adults (average age 72.2 ± 6.4 years) provided blood samples at two time points separated on average by 4.2 years while participating in an annual memory screening that included the MoCA (Montreal Cognitive Assessment) and GDS (Geriatric Depression Scale). Both mBDNF and proBDNF from serum were quantified at each time point. Whole blood samples were genotyped for
    Results: Using logistic regression analysis controlling for age, sex, baseline MoCA score,
    Discussion: This study further supports that mBDNF measured in the serum of older adults may reflect a protective role while proBDNF requires further investigation.
    MeSH term(s) Humans ; Aged ; Brain-Derived Neurotrophic Factor/genetics ; Independent Living ; Cognition ; Cognitive Dysfunction/diagnosis ; Cognitive Dysfunction/genetics ; Apolipoproteins E
    Chemical Substances Brain-Derived Neurotrophic Factor ; Apolipoproteins E
    Language English
    Publishing date 2024-01-22
    Publishing country England
    Document type Journal Article
    ZDB-ID 424428-x
    ISSN 1743-1328 ; 0161-6412
    ISSN (online) 1743-1328
    ISSN 0161-6412
    DOI 10.1080/01616412.2023.2294581
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1491: Show issues Location:
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  2. Article ; Online: Bacopa monnieri

    Keegan, Andrew P / Stough, Con / Paris, Daniel / Luis, Cheryl A / Abdullah, Laila / Ait-Ghezala, Ghania / Crawford, Fiona / Mullan, Michael

    Journal of clinical and translational research

    2023  Volume 9, Issue 1, Page(s) 50–58

    Abstract: Background and aim: Bacopa monnieri: Methods: Bacopa was administered in an open-labeled study to cognitively healthy controls over a 3-month period. Cognition and mood were assessed using the Montreal Cognitive Assessment (MoCA) and geriatric ... ...

    Abstract Background and aim: Bacopa monnieri
    Methods: Bacopa was administered in an open-labeled study to cognitively healthy controls over a 3-month period. Cognition and mood were assessed using the Montreal Cognitive Assessment (MoCA) and geriatric depression scale (GDS) at the baseline and 3-month visit. Laboratories were assessed for safety and serum levels of mature (mBDNF) and proBDNF were quantified. In a subset of subjects, intracellular signaling processes were assessed using western blot analysis.
    Results: Bacopa was provided to 35 subjects and was well-tolerated except for 4 (11%) subjects who early terminated due to known, reversible, and gastrointestinal side effects (i.e., nausea, diarrhea). Over the 3 months, the GDS and the total MoCA did not significantly change; however, the delayed-recall subscale significantly improved (baseline: 3.8 ± 1.2, 3-months: 4.3 ± 0.9;
    Conclusion: These results suggest that Bacopa may exert an anti-inflammatory effect through NF-κB and improve intracellular signaling processes associated with synaptogenesis (CREB). The future placebo-controlled studies are recommended.
    Relevance for patients: B. monnieri
    Language English
    Publishing date 2023-01-17
    Publishing country Singapore
    Document type Journal Article
    ZDB-ID 3019815-X
    ISSN 2424-810X ; 2382-6533
    ISSN (online) 2424-810X
    ISSN 2382-6533
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  3. Article ; Online: Sex-Specific Regulation of β-Secretase: A Novel Estrogen Response Element (ERE)-Dependent Mechanism in Alzheimer's Disease.

    Cui, Jie / Ait-Ghezala, Ghania / Sambamurti, Kumar / Gao, Feng / Shen, Yong / Li, Rena

    The Journal of neuroscience : the official journal of the Society for Neuroscience

    2021  Volume 42, Issue 6, Page(s) 1154–1165

    Abstract: Women have a higher prevalence and incidence of Alzheimer's disease (AD) than age-matched men, and loss of estrogen might be partially responsible for the higher risk of AD in aged women. While β-secretase (BACE1) plays an important role in AD ... ...

    Abstract Women have a higher prevalence and incidence of Alzheimer's disease (AD) than age-matched men, and loss of estrogen might be partially responsible for the higher risk of AD in aged women. While β-secretase (BACE1) plays an important role in AD pathogenesis, whether BACE1 involved the sex difference in AD pathology remains unclear. This study investigated the hypothesis that estrogen regulates BACE1 transcription via the estrogen response element (ERE) and designated pathways. Using estrogen receptor (ER) knock-out mice and mutagenesis of EREs in HEK293 cells, we demonstrated sex-specific inhibition of BACE1 transcription by estrogen via direct binding to ERE sites and ERα. We also used a repressor of estrogen receptor activity (REA) and showed that an REA-ERE complex downregulated BACE1. A chromatin immunoprecipitation assay analysis determined that all three EREs at the BACE1 promoter were required for estradiol-mediated downregulation of BACE1 transcription in mice. Last, we confirmed the impairment of the REA pathway in the cortex of female AD patients. Our study identified an estrogen-specific BACE1 transcriptional regulation pathway from cell and animal models to AD patients.
    MeSH term(s) Alzheimer Disease/metabolism ; Amyloid Precursor Protein Secretases/biosynthesis ; Animals ; Estrogen Receptor alpha/metabolism ; Estrogens/metabolism ; Female ; Gene Expression Regulation/physiology ; HEK293 Cells ; Humans ; Male ; Mice ; Mice, Knockout ; Response Elements/physiology ; Sex Characteristics ; Transcription, Genetic
    Chemical Substances Estrogen Receptor alpha ; Estrogens ; Amyloid Precursor Protein Secretases (EC 3.4.-)
    Language English
    Publishing date 2021-12-13
    Publishing country United States
    Document type Journal Article
    ZDB-ID 604637-x
    ISSN 1529-2401 ; 0270-6474
    ISSN (online) 1529-2401
    ISSN 0270-6474
    DOI 10.1523/JNEUROSCI.0864-20.2021
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1668: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: MMP9 modulation improves specific neurobehavioral deficits in a mouse model of Alzheimer's disease.

    Ringland, Charis / Schweig, Jonas Elias / Eisenbaum, Maxwell / Paris, Daniel / Ait-Ghezala, Ghania / Mullan, Michael / Crawford, Fiona / Abdullah, Laila / Bachmeier, Corbin

    BMC neuroscience

    2021  Volume 22, Issue 1, Page(s) 39

    Abstract: Background: Matrix metallopeptidase 9 (MMP9) has been implicated in a variety of neurological disorders, including Alzheimer's disease (AD), where MMP9 levels are elevated in the brain and cerebrovasculature. Previously our group demonstrated ... ...

    Abstract Background: Matrix metallopeptidase 9 (MMP9) has been implicated in a variety of neurological disorders, including Alzheimer's disease (AD), where MMP9 levels are elevated in the brain and cerebrovasculature. Previously our group demonstrated apolipoprotein E4 (apoE4) was less efficient in regulating MMP9 activity in the brain than other apoE isoforms, and that MMP9 inhibition facilitated beta-amyloid (Aβ) elimination across the blood-brain barrier (BBB) METHODS: In the current studies, we evaluated the impact of MMP9 modulation on Aβ disposition and neurobehavior in AD using two approaches, (1) pharmacological inhibition of MMP9 with SB-3CT in apoE4 x AD (E4FAD) mice, and (2) gene deletion of MMP9 in AD mice (MMP9KO/5xFAD) RESULTS: Treatment with the MMP9 inhibitor SB-3CT in E4FAD mice led to reduced anxiety compared to placebo using the elevated plus maze. Deletion of the MMP9 gene in 5xFAD mice also reduced anxiety using the open field test, in addition to improving sociability and social recognition memory, particularly in male mice, as assessed through the three-chamber task, indicating certain behavioral alterations in AD may be mediated by MMP9. However, neither pharmacological inhibition of MMP9 or gene deletion of MMP9 affected spatial learning or memory in the AD animals, as determined through the radial arm water maze. Moreover, the effect of MMP9 modulation on AD neurobehavior was not due to changes in Aβ disposition, as both brain and plasma Aβ levels were unchanged in the SB-3CT-treated E4FAD animals and MMP9KO/AD mice compared to their respective controls.
    Conclusions: In total, while MMP9 inhibition did improve specific neurobehavioral deficits associated with AD, such as anxiety and social recognition memory, modulation of MMP9 did not alter spatial learning and memory or Aβ tissue levels in AD animals. While targeting MMP9 may represent a therapeutic strategy to mitigate aspects of neurobehavioral decline in AD, further work is necessary to understand the nature of the relationship between MMP9 activity and neurological dysfunction.
    MeSH term(s) Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Alzheimer Disease/psychology ; Amyloid beta-Peptides/genetics ; Animals ; Anxiety/drug therapy ; Anxiety/genetics ; Anxiety/metabolism ; Anxiety/psychology ; Brain/metabolism ; Female ; Heterocyclic Compounds, 1-Ring/pharmacology ; Heterocyclic Compounds, 1-Ring/therapeutic use ; Male ; Matrix Metalloproteinase 9/deficiency ; Matrix Metalloproteinase 9/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Motor Activity/drug effects ; Motor Activity/physiology ; Presenilin-1/genetics ; Social Interaction/drug effects ; Spatial Learning/drug effects ; Spatial Learning/physiology ; Sulfones/pharmacology ; Sulfones/therapeutic use
    Chemical Substances Amyloid beta-Peptides ; Heterocyclic Compounds, 1-Ring ; Presenilin-1 ; SB 3CT compound ; Sulfones ; presenilin 1, mouse ; Matrix Metalloproteinase 9 (EC 3.4.24.35) ; Mmp9 protein, mouse (EC 3.4.24.35)
    Language English
    Publishing date 2021-05-25
    Publishing country England
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2041344-0
    ISSN 1471-2202 ; 1471-2202
    ISSN (online) 1471-2202
    ISSN 1471-2202
    DOI 10.1186/s12868-021-00643-2
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  5. Article ; Online: Novel, natural allosteric inhibitors and enhancers of Candida rugosa lipase activity.

    Menden, Ariane / Crynen, Stefan / Mathura, Venkatarian / Paris, Daniel / Crawford, Fiona / Mullan, Michael / Ait-Ghezala, Ghania

    Bioorganic chemistry

    2021  Volume 109, Page(s) 104732

    Abstract: Candida rugosa lipase (CRL) is an enzyme commonly used in medicinal and biotechnological applications. Allosteric modulators of CRL could aid in modifying lipase-related diseases as well as improving biotechnological processes. Thus, a combinatorial ... ...

    Abstract Candida rugosa lipase (CRL) is an enzyme commonly used in medicinal and biotechnological applications. Allosteric modulators of CRL could aid in modifying lipase-related diseases as well as improving biotechnological processes. Thus, a combinatorial approach of computational in-silico and high-throughput in-vitro screening was used to identify allosteric modulators of CRL. The screening of natural product libraries resulted in 132 compounds of which 53 were tested in-vitro. Subsequently, four inhibitors and three enhancers were identified of which rutin and cynaroside represented the strongest inhibitors of CRL activity (IC50: 227 ± 26 µM and 446 ± 15 µM, respectively) and NP-008496 the strongest enhancer (EC50: 425 ± 18 µM). All three compounds were predicted to bind the same allosteric site suggesting a common mechanism. Therefore, the present study demonstrated a reliable work-flow, identified an allosteric site of CRL and determined inhibitors and enhancers with numerous potential medical and biotechnological applications.
    MeSH term(s) Allosteric Site/drug effects ; Biological Products/chemical synthesis ; Biological Products/chemistry ; Biological Products/pharmacology ; Dose-Response Relationship, Drug ; Enzyme Inhibitors/chemical synthesis ; Enzyme Inhibitors/chemistry ; Enzyme Inhibitors/pharmacology ; Kinetics ; Lipase/metabolism ; Molecular Docking Simulation ; Molecular Structure ; Saccharomycetales/enzymology ; Structure-Activity Relationship
    Chemical Substances Biological Products ; Enzyme Inhibitors ; Lipase (EC 3.1.1.3)
    Language English
    Publishing date 2021-02-16
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 120080-x
    ISSN 1090-2120 ; 0045-2068
    ISSN (online) 1090-2120
    ISSN 0045-2068
    DOI 10.1016/j.bioorg.2021.104732
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    Zs.A 4207: Show issues Location:
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  6. Article ; Online: Adaptive Immune Responses Associated with the Central Nervous System Pathology of Gulf War Illness.

    Nkiliza, Aurore / Joshi, Utsav / Evans, James E / Ait-Ghezala, Ghania / Parks, Megan / Crawford, Fiona / Mullan, Michael / Abdullah, Laila

    Neuroscience insights

    2021  Volume 16, Page(s) 26331055211018458

    Abstract: Gulf War Illness is a multisymptomatic condition which affects 30% of veterans from the 1991 Gulf War. While there is evidence for a role of peripheral cellular and humoral adaptive immune responses in Gulf War Illness, a potential role of the adaptive ... ...

    Abstract Gulf War Illness is a multisymptomatic condition which affects 30% of veterans from the 1991 Gulf War. While there is evidence for a role of peripheral cellular and humoral adaptive immune responses in Gulf War Illness, a potential role of the adaptive immune system in the central nervous system pathology of this condition remains unknown. Furthermore, many of the clinical features of Gulf War Illness resembles those of autoimmune diseases, but the biological processes are likely different as the etiology of Gulf War Illness is linked to hazardous chemical exposures specific to the Gulf War theatre. This review discusses Gulf War chemical-induced maladaptive immune responses and a potential role of cellular and humoral immune responses that may be relevant to the central nervous system symptoms and pathology of Gulf War Illness. The discussion may stimulate investigations into adaptive immunity for developing novel therapies for Gulf War Illness.
    Language English
    Publishing date 2021-05-25
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2633-1055
    ISSN (online) 2633-1055
    DOI 10.1177/26331055211018458
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  7. Article ; Online: Impact of gulf war toxic exposures after mild traumatic brain injury.

    Ferguson, Scott / McCartan, Robyn / Browning, Mackenzie / Hahn-Townsend, Coral / Gratkowski, Arissa / Morin, Alexander / Abdullah, Laila / Ait-Ghezala, Ghania / Ojo, Joseph / Sullivan, Kimberly / Mullan, Michael / Crawford, Fiona / Mouzon, Benoit

    Acta neuropathologica communications

    2022  Volume 10, Issue 1, Page(s) 147

    Abstract: Chemical and pharmaceutical exposures have been associated with the development of Gulf War Illness (GWI), but how these factors interact with the pathophysiology of traumatic brain injury (TBI) remains an area of study that has received little attention ...

    Abstract Chemical and pharmaceutical exposures have been associated with the development of Gulf War Illness (GWI), but how these factors interact with the pathophysiology of traumatic brain injury (TBI) remains an area of study that has received little attention thus far. We studied the effects of pyridostigmine bromide (an anti-nerve agent) and permethrin (a pesticide) exposure in a mouse model of repetitive mild TBI (r-mTBI), with 5 impacts over a 9-day period, followed by Gulf War (GW) toxicant exposure for 10 days beginning 30 days after the last head injury. We then assessed the chronic behavioral and pathological sequelae 5 months after GW agent exposure. We observed that r-mTBI and GWI cumulatively affect the spatial memory of mice in the Barnes maze and result in a shift of search strategies employed by r-mTBI/GW exposed mice. GW exposure also produced anxiety-like behavior in sham animals, but r-mTBI produced disinhibition in both the vehicle and GW treated mice. Pathologically, GW exposure worsened r-mTBI dependent axonal degeneration and neuroinflammation, increased oligodendrocyte cell counts, and increased r-mTBI dependent phosphorylated tau, which was found to colocalize with oligodendrocytes in the corpus callosum. These results suggest that GW exposures may worsen TBI-related deficits. Veterans with a history of both GW chemical exposures as well as TBI may be at higher risk for worse symptoms and outcomes. Subsequent exposure to various toxic substances can influence the chronic nature of mTBI and should be considered as an etiological factor influencing mTBI recovery.
    MeSH term(s) Mice ; Animals ; Gulf War ; Brain Concussion/complications ; Pyridostigmine Bromide/toxicity ; Permethrin/toxicity ; Disease Models, Animal ; Brain Injuries, Traumatic ; Pesticides ; Pharmaceutical Preparations
    Chemical Substances Pyridostigmine Bromide (KVI301NA53) ; Permethrin (509F88P9SZ) ; Pesticides ; Pharmaceutical Preparations
    Language English
    Publishing date 2022-10-18
    Publishing country England
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2715589-4
    ISSN 2051-5960 ; 2051-5960
    ISSN (online) 2051-5960
    ISSN 2051-5960
    DOI 10.1186/s40478-022-01449-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Exogenous lipase administration alters gut microbiota composition and ameliorates Alzheimer's disease-like pathology in APP/PS1 mice.

    Menden, Ariane / Hall, Davane / Hahn-Townsend, Coral / Broedlow, Courtney A / Joshi, Utsav / Pearson, Andrew / Crawford, Fiona / Evans, James E / Klatt, Nichole / Crynen, Stefan / Mullan, Michael / Ait-Ghezala, Ghania

    Scientific reports

    2022  Volume 12, Issue 1, Page(s) 4797

    Abstract: Alzheimer's disease (AD) represents the most common form of dementia in the elderly with no available disease modifying treatments. Altered gut microbial composition has been widely acknowledged as a common feature of AD, which potentially contributes to ...

    Abstract Alzheimer's disease (AD) represents the most common form of dementia in the elderly with no available disease modifying treatments. Altered gut microbial composition has been widely acknowledged as a common feature of AD, which potentially contributes to progression or onset of AD. To assess the hypothesis that Candida rugosa lipase (CRL), which has been shown to enhance gut microbiome and metabolite composition, can rebalance the gut microbiome composition and reduce AD pathology, the treatment effects in APPswe/PS1de9 (APP/PS1) mice were investigated. The analysis revealed an increased abundance of Acetatifactor and Clostridiales vadin BB60 genera in the gut; increased lipid hydrolysis in the gut lumen, normalization of peripheral unsaturated fatty acids, and reduction of neuroinflammation and memory deficits post treatment. Finally, we demonstrated that the evoked benefits on memory could be transferred via fecal matter transplant (FMT) into antibiotic-induced microbiome-depleted (AIMD) wildtype mice, ameliorating their memory deficits. The findings herein contributed to improve our understanding of the role of the gut microbiome in AD's complex networks and suggested that targeted modification of the gut could contribute to amelioration of AD neuropathology.
    MeSH term(s) Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Animals ; Clostridiales/metabolism ; Disease Models, Animal ; Gastrointestinal Microbiome/physiology ; Lipase ; Memory Disorders ; Mice ; Mice, Transgenic
    Chemical Substances Amyloid beta-Peptides ; Lipase (EC 3.1.1.3)
    Language English
    Publishing date 2022-03-21
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-022-08840-7
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  9. Article ; Online: Candida rugosa lipase alters the gastrointestinal environment in wild-type mice.

    Menden, Ariane / Hall, Davane / Broedlow, Courtney Ann / Darcey, Teresa / Crawford, Fiona / Klatt, Nichole / Crynen, Stefan / Mullan, Michael / Ait-Ghezala, Ghania

    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

    2020  Volume 130, Page(s) 110579

    Abstract: Diet and commercially available supplements can significantly impact the gut microbial composition; however, the effects of supplements often lack scientific data demonstrating the effects on healthy and diseased individuals. Hence, it was investigated, ... ...

    Abstract Diet and commercially available supplements can significantly impact the gut microbial composition; however, the effects of supplements often lack scientific data demonstrating the effects on healthy and diseased individuals. Hence, it was investigated, whether a frequently used supplement in humans, Candida rugosa lipase (CRL), gets delivered active beyond the stomach in the intestinal tract of C57BL/6 J mice and its impact on the gut microbial community and environment. We showed for the first time the movement of CRL in an active state through the mouse digestive tract by determination of intestinal CRL activity and free fatty acids concentrations. The short- and long-term administration of CRL resulted in significant alterations of the gut microbiome, favoring the growth of, for instance, Verrucomicrobia but also other species associated with normal body mass index (BMI) or butyrate expression, both considered beneficial. In addition, we showed that these changes persisted after supplementation and that gut barrier integrity was unaffected by the treatment. In conclusion, CRL can be delivered in an active state beyond the stomach and supplementation altered the murine gut microbiome favoring beneficial bacterial species, which may be of relevance in humans in healthy but also potentially in disease states.
    MeSH term(s) Animals ; Bacteria/genetics ; Gastrointestinal Microbiome/drug effects ; Gastrointestinal Tract/drug effects ; Gastrointestinal Tract/microbiology ; Lipase/pharmacology ; Mice, Inbred C57BL ; RNA, Ribosomal, 16S/genetics ; Saccharomycetales/enzymology
    Chemical Substances RNA, Ribosomal, 16S ; Lipase (EC 3.1.1.3)
    Language English
    Publishing date 2020-08-06
    Publishing country France
    Document type Journal Article
    ZDB-ID 392415-4
    ISSN 1950-6007 ; 0753-3322 ; 0300-0893
    ISSN (online) 1950-6007
    ISSN 0753-3322 ; 0300-0893
    DOI 10.1016/j.biopha.2020.110579
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    In stock of ZB MED Cologne/Königswinter

    Ud II Zs.198: Show issues Location:
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  10. Article: Proteomic Identification of Pathways Responsible for the Estradiol Therapeutic Window in AD Animal Models.

    Cui, Jie / Reed, Jon / Crynen, Gogce / Ait-Ghezala, Ghania / Crawford, Fiona / Shen, Yong / Li, Rena

    Frontiers in cellular neuroscience

    2019  Volume 13, Page(s) 437

    Abstract: Benefits and risks were reported for hormone therapy (HT) to prevent chronic disease, including Alzheimer's disease (AD). While the Women's Health Initiative (WHI) found no protective effect of HT on the cognitive function of women whose treatment was ... ...

    Abstract Benefits and risks were reported for hormone therapy (HT) to prevent chronic disease, including Alzheimer's disease (AD). While the Women's Health Initiative (WHI) found no protective effect of HT on the cognitive function of women whose treatment was initiated far past the onset of menopause, other studies showed reduced risk of AD with midlife treatment, versus increased risk of AD with late treatment. These suggest a critical window during which estradiol must be administered to prevent cognitive decline and AD in women. Our published work supports this, by demonstrating that early and long-term estradiol treatment improves cognitive function and reduce Aβ accumulation in AD mouse models with estradiol deficiency, while there is no effect of late and short-term estradiol treatment on AD neuropathogenesis. However, little is known about the molecular mechanisms underlying the critical window and whether different protein networks are responsible for the brain estradiol deficiency-associated risk of AD in females. In this study, we used proteomics to identify target protein pathways that are activated during the estradiol therapeutic window in AD mouse model. Our results showed that different signaling pathways were involved in the regulatory effects of estradiol on MAP1A and hemoglobin α. Estradiol treatment increased the level of MAP1A through the phosphorylation of ERK1/2 and increased the level of hemoglobin α through the phosphorylation of AKT. This study has provided molecular insights into the "critical window" theory and identifies specific target proteins of therapeutic responsiveness that may lead to improved treatment strategies and optimal estradiol therapy.
    Language English
    Publishing date 2019-10-15
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2452963-1
    ISSN 1662-5102
    ISSN 1662-5102
    DOI 10.3389/fncel.2019.00437
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