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  1. AU="Sonntag, William E"
  2. AU="Tamagawa, Masumi"
  3. AU="Subhan, Fazli"
  4. AU="Parisi, A"
  5. AU="Calisher, C H"
  6. AU="Altaş, İrem"

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  1. Article: Systemic Listeria monocytogenes infection in aged mice induces long-term neuroinflammation: the role of miR-155.

    Cassidy, Benjamin R / Sonntag, William E / Leenen, Pieter J M / Drevets, Douglas A

    Immunity & ageing : I & A

    2022  Volume 19, Issue 1, Page(s) 25

    Abstract: Background: Understanding mechanisms of pathologic neuroinflammation is essential for improving outcomes after central nervous system infections. Brain tissue-resident memory T cells (bT: Methods: Young (2 mo) and aged (> 18 mo) male C57BL/6 mice ... ...

    Abstract Background: Understanding mechanisms of pathologic neuroinflammation is essential for improving outcomes after central nervous system infections. Brain tissue-resident memory T cells (bT
    Methods: Young (2 mo) and aged (> 18 mo) male C57BL/6 mice were infected intra-peritoneally with wild-type Lm, or avirulent Lm mutants lacking the genes required for intracellular motility (ΔactA) or phagosomal escape (Δhly), then were given antibiotics. Brain leukocytes and their intracellular cytokine production were quantified by flow cytometry >28d post-infection (p.i.). The role of miR-155 was tested by injecting mice with anti-miR-155 or control oligonucleotides along with antibiotics.
    Results: Aged mice had significantly more homeostatic CD8
    Conclusions: Systemic infection with Lm ΔactA is a novel model for studying infection-induced brain inflammation in aged mice without excessive mortality. CD8
    Language English
    Publishing date 2022-05-25
    Publishing country England
    Document type Journal Article
    ZDB-ID 2168941-6
    ISSN 1742-4933
    ISSN 1742-4933
    DOI 10.1186/s12979-022-00281-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Progressive cognitive impairment after recovery from neuroinvasive and non-neuroinvasive

    Cassidy, Benjamin R / Logan, Sreemathi / Farley, Julie A / Owen, Daniel B / Sonntag, William E / Drevets, Douglas A

    Frontiers in immunology

    2023  Volume 14, Page(s) 1146690

    Abstract: Background: Neuro-cognitive impairment is a deleterious complication of bacterial infections that is difficult to treat or prevent. : Methods: Male C57BL/6J mice (age 8 wks) were injected with neuroinvasive : Results: Changes suggesting cognitive ... ...

    Abstract Background: Neuro-cognitive impairment is a deleterious complication of bacterial infections that is difficult to treat or prevent.
    Methods: Male C57BL/6J mice (age 8 wks) were injected with neuroinvasive
    Results: Changes suggesting cognitive decline were observed 1 mo p.i. in both groups of infected mice compared with uninfected controls, but were more widespread and significantly worse 4 mo p.i. and most notably after
    Conclusions: Systemic infection by neuroinvasive as well as non-neuroinvasive
    MeSH term(s) Mice ; Male ; Animals ; Listeria monocytogenes ; CD8-Positive T-Lymphocytes ; Mice, Inbred C57BL ; Listeriosis ; Cognitive Dysfunction/etiology
    Language English
    Publishing date 2023-04-18
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1146690
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Neuroinvasive Listeria monocytogenes infection triggers accumulation of brain CD8

    Cassidy, Benjamin R / Zhang, Miao / Sonntag, William E / Drevets, Douglas A

    Journal of neuroinflammation

    2020  Volume 17, Issue 1, Page(s) 259

    Abstract: Background: Brain inflammation is a key cause of cognitive decline after central nervous system (CNS) infections. A thorough understanding of immune responses to CNS infection is essential for developing anti-inflammatory interventions that improve ... ...

    Abstract Background: Brain inflammation is a key cause of cognitive decline after central nervous system (CNS) infections. A thorough understanding of immune responses to CNS infection is essential for developing anti-inflammatory interventions that improve outcomes. Tissue-resident memory T cells (T
    Methods: C57BL/6J mice were infected by intraperitoneal injection with a lethal inoculum of Listeria monocytogenes (Lm) then treated with antibiotics. Flow cytometry was used to quantify specific populations of brain leukocytes 28-29 days (d) post-infection (p.i.). To test the degree to which miR-155 altered leukocyte influxes into the brain, infected mice were injected with a miR-155 inhibitor or locked nucleic acid (LNA) scramble control 2d, 4d, 6d, and 8d p.i. along with antibiotic treatment. Bacterial loads in spleen and liver and body weights were measured up to 7d p.i. Brain leukocytes were analyzed 14d and 28d p.i. Confirmatory studies were performed in mutated mice lacking miR-155 (miR-155
    Conclusions: Brain CD8
    Language English
    Publishing date 2020-09-02
    Publishing country England
    Document type Journal Article
    ISSN 1742-2094
    ISSN (online) 1742-2094
    DOI 10.1186/s12974-020-01929-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: GeroScience: understanding the interaction of processes of aging and chronic diseases.

    Sonntag, William E / Ungvari, Zoltan

    Age (Dordrecht, Netherlands)

    2016  Volume 38, Issue 5-6, Page(s) 377–378

    MeSH term(s) Aged ; Aging ; Biomedical Research ; Chronic Disease ; Humans
    Language English
    Publishing date 2016-12-06
    Publishing country Netherlands
    Document type Editorial
    ZDB-ID 423714-6
    ISSN 1574-4647 ; 0161-9152
    ISSN (online) 1574-4647
    ISSN 0161-9152
    DOI 10.1007/s11357-016-9953-7
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  5. Article ; Online: Cognitive heterogeneity reveals molecular signatures of age-related impairment.

    Logan, Sreemathi / Baier, Matthew P / Owen, Daniel B / Peasari, John / Jones, Kenneth L / Ranjit, Rojina / Yarbrough, Hannah P / Masingale, Anthony M / Bhandari, Suyesha / Rice, Heather C / Kinter, Michael T / Sonntag, William E

    PNAS nexus

    2023  Volume 2, Issue 4, Page(s) pgad101

    Abstract: The greatest risk factor for cognitive decline is aging. The biological mechanisms for this decline remain enigmatic due, in part, to the confounding of normal aging mechanisms and those that contribute to cognitive impairment. Importantly, many ... ...

    Abstract The greatest risk factor for cognitive decline is aging. The biological mechanisms for this decline remain enigmatic due, in part, to the confounding of normal aging mechanisms and those that contribute to cognitive impairment. Importantly, many individuals exhibit impaired cognition in age, while some retain functionality despite their age. Here, we establish a behavioral testing paradigm to characterize age-related cognitive heterogeneity in inbred aged C57BL/6 mice and reliably separate animals into cognitively "intact" (resilient) and "impaired" subgroups using a high-resolution home-cage testing paradigm for spatial discrimination. RNA sequencing and subsequent pathway analyses of cognitively stratified mice revealed molecular signatures unique to cognitively impaired animals, including transcriptional down-regulation of genes involved in mitochondrial oxidative phosphorylation (OXPHOS) and sirtuin (
    Language English
    Publishing date 2023-03-27
    Publishing country England
    Document type Journal Article
    ISSN 2752-6542
    ISSN (online) 2752-6542
    DOI 10.1093/pnasnexus/pgad101
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  6. Article ; Online: Interleukin 6 reduces allopregnanolone synthesis in the brain and contributes to age-related cognitive decline in mice.

    Parks, Eileen E / Logan, Sreemathi / Yeganeh, Alexander / Farley, Julie A / Owen, Daniel B / Sonntag, William E

    Journal of lipid research

    2020  Volume 61, Issue 10, Page(s) 1308–1319

    Abstract: Cognitive decline with age is a harmful process that can reduce quality of life. Multiple factors have been established to contribute to cognitive decline, but the overall etiology remains unknown. Here, we hypothesized that cognitive dysfunction is ... ...

    Abstract Cognitive decline with age is a harmful process that can reduce quality of life. Multiple factors have been established to contribute to cognitive decline, but the overall etiology remains unknown. Here, we hypothesized that cognitive dysfunction is mediated, in part, by increased levels of inflammatory cytokines that alter allopregnanolone (AlloP) levels, an important neurosteroid in the brain. We assessed the levels and regulation of AlloP and the effects of AlloP supplementation on cognitive function in 4-month-old and 24-month-old male C57BL/6 mice. With age, the expression of enzymes involved in the AlloP synthetic pathway was decreased and corticosterone (CORT) synthesis increased. Supplementation of AlloP improved cognitive function. Interestingly, interleukin 6 (IL-6) infusion in young animals significantly reduced the production of AlloP compared with controls. It is notable that inhibition of IL-6 with its natural inhibitor, soluble membrane glycoprotein 130, significantly improved spatial memory in aged mice. These findings were supported by in vitro experiments in primary murine astrocyte cultures, indicating that IL-6 decreases production of AlloP and increases CORT levels. Our results indicate that age-related increases in IL-6 levels reduce progesterone substrate availability, resulting in a decline in AlloP levels and an increase in CORT. Furthermore, our results indicate that AlloP is a critical link between inflammatory cytokines and the age-related decline in cognitive function.
    MeSH term(s) Aging/metabolism ; Aging/physiology ; Animals ; Brain/metabolism ; Brain/physiology ; Cognition ; Interleukin-6/metabolism ; Male ; Mice ; Pregnanolone/biosynthesis
    Chemical Substances Interleukin-6 ; Pregnanolone (BXO86P3XXW)
    Language English
    Publishing date 2020-07-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80154-9
    ISSN 1539-7262 ; 0022-2275
    ISSN (online) 1539-7262
    ISSN 0022-2275
    DOI 10.1194/jlr.RA119000479
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    Zs.A 175: Show issues Location:
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  7. Article ; Online: Brain and cerebrovascular aging--new mechanisms and insights.

    Ungvari, Zoltan / Sonntag, William E

    The journals of gerontology. Series A, Biological sciences and medical sciences

    2014  Volume 69, Issue 11, Page(s) 1307–1310

    MeSH term(s) Aging/physiology ; Aging/psychology ; Animals ; Brain/blood supply ; Brain/physiology ; Cerebrovascular Circulation/physiology ; Humans ; Models, Neurological
    Language English
    Publishing date 2014-10-09
    Publishing country United States
    Document type Editorial ; Introductory Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1223643-3
    ISSN 1758-535X ; 1079-5006
    ISSN (online) 1758-535X
    ISSN 1079-5006
    DOI 10.1093/gerona/glu187
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    Uc I Zs.242/A: Show issues Location:
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  8. Article ; Online: Aging, synaptic dysfunction, and insulin-like growth factor (IGF)-1.

    Deak, Ferenc / Sonntag, William E

    The journals of gerontology. Series A, Biological sciences and medical sciences

    2012  Volume 67, Issue 6, Page(s) 611–625

    Abstract: Insulin-like growth factor (IGF)-1 is an important neurotrophic hormone. Deficiency of this hormone has been reported to influence the genesis of cognitive impairment and dementia in the elderly patients. Nevertheless, there are studies indicating that ... ...

    Abstract Insulin-like growth factor (IGF)-1 is an important neurotrophic hormone. Deficiency of this hormone has been reported to influence the genesis of cognitive impairment and dementia in the elderly patients. Nevertheless, there are studies indicating that cognitive function can be maintained into old age even in the absence of circulating IGF-1 and studies that link IGF-1 to an acceleration of neurological diseases. Although IGF-1 has a complex role in brain function, synaptic effects appear to be central to the IGF-1-induced improvement in learning and memory. In this review, synaptic mechanisms of learning and memory and the effects of IGF-1 on synaptic communication are discussed. The emerging data indicate that synaptic function decreases with age and that IGF-1 contributes to information processing in the brain. Further studies that detail the specific actions of this important neurotrophic hormone will likely lead to therapies that result in improved cognitive function for the elderly patients.
    MeSH term(s) Aging/metabolism ; Aging/physiology ; Animals ; Cognition Disorders/metabolism ; Cognition Disorders/physiopathology ; Female ; Humans ; Insulin-Like Growth Factor I/metabolism ; Learning/physiology ; Long-Term Potentiation/physiology ; Male ; Mice ; Rats ; Synapses/metabolism ; Synapses/physiology
    Chemical Substances Insulin-Like Growth Factor I (67763-96-6)
    Language English
    Publishing date 2012-04-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1223643-3
    ISSN 1758-535X ; 1079-5006
    ISSN (online) 1758-535X
    ISSN 1079-5006
    DOI 10.1093/gerona/gls118
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  9. Article ; Online: Elimination of senescent cells by treatment with Navitoclax/ABT263 reverses whole brain irradiation-induced blood-brain barrier disruption in the mouse brain.

    Gulej, Rafal / Nyúl-Tóth, Ádám / Ahire, Chetan / DelFavero, Jordan / Balasubramanian, Priya / Kiss, Tamas / Tarantini, Stefano / Benyo, Zoltan / Pacher, Pal / Csik, Boglarka / Yabluchanskiy, Andriy / Mukli, Peter / Kuan-Celarier, Anna / Krizbai, István A / Campisi, Judith / Sonntag, William E / Csiszar, Anna / Ungvari, Zoltan

    GeroScience

    2023  Volume 45, Issue 5, Page(s) 2983–3002

    Abstract: Whole brain irradiation (WBI), a commonly employed therapy for multiple brain metastases and as a prophylactic measure after cerebral metastasis resection, is associated with a progressive decline in neurocognitive function, significantly impacting the ... ...

    Abstract Whole brain irradiation (WBI), a commonly employed therapy for multiple brain metastases and as a prophylactic measure after cerebral metastasis resection, is associated with a progressive decline in neurocognitive function, significantly impacting the quality of life for approximately half of the surviving patients. Recent preclinical investigations have shed light on the multifaceted cerebrovascular injury mechanisms underlying this side effect of WBI. In this study, we aimed to test the hypothesis that WBI induces endothelial senescence, contributing to chronic disruption of the blood-brain barrier (BBB) and microvascular rarefaction. To accomplish this, we utilized transgenic p16-3MR mice, which enable the identification and selective elimination of senescent cells. These mice were subjected to a clinically relevant fractionated WBI protocol (5 Gy twice weekly for 4 weeks), and cranial windows were applied to both WBI-treated and control mice. Quantitative assessment of BBB permeability and capillary density was performed using two-photon microscopy at the 6-month post-irradiation time point. The presence of senescent microvascular endothelial cells was assessed by imaging flow cytometry, immunolabeling, and single-cell RNA-sequencing (scRNA-seq). WBI induced endothelial senescence, which associated with chronic BBB disruption and a trend for decreased microvascular density in the mouse cortex. In order to investigate the cause-and-effect relationship between WBI-induced senescence and microvascular injury, senescent cells were selectively removed from animals subjected to WBI treatment using Navitoclax/ABT263, a well-known senolytic drug. This intervention was carried out at the 3-month post-WBI time point. In WBI-treated mice, Navitoclax/ABT263 effectively eliminated senescent endothelial cells, which was associated with decreased BBB permeability and a trend for increased cortical capillarization. Our findings provide additional preclinical evidence that senolytic treatment approaches may be developed for prevention of the side effects of WBI.
    MeSH term(s) Humans ; Mice ; Animals ; Blood-Brain Barrier ; Endothelial Cells ; Quality of Life ; Senotherapeutics ; Brain/blood supply ; Cellular Senescence
    Chemical Substances navitoclax (XKJ5VVK2WD) ; Senotherapeutics
    Language English
    Publishing date 2023-08-29
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2886586-8
    ISSN 2509-2723 ; 2509-2715
    ISSN (online) 2509-2723
    ISSN 2509-2715
    DOI 10.1007/s11357-023-00870-x
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  10. Article ; Online: Measurements of cerebral microvascular blood flow, oxygenation, and morphology in a mouse model of whole-brain irradiation-induced cognitive impairment by two-photon microscopy and optical coherence tomography: evidence for microvascular injury in the cerebral white matter.

    Li, Baoqiang / Yabluchanskiy, Andriy / Tarantini, Stefano / Allu, Srinivasa Rao / Şencan-Eğilmez, Ikbal / Leng, Ji / Alfadhel, Mohammed Ali H / Porter, Jason E / Fu, Buyin / Ran, Chongzhao / Erdener, Sefik Evren / Boas, David A / Vinogradov, Sergei A / Sonntag, William E / Csiszar, Anna / Ungvari, Zoltan / Sakadžić, Sava

    GeroScience

    2023  Volume 45, Issue 3, Page(s) 1491–1510

    Abstract: Whole-brain irradiation (WBI, also known as whole-brain radiation therapy) is a mainstay treatment modality for patients with multiple brain metastases. It is also used as a prophylactic treatment for microscopic tumors that cannot be detected by ... ...

    Abstract Whole-brain irradiation (WBI, also known as whole-brain radiation therapy) is a mainstay treatment modality for patients with multiple brain metastases. It is also used as a prophylactic treatment for microscopic tumors that cannot be detected by magnetic resonance imaging. WBI induces a progressive cognitive decline in ~ 50% of the patients surviving over 6 months, significantly compromising the quality of life. There is increasing preclinical evidence that radiation-induced injury to the cerebral microvasculature and accelerated neurovascular senescence plays a central role in this side effect of WBI. To better understand this side effect, male C57BL/6 mice were first subjected to a clinically relevant protocol of fractionated WBI (5 Gy, two doses per week, for 4 weeks). Nine months post the WBI treatment, we applied two-photon microscopy and Doppler optical coherence tomography to measure capillary red-blood-cell (RBC) flux, capillary morphology, and microvascular oxygen partial pressure (PO
    MeSH term(s) Mice ; Male ; Animals ; Microcirculation ; White Matter/diagnostic imaging ; Microscopy ; Cerebrovascular Circulation/physiology ; Tomography, Optical Coherence ; Brain Neoplasms ; Quality of Life ; Cranial Irradiation ; Mice, Inbred C57BL ; Brain/blood supply ; Cognitive Dysfunction ; Disease Models, Animal ; Oxygen
    Chemical Substances Oxygen (S88TT14065)
    Language English
    Publishing date 2023-02-16
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2886586-8
    ISSN 2509-2723 ; 2509-2715
    ISSN (online) 2509-2723
    ISSN 2509-2715
    DOI 10.1007/s11357-023-00735-3
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