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  1. Book ; Conference proceedings: Symposium: Oxidative Stress in Neurological Disease

    Love, Seth

    [circa 1999]

    1999  

    Title variant Oxidative stress in neurological disease
    Institution Symposium Oxidative Stress in Neurological Disease
    Author's details ed. by Seth Love
    Language English
    Publishing country United States
    Document type Book ; Conference proceedings
    Note In: Brain pathology. - ISSN 1015-6305. - 9 (1999),1, S. 55 - 186
    HBZ-ID HT009973045
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Zs A 3585 -9- not available for loan Zeitschriften-Lesesaal

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  2. Book: Neuropathology

    Black, M. / Love, Seth

    a guide for practising pathologists

    (Current topics in pathology ; 95)

    2001  

    Author's details S. Love (ed.). Contributors M. Black
    Series title Current topics in pathology ; 95
    Collection
    Keywords Nervous System Diseases / pathology ; Nervensystem ; Krankheit
    Subject Erkrankung ; Krankheitszustand ; Krankheiten ; Morbus ; Nosos ; Pathos ; Systema nervosum ; NS
    Language English
    Size VI, 284 S. : Ill.
    Publisher Springer
    Publishing place Berlin u.a.
    Publishing country Germany
    Document type Book
    HBZ-ID HT013070925
    ISBN 3-540-67721-6 ; 978-3-540-67721-5
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Ud II Zs 15 -95- verfügbar in Königswinter Königswinter

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  3. Article ; Online: Pathological changes within the cerebral vasculature in Alzheimer's disease: New perspectives.

    Fisher, Robert A / Miners, J Scott / Love, Seth

    Brain pathology (Zurich, Switzerland)

    2022  Volume 32, Issue 6, Page(s) e13061

    Abstract: Cerebrovascular disease underpins vascular dementia (VaD), but structural and functional changes to the cerebral vasculature contribute to disease pathology and cognitive decline in Alzheimer's disease (AD). In this review, we discuss the contribution of ...

    Abstract Cerebrovascular disease underpins vascular dementia (VaD), but structural and functional changes to the cerebral vasculature contribute to disease pathology and cognitive decline in Alzheimer's disease (AD). In this review, we discuss the contribution of cerebral amyloid angiopathy and non-amyloid small vessel disease in AD, and the accompanying changes to the density, maintenance and remodelling of vessels (including alterations to the composition and function of the cerebrovascular basement membrane). We consider how abnormalities of the constituent cells of the neurovascular unit - particularly of endothelial cells and pericytes - and impairment of the blood-brain barrier (BBB) impact on the pathogenesis of AD. We also discuss how changes to the cerebral vasculature are likely to impair Aβ clearance - both intra-periarteriolar drainage (IPAD) and transport of Aβ peptides across the BBB, and how impaired neurovascular coupling and reduced blood flow in relation to metabolic demand increase amyloidogenic processing of APP and the production of Aβ. We review the vasoactive properties of Aβ peptides themselves, and the probable bi-directional relationship between vascular dysfunction and Aβ accumulation in AD. Lastly, we discuss recent methodological advances in transcriptomics and imaging that have provided novel insights into vascular changes in AD, and recent advances in assessment of the retina that allow in vivo detection of vascular changes in the early stages of AD.
    MeSH term(s) Humans ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Endothelial Cells/pathology ; Cerebral Amyloid Angiopathy/pathology ; Blood-Brain Barrier/pathology ; Brain/pathology
    Chemical Substances Amyloid beta-Peptides
    Language English
    Publishing date 2022-03-14
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 1051484-3
    ISSN 1750-3639 ; 1015-6305
    ISSN (online) 1750-3639
    ISSN 1015-6305
    DOI 10.1111/bpa.13061
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    Zs.A 3585: Show issues Location:
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    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: SARS-CoV-2 targets pericytes to restrict blood flow within the brain.

    Miners, J Scott / Fisher, Robert A / Love, Seth

    Brain : a journal of neurology

    2022  Volume 146, Issue 2, Page(s) 418–420

    MeSH term(s) Humans ; SARS-CoV-2 ; Pericytes/physiology ; Constriction ; COVID-19/physiopathology ; Brain/physiopathology ; Blood-Brain Barrier/physiopathology
    Language English
    Publishing date 2022-12-16
    Publishing country England
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 80072-7
    ISSN 1460-2156 ; 0006-8950
    ISSN (online) 1460-2156
    ISSN 0006-8950
    DOI 10.1093/brain/awac481
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    Ui II Zs.26: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: Brain Pathology moves to open access.

    Glatzel, Markus / Love, Seth

    Brain pathology (Zurich, Switzerland)

    2020  Volume 30, Issue 6, Page(s) 1011

    MeSH term(s) Humans ; Neuropathology ; Open Access Publishing
    Language English
    Publishing date 2020-12-10
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 1051484-3
    ISSN 1750-3639 ; 1015-6305
    ISSN (online) 1750-3639
    ISSN 1015-6305
    DOI 10.1111/bpa.12913
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  6. Article: Pericyte Contractile Responses to Endothelin-1 and Aβ Peptides: Assessment by Electrical Impedance Assay.

    Hibbs, Elliott / Love, Seth / Miners, J Scott

    Frontiers in cellular neuroscience

    2021  Volume 15, Page(s) 723953

    Abstract: Pericytes are vascular mural cells that contract and relax in response to vasoactive stimuli to regulate neurovascular coupling and cerebral blood flow. Pericytes are damaged and degenerate in Alzheimer's disease (AD). We previously showed that the level ...

    Abstract Pericytes are vascular mural cells that contract and relax in response to vasoactive stimuli to regulate neurovascular coupling and cerebral blood flow. Pericytes are damaged and degenerate in Alzheimer's disease (AD). We previously showed that the level of the regulatory vasoconstrictor, endothelin-1 (EDN1), is elevated in AD cerebral cortex and upregulated by amyloid-beta (Aβ). We have used electrical impedance analysis to monitor the contractile and proliferative response of cultured human fetal and adult brain-derived pericytes to EDN1 in real-time. EDN1 caused transient, dose-dependent contraction of fetal and adult brain pericytes that was mediated by EDN1 type A receptors and increased the subsequent proliferation of fetal but not adult cells. The contractile responses to EDN1 were weaker in the adult pericytes. The EDN1-mediated contractile response of fetal pericytes was unchanged after exposure to Aβ
    Language English
    Publishing date 2021-08-20
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2452963-1
    ISSN 1662-5102
    ISSN 1662-5102
    DOI 10.3389/fncel.2021.723953
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  7. Article ; Online: APOE ε4, Alzheimer's disease neuropathology and sleep disturbance, in individuals with and without dementia.

    Blackman, Jonathan / Love, Seth / Sinclair, Lindsey / Cain, Richard / Coulthard, Elizabeth

    Alzheimer's research & therapy

    2022  Volume 14, Issue 1, Page(s) 47

    Abstract: Background: Apolipoprotein E epsilon 4 (APOE-ε4) carrier status is an established risk factor for Alzheimer's disease (AD) dementia. It has also been linked with sleep disturbance in healthy older adults and increased insomnia risk. This association may ...

    Abstract Background: Apolipoprotein E epsilon 4 (APOE-ε4) carrier status is an established risk factor for Alzheimer's disease (AD) dementia. It has also been linked with sleep disturbance in healthy older adults and increased insomnia risk. This association may be driven by the effect of APOE-ε4 on AD pathological change, itself associated with sleep abnormalities. To assess this relationship, we have evaluated post-mortem neuropathological findings in patients with and without cognitive impairment and AD pathology, who had extensive clinical assessment within 12 months of death.
    Methods: This retrospective cohort study used UK Brain Banks Network data. Eligible subjects were aged over 50, with pre-mortem neuropsychiatry inventory scores of sleep disturbance (NPI-K), neurocognitive testing and functional cognitive status assessment (Clinical Dementia Rating scale). Neuropathological data included Thal phase, Braak stage and CERAD scores (measures of Aβ plaque distribution, tangle distribution and neuritic plaque density, respectively) combined to form the National Institute on Aging Alzheimer's Association (NIA-AA) ABC score reflecting AD neuropathology. Participants with other significant intracerebral pathology or pathological features of non-AD dementia were excluded. Multivariate linear regression was performed with NPIK Global Score (NPIK frequency score multiplied by severity score) as the dependent variable and APOE-ε4 heterozygosity or homozygosity as independent variables. Covariates included age, gender, APOE-ε2 status and ABC NPI measures reflecting depression and anxiety. Further models stratified by ABC score and functional cognitive status were also produced.
    Results: Seven hundred twenty-eight records were identified. Two hundred two participants were included in the final analysis: mean (SD) age 84.0 (9.2) and MMSE 14.0 (11.8). Mean sleep disturbance scores were highest in ε4 homozygosity (n=11), 4.55 (5.4); intermediate in ε4 heterozygosity (n=95), 2.03 (4.0); and lowest in non-ε4 carriers (n=96), 1.36 (3.3). Within the full sample, controlling for pathological status, age, gender, depression, anxiety and CDR-SOB status, APOE-ε4 homozygosity was associated with sleep disturbance (β 2.53, p=0.034). APOE-ε4 heterozygosity was similarly associated in individuals without dementia (β 1.21, p=0.048).
    Conclusion: These findings lend weight to the hypothesis that APOE-ε4 affects sleep by mechanisms independent of AD pathological change. Evaluation of those mechanisms would enhance understanding of sleep disturbance pathways and potentially provide treatment targets.
    MeSH term(s) Aged ; Aged, 80 and over ; Alzheimer Disease/complications ; Alzheimer Disease/genetics ; Alzheimer Disease/pathology ; Apolipoprotein E4/genetics ; Apolipoproteins E ; Humans ; Retrospective Studies ; Sleep ; Sleep Wake Disorders/complications ; Sleep Wake Disorders/genetics
    Chemical Substances Apolipoprotein E4 ; Apolipoproteins E
    Language English
    Publishing date 2022-03-30
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2506521-X
    ISSN 1758-9193 ; 1758-9193
    ISSN (online) 1758-9193
    ISSN 1758-9193
    DOI 10.1186/s13195-022-00992-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Elevated late-life blood pressure may maintain brain oxygenation and slow amyloid-β accumulation at the expense of cerebral vascular damage.

    Tayler, Hannah M / MacLachlan, Robert / Güzel, Özge / Miners, J Scott / Love, Seth

    Brain communications

    2023  Volume 5, Issue 2, Page(s) fcad112

    Abstract: Hypertension in midlife contributes to cognitive decline and is a modifiable risk factor for dementia. The relationship between late-life hypertension and dementia is less clear. We have investigated the relationship of blood pressure and hypertensive ... ...

    Abstract Hypertension in midlife contributes to cognitive decline and is a modifiable risk factor for dementia. The relationship between late-life hypertension and dementia is less clear. We have investigated the relationship of blood pressure and hypertensive status during late life (after 65 years) to post-mortem markers of Alzheimer's disease (amyloid-β and tau loads); arteriolosclerosis and cerebral amyloid angiopathy; and to biochemical measures of ante-mortem cerebral oxygenation (the myelin-associated glycoprotein:proteolipid protein-1 ratio, which is reduced in chronically hypoperfused brain tissue, and the level of vascular endothelial growth factor-A, which is upregulated by tissue hypoxia); blood-brain barrier damage (indicated by an increase in parenchymal fibrinogen); and pericyte content (platelet-derived growth factor receptor β, which declines with pericyte loss), in Alzheimer's disease (
    Language English
    Publishing date 2023-04-04
    Publishing country England
    Document type Journal Article
    ISSN 2632-1297
    ISSN (online) 2632-1297
    DOI 10.1093/braincomms/fcad112
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  9. Article ; Online: Dear Reader: Data citation in changing times.

    Glatzel, Markus / Love, Seth

    Brain pathology (Zurich, Switzerland)

    2019  Volume 29, Issue 2, Page(s) 153–154

    MeSH term(s) Animals ; Big Data/supply & distribution ; Data Science/methods ; Editorial Policies ; Humans
    Language English
    Publishing date 2019-03-22
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 1051484-3
    ISSN 1750-3639 ; 1015-6305
    ISSN (online) 1750-3639
    ISSN 1015-6305
    DOI 10.1111/bpa.12702
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  10. Article ; Online: Correction: Is later‑life depression a risk factor for Alzheimer's disease or a prodromal symptom: a study using post‑mortem human brain tissue?

    Sinclair, Lindsey I / Mohr, Asher / Morisaki, Mizuki / Edmondson, Martin / Chan, Selina / Bone-Connaughton, A / Turecki, Gustavo / Love, Seth

    Alzheimer's research & therapy

    2024  Volume 16, Issue 1, Page(s) 33

    Language English
    Publishing date 2024-02-13
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2506521-X
    ISSN 1758-9193 ; 1758-9193
    ISSN (online) 1758-9193
    ISSN 1758-9193
    DOI 10.1186/s13195-024-01404-z
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