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  1. Book: Immunotherapy and biomarkers in neurodegenerative disorders

    Ingelsson, Martin / Lannfelt, Lars

    (Methods in pharmacology and toxicology ; Springer protocols)

    2016  

    Author's details edited by Martin Ingelsson and Lars Lannfelt, Department of Public Health and Caring Sciences/Geriatrics, Uppsala University, Uppsala, Sweden
    Series title Methods in pharmacology and toxicology
    Springer protocols
    Language English
    Size X, 289 Seiten, Illustrationen, Diagramme
    Publisher Humana Press
    Publishing place New York
    Publishing country United States
    Document type Book
    HBZ-ID HT018964217
    ISBN 978-1-4939-3558-1 ; 9781493935604 ; 1-4939-3558-5 ; 1493935607
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2016 A 1706 available for loan (reading room) Lesesaal EG

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  2. Article ; Online: Targeted Gene Therapy to Treat Disorders of the Central Nervous System.

    Sasikumar, Sanskriti / Ingelsson, Martin

    Movement disorders : official journal of the Movement Disorder Society

    2022  Volume 37, Issue 5, Page(s) 892

    MeSH term(s) Central Nervous System ; Central Nervous System Diseases/genetics ; Central Nervous System Diseases/therapy ; Genetic Therapy ; Humans
    Language English
    Publishing date 2022-04-01
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 607633-6
    ISSN 1531-8257 ; 0885-3185
    ISSN (online) 1531-8257
    ISSN 0885-3185
    DOI 10.1002/mds.29017
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2555: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 238: Show issues

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  3. Article ; Online: Astrocytic accumulation of tau fibrils isolated from Alzheimer's disease brains induces inflammation, cell-to-cell propagation and neuronal impairment.

    Eltom, Khalid / Mothes, Tobias / Libard, Sylwia / Ingelsson, Martin / Erlandsson, Anna

    Acta neuropathologica communications

    2024  Volume 12, Issue 1, Page(s) 34

    Abstract: Accumulating evidence highlights the involvement of astrocytes in Alzheimer's disease (AD) progression. We have previously demonstrated that human iPSC-derived astrocytes ingest and modify synthetic tau fibrils in a way that enhances their seeding ... ...

    Abstract Accumulating evidence highlights the involvement of astrocytes in Alzheimer's disease (AD) progression. We have previously demonstrated that human iPSC-derived astrocytes ingest and modify synthetic tau fibrils in a way that enhances their seeding efficiency. However, synthetic tau fibrils differ significantly from in vivo formed fibrils. To mimic the situation in the brain, we here analyzed astrocytes' processing of human brain-derived tau fibrils and its consequences for cellular physiology. Tau fibrils were extracted from both AD and control brains, aiming to examine any potential differences in astrocyte response depending on the origin of fibrils. Our results show that human astrocytes internalize, but fail to degrade, both AD and control tau fibrils. Instead, pathogenic, seeding capable tau proteoforms are spread to surrounding cells via tunneling nanotubes and exocytosis. Notably, accumulation of AD tau fibrils induces a stronger reactive state in astrocytes, compared to control fibrils, evident by the augmented expression of vimentin and GFAP, as well as by an increased secretion of the pro-inflammatory cytokines IL-8 and MCP-1. Moreover, conditioned media from astrocytes with AD tau fibril deposits induce synapse and metabolic impairment in human iPSC-derived neurons. Taken together, our data suggest that the accumulation of brain-derived AD tau fibrils induces a more robust inflammatory and neurotoxic phenotype in human astrocytes, accentuating the nature of tau fibrils as an important contributing factor to inflammation and neurodegeneration in AD.
    MeSH term(s) Humans ; Alzheimer Disease/pathology ; Astrocytes/metabolism ; tau Proteins/metabolism ; Brain/pathology ; Neurons/metabolism ; Inflammation/metabolism
    Chemical Substances tau Proteins
    Language English
    Publishing date 2024-02-26
    Publishing country England
    Document type Journal Article
    ZDB-ID 2715589-4
    ISSN 2051-5960 ; 2051-5960
    ISSN (online) 2051-5960
    ISSN 2051-5960
    DOI 10.1186/s40478-024-01745-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Altered Distribution of SNARE Proteins in Primary Neurons Exposed to Different Alpha-Synuclein Proteoforms.

    Brolin, Emma / Ingelsson, Martin / Bergström, Joakim / Erlandsson, Anna

    Cellular and molecular neurobiology

    2023  Volume 43, Issue 6, Page(s) 3023–3035

    Abstract: Growing evidence indicates that the pathological alpha-synuclein (α-syn) aggregation in Parkinson's disease (PD) and dementia with Lewy bodies (DLB) starts at the synapses. Physiologic α-syn is involved in regulating neurotransmitter release by binding ... ...

    Abstract Growing evidence indicates that the pathological alpha-synuclein (α-syn) aggregation in Parkinson's disease (PD) and dementia with Lewy bodies (DLB) starts at the synapses. Physiologic α-syn is involved in regulating neurotransmitter release by binding to the SNARE complex protein VAMP-2 on synaptic vesicles. However, in which way the SNARE complex formation is affected by α-syn pathology remains unclear. In this study, primary cortical neurons were exposed to either α-syn monomers or preformed fibrils (PFFs) for different time points and the effect on SNARE protein distribution was analyzed with a novel proximity ligation assay (PLA). Short-term exposure to monomers or PFFs for 24 h increased the co-localization of VAMP-2 and syntaxin-1, but reduced the co-localization of SNAP-25 and syntaxin-1, indicating a direct effect of the added α-syn on SNARE protein distribution. Long-term exposure to α-syn PFFs for 7 d reduced VAMP-2 and SNAP-25 co-localization, although there was only a modest induction of ser129 phosphorylated (pS129) α-syn. Similarly, exposure to extracellular vesicles collected from astrocytes treated with α-syn PFFs for 7 d influenced VAMP-2 and SNAP-25 co-localization despite only low levels of pS129 α-syn being formed. Taken together, our results demonstrate that different α-syn proteoforms have the potential to alter the distribution of SNARE proteins at the synapse.
    MeSH term(s) alpha-Synuclein/metabolism ; Vesicle-Associated Membrane Protein 2/metabolism ; SNARE Proteins ; Neurons/metabolism ; Qa-SNARE Proteins
    Chemical Substances alpha-Synuclein ; Vesicle-Associated Membrane Protein 2 ; SNARE Proteins ; Qa-SNARE Proteins
    Language English
    Publishing date 2023-05-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 283404-2
    ISSN 1573-6830 ; 0272-4340
    ISSN (online) 1573-6830
    ISSN 0272-4340
    DOI 10.1007/s10571-023-01355-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1727: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article: Alpha-Synuclein Oligomers-Neurotoxic Molecules in Parkinson's Disease and Other Lewy Body Disorders.

    Ingelsson, Martin

    Frontiers in neuroscience

    2016  Volume 10, Page(s) 408

    Abstract: Adverse intra- and extracellular effects of toxic α-synuclein are believed to be central to the pathogenesis in Parkinson's disease and other disorders with Lewy body pathology in the nervous system. One of the physiological roles of α-synuclein relates ... ...

    Abstract Adverse intra- and extracellular effects of toxic α-synuclein are believed to be central to the pathogenesis in Parkinson's disease and other disorders with Lewy body pathology in the nervous system. One of the physiological roles of α-synuclein relates to the regulation of neurotransmitter release at the presynapse, although it is still unclear whether this mechanism depends on the action of monomers or smaller oligomers. As for the pathogenicity, accumulating evidence suggest that prefibrillar species, rather than the deposits per se, are responsible for the toxicity in affected cells. In particular, larger oligomers or protofibrils of α-synuclein have been shown to impair protein degradation as well as the function of several organelles, such as the mitochondria and the endoplasmic reticulum. Accumulating evidence further suggest that oligomers/protofibrils may have a toxic effect on the synapse, which may lead to disrupted electrophysiological properties. In addition, recent data indicate that oligomeric α-synuclein species can spread between cells, either as free-floating proteins or via extracellular vesicles, and thereby act as seeds to propagate disease between interconnected brain regions. Taken together, several lines of evidence suggest that α-synuclein have neurotoxic properties and therefore should be an appropriate molecular target for therapeutic intervention in Parkinson's disease and other disorders with Lewy pathology. In this context, immunotherapy with monoclonal antibodies against α-synuclein oligomers/protofibrils should be a particularly attractive treatment option.
    Language English
    Publishing date 2016-09-05
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2411902-7
    ISSN 1662-453X ; 1662-4548
    ISSN (online) 1662-453X
    ISSN 1662-4548
    DOI 10.3389/fnins.2016.00408
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Studies on alpha-synuclein and islet amyloid polypeptide interaction.

    Wang, Ye / Bergström, Joakim / Ingelsson, Martin / Westermark, Gunilla T

    Frontiers in molecular biosciences

    2023  Volume 10, Page(s) 1080112

    Abstract: Introduction: ...

    Abstract Introduction:
    Language English
    Publishing date 2023-01-30
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2814330-9
    ISSN 2296-889X
    ISSN 2296-889X
    DOI 10.3389/fmolb.2023.1080112
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Mixed Pathologies in a Subject with a Novel PSEN1 G206R Mutation.

    Libard, Sylwia / Giedraitis, Vilmantas / Kilander, Lena / Ingelsson, Martin / Alafuzoff, Irina

    Journal of Alzheimer's disease : JAD

    2022  Volume 90, Issue 4, Page(s) 1601–1614

    Abstract: Background: There are more than 300 presenilin-1 (PSEN1) mutations identified but a thorough postmortem neuropathological assessment of the mutation carriers is seldom performed.: Objective: To assess neuropathological changes (NC) in a 73-year-old ... ...

    Abstract Background: There are more than 300 presenilin-1 (PSEN1) mutations identified but a thorough postmortem neuropathological assessment of the mutation carriers is seldom performed.
    Objective: To assess neuropathological changes (NC) in a 73-year-old subject with the novel PSEN1 G206R mutation suffering from cognitive decline in over 20 years. To compare these findings with an age- and gender-matched subject with sporadic Alzheimer's disease (sAD).
    Methods: The brains were assessed macro- and microscopically and the proteinopathies were staged according to current recommendations.
    Results: The AD neuropathological change (ADNC) was more extensive in the mutation carrier, although both individuals reached a high level of ADNC. The transactive DNA binding protein 43 pathology was at the end-stage in the index subject, a finding not previously described in familial AD. This pathology was moderate in the sAD subject. The PSEN1 G206R subject displayed full-blown alpha-synuclein pathology, while this proteinopathy was absent in the sAD case. Additionally, the mutation carrier displayed pronounced neuroinflammation, not previously described in association with PSEN1 mutations.
    Conclusion: Our findings are exceptional, as the PSEN1 G206R subject displayed an end-stage pathology of every common proteinopathy. It is unclear whether the observed alterations are caused by the mutation or are related to a cross-seeding mechanisms. The pronounced neuroinflammation in the index patient can be reactive to the extensive NC or a contributing factor to the proteinopathies. Thorough postmortem neuropathological and genetic assessment of subjects with familial AD is warranted, for further understanding of a dementing illness.
    Language English
    Publishing date 2022-10-31
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 1440127-7
    ISSN 1875-8908 ; 1387-2877
    ISSN (online) 1875-8908
    ISSN 1387-2877
    DOI 10.3233/JAD-220655
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6084: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  8. Article ; Online: Modeling Parkinson's disease-related symptoms in alpha-synuclein overexpressing mice.

    Aniszewska, Agata / Bergström, Joakim / Ingelsson, Martin / Ekmark-Lewén, Sara

    Brain and behavior

    2022  Volume 12, Issue 7, Page(s) e2628

    Abstract: Background: Intracellular deposition of alpha-synuclein (α-syn) as Lewy bodies and Lewy neurites is a central event in the pathogenesis of Parkinson's disease (PD) and other α-synucleinopathies. Transgenic mouse models overexpressing human α-syn, are ... ...

    Abstract Background: Intracellular deposition of alpha-synuclein (α-syn) as Lewy bodies and Lewy neurites is a central event in the pathogenesis of Parkinson's disease (PD) and other α-synucleinopathies. Transgenic mouse models overexpressing human α-syn, are useful research tools in preclinical studies of pathogenetic mechanisms. Such mice develop α-syn inclusions as well as neurodegeneration with a topographical distribution that varies depending on the choice of promoter and which form of α-syn that is overexpressed. Moreover, they display motor symptoms and cognitive disturbances that to some extent resemble the human conditions.
    Purpose: One of the main motives for assessing behavior in these mouse models is to evaluate the potential of new treatment strategies, including their impact on motor and cognitive symptoms. However, due to a high within-group variability with respect to such features, the behavioral studies need to be applied with caution. In this review, we discuss how to make appropriate choices in the experimental design and which tests that are most suitable for the evaluation of PD-related symptoms in such studies.
    Methods: We have evaluated published results on two selected transgenic mouse models overexpressing wild type (L61) and mutated (A30P) α-syn in the context of their validity and utility for different types of behavioral studies.
    Conclusions: By applying appropriate behavioral tests, α-syn transgenic mouse models provide an appropriate experimental platform for studies of symptoms related to PD and other α-synucleinopathies.
    MeSH term(s) Animals ; Disease Models, Animal ; Humans ; Lewy Bodies/pathology ; Mice ; Mice, Transgenic ; Parkinson Disease/genetics ; Parkinson Disease/pathology ; Synucleinopathies/genetics ; alpha-Synuclein/genetics
    Chemical Substances SNCA protein, human ; alpha-Synuclein
    Language English
    Publishing date 2022-06-01
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2623587-0
    ISSN 2162-3279 ; 2162-3279
    ISSN (online) 2162-3279
    ISSN 2162-3279
    DOI 10.1002/brb3.2628
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Impact of risk factors for major cardiovascular diseases: a comparison of life-time observational and Mendelian randomisation findings.

    Lind, Lars / Ingelsson, Martin / Sundstrom, Johan / Ärnlöv, Johan

    Open heart

    2021  Volume 8, Issue 2

    Abstract: Background: This study compared the strength and causality of associations between major risk factors for cardiovascular disease (CVD) and the four major CVDs: myocardial infarction, ischaemic stroke, heart failure and atrial fibrillation. Both a long- ... ...

    Abstract Background: This study compared the strength and causality of associations between major risk factors for cardiovascular disease (CVD) and the four major CVDs: myocardial infarction, ischaemic stroke, heart failure and atrial fibrillation. Both a long-term follow-up in an observational cohort and Mendelian randomisation (MR) were used for this aim.
    Methods: In the Uppsala Longitudinal Study of Adult Men study, 2322 men, all aged 50 years, were assessed for CVD risk factors and then followed for four decades regarding incident CVDs. The two-sample MR part used public available Genome-Wide Association Study (GWAS) data.
    Results: In multivariate analyses, systolic blood pressure was overall by far the most important risk factor, since it was related to all four CVDs, both in observational and MR analyses. Body mass index was the second most overall important risk factor, being linked to all four CVDs, except ischaemic stroke, both in observational and MR analyses. Smoking was an important risk factor for ischaemic stroke and heart failure, both in observational and MR analyses, while low-density lipoprotein-cholesterol mainly was related to myocardial infarction. Diabetes was mainly a causal risk factor for incident myocardial infarction and heart failure. Neither HDL-cholesterol nor triglycerides were of major importance as risk factors in these multivariable models.
    Conclusion: By combining long-term observational data with genetic data, we show that the impact and causal role of specific established cardiovascular risk factors varies between different major CVDs. Systolic blood pressure was causally related to all four cardiovascular outcomes and was therefore, overall, the most important risk factor.
    MeSH term(s) Cardiovascular Diseases/diagnosis ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/genetics ; Cause of Death/trends ; Follow-Up Studies ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; Incidence ; Male ; Mendelian Randomization Analysis/methods ; Middle Aged ; Retrospective Studies ; Risk Factors ; Smoking/adverse effects ; Smoking/epidemiology ; Survival Rate/trends ; Sweden/epidemiology
    Language English
    Publishing date 2021-09-14
    Publishing country England
    Document type Comparative Study ; Journal Article ; Multicenter Study ; Observational Study ; Research Support, Non-U.S. Gov't
    ZDB-ID 2747269-3
    ISSN 2053-3624
    ISSN 2053-3624
    DOI 10.1136/openhrt-2021-001735
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Book: Immunotherapy and biomarkers in neurodegenerative disorders

    Ingelsson, Martin / Lannfelt, Lars

    (Methods in pharmacology and toxicology, ; Springer protocols)

    2016  

    Author's details edited by Martin Ingelsson and Lars Lannfelt
    Series title Methods in pharmacology and toxicology,
    Springer protocols
    MeSH term(s) Nervous System Diseases/therapy ; Immunotherapy ; Biomarkers
    Language English
    Size x, 289 pages :, illustrations (some color) ;, 26 cm.
    Document type Book
    ISBN 9781493935581 ; 1493935585 ; 9781493935604 ; 1493935607
    Database Catalogue of the US National Library of Medicine (NLM)

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