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  1. Article ; Online: Using Neuroimaging to Study Cerebral Amyloid Angiopathy and Its Relationship to Alzheimer's Disease.

    Wheeler, Koral V / Irimia, Andrei / Braskie, Meredith N

    Journal of Alzheimer's disease : JAD

    2024  Volume 97, Issue 4, Page(s) 1479–1502

    Abstract: Cerebral amyloid angiopathy (CAA) is characterized by amyloid-β aggregation in the media and adventitia of the leptomeningeal and cortical blood vessels. CAA is one of the strongest vascular contributors to Alzheimer's disease (AD). It frequently co- ... ...

    Abstract Cerebral amyloid angiopathy (CAA) is characterized by amyloid-β aggregation in the media and adventitia of the leptomeningeal and cortical blood vessels. CAA is one of the strongest vascular contributors to Alzheimer's disease (AD). It frequently co-occurs in AD patients, but the relationship between CAA and AD is incompletely understood. CAA may drive AD risk through damage to the neurovascular unit and accelerate parenchymal amyloid and tau deposition. Conversely, early AD may also drive CAA through cerebrovascular remodeling that impairs blood vessels from clearing amyloid-β. Sole reliance on autopsy examination to study CAA limits researchers' ability to investigate CAA's natural disease course and the effect of CAA on cognitive decline. Neuroimaging allows for in vivo assessment of brain function and structure and can be leveraged to investigate CAA staging and explore its associations with AD. In this review, we will discuss neuroimaging modalities that can be used to investigate markers associated with CAA that may impact AD vulnerability including hemorrhages and microbleeds, blood-brain barrier permeability disruption, reduced cerebral blood flow, amyloid and tau accumulation, white matter tract disruption, reduced cerebrovascular reactivity, and lowered brain glucose metabolism. We present possible areas for research inquiry to advance biomarker discovery and improve diagnostics.
    MeSH term(s) Humans ; Alzheimer Disease/metabolism ; Cerebral Amyloid Angiopathy/complications ; Cerebral Amyloid Angiopathy/diagnostic imaging ; Cerebral Amyloid Angiopathy/metabolism ; Brain/metabolism ; Amyloid beta-Peptides/metabolism ; Neuroimaging ; Amyloid/metabolism ; Amyloidogenic Proteins/metabolism
    Chemical Substances Amyloid beta-Peptides ; Amyloid ; Amyloidogenic Proteins
    Language English
    Publishing date 2024-02-02
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 1440127-7
    ISSN 1875-8908 ; 1387-2877
    ISSN (online) 1875-8908
    ISSN 1387-2877
    DOI 10.3233/JAD-230553
    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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  2. Article ; Online: White matter hyperintensity volume modifies the association between CSF vascular inflammatory biomarkers and regional FDG-PET along the Alzheimer's disease continuum.

    Tubi, Meral A / Wheeler, Koral / Matsiyevskiy, Elizabeth / Hapenney, Matthew / Mack, Wendy J / Chui, Helena C / King, Kevin / Thompson, Paul M / Braskie, Meredith N

    Neurobiology of aging

    2023  Volume 132, Page(s) 1–12

    Abstract: In older adults with abnormal levels of Alzheimer's disease neuropathology, lower cerebrospinal fluid (CSF) vascular endothelial growth factor (VEGF) levels are associated with lower [¹⁸F]-fluorodeoxyglucose positron emission tomography (FDG-PET) signal, ...

    Abstract In older adults with abnormal levels of Alzheimer's disease neuropathology, lower cerebrospinal fluid (CSF) vascular endothelial growth factor (VEGF) levels are associated with lower [¹⁸F]-fluorodeoxyglucose positron emission tomography (FDG-PET) signal, but whether this association is (1) specific to VEGF or broadly driven by vascular inflammation, or (2) modified by vascular risk (e.g., white matter hyperintensities [WMHs]) remains unknown. To address this and build upon our past work, we evaluated whether 5 CSF vascular inflammation biomarkers (vascular cell adhesion molecule 1, VEGF, C-reactive protein, fibrinogen, and von Willebrand factor)-previously associated with CSF amyloid levels-were related to FDG-PET signal and whether WMH volume modified these associations in 158 Alzheimer's Disease Neuroimaging Initiative participants (55-90 years old, 39 cognitively normal, 80 mild cognitive impairment, 39 Alzheimer's disease). We defined regions both by cortical boundary and by the 3 major vascular territories: anterior, middle, and posterior cerebral arteries. We found that WMH volume had interactive effects with CSF biomarkers (VEGF and C-reactive protein) on FDG-PET throughout the cortex in both vascular territories and conventionally defined regions of interest.
    MeSH term(s) Humans ; Aged ; Aged, 80 and over ; Alzheimer Disease/metabolism ; Fluorodeoxyglucose F18/metabolism ; Vascular Endothelial Growth Factor A/metabolism ; White Matter/pathology ; C-Reactive Protein ; Brain/metabolism ; Positron-Emission Tomography/methods ; Biomarkers/cerebrospinal fluid ; Cognitive Dysfunction/metabolism ; Inflammation/metabolism ; Amyloid beta-Peptides/metabolism ; Magnetic Resonance Imaging
    Chemical Substances Fluorodeoxyglucose F18 (0Z5B2CJX4D) ; Vascular Endothelial Growth Factor A ; C-Reactive Protein (9007-41-4) ; Biomarkers ; Amyloid beta-Peptides
    Language English
    Publishing date 2023-08-10
    Publishing country United States
    Document type Journal Article
    ZDB-ID 604505-4
    ISSN 1558-1497 ; 0197-4580
    ISSN (online) 1558-1497
    ISSN 0197-4580
    DOI 10.1016/j.neurobiolaging.2023.08.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1685: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
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    Zs.MG 10: Show issues

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  3. Article ; Online: Transplantation of human neural progenitor cells secreting GDNF into the spinal cord of patients with ALS: a phase 1/2a trial.

    Baloh, Robert H / Johnson, J Patrick / Avalos, Pablo / Allred, Peggy / Svendsen, Soshana / Gowing, Genevieve / Roxas, Kristina / Wu, Amanda / Donahue, Becky / Osborne, Sheryl / Lawless, George / Shelley, Brandon / Wheeler, Koral / Prina, Carolyn / Fine, Dana / Kendra-Romito, Tami / Stokes, Haniah / Manoukian, Vicki / Muthukumaran, Abirami /
    Garcia, Leslie / Bañuelos, Maria G / Godoy, Marlesa / Bresee, Catherine / Yu, Hong / Drazin, Doniel / Ross, Lindsey / Naruse, Robert / Babu, Harish / Macklin, Eric A / Vo, Ashley / Elsayegh, Ashraf / Tourtellotte, Warren / Maya, Marcel / Burford, Matthew / Diaz, Frank / Patil, Chirag G / Lewis, Richard A / Svendsen, Clive N

    Nature medicine

    2022  Volume 28, Issue 9, Page(s) 1813–1822

    Abstract: Amyotrophic lateral sclerosis (ALS) involves progressive motor neuron loss, leading to paralysis and death typically within 3-5 years of diagnosis. Dysfunctional astrocytes may contribute to disease and glial cell line-derived neurotrophic factor (GDNF) ... ...

    Abstract Amyotrophic lateral sclerosis (ALS) involves progressive motor neuron loss, leading to paralysis and death typically within 3-5 years of diagnosis. Dysfunctional astrocytes may contribute to disease and glial cell line-derived neurotrophic factor (GDNF) can be protective. Here we show that human neural progenitor cells transduced with GDNF (CNS10-NPC-GDNF) differentiated to astrocytes protected spinal motor neurons and were safe in animal models. CNS10-NPC-GDNF were transplanted unilaterally into the lumbar spinal cord of 18 ALS participants in a phase 1/2a study (NCT02943850). The primary endpoint of safety at 1 year was met, with no negative effect of the transplant on motor function in the treated leg compared with the untreated leg. Tissue analysis of 13 participants who died of disease progression showed graft survival and GDNF production. Benign neuromas near delivery sites were common incidental findings at post-mortem. This study shows that one administration of engineered neural progenitors can provide new support cells and GDNF delivery to the ALS patient spinal cord for up to 42 months post-transplantation.
    MeSH term(s) Amyotrophic Lateral Sclerosis/therapy ; Animals ; Disease Models, Animal ; Glial Cell Line-Derived Neurotrophic Factor/genetics ; Humans ; Neural Stem Cells ; Spinal Cord ; Superoxide Dismutase
    Chemical Substances Glial Cell Line-Derived Neurotrophic Factor ; Superoxide Dismutase (EC 1.15.1.1)
    Language English
    Publishing date 2022-09-05
    Publishing country United States
    Document type Clinical Trial, Phase I ; Clinical Trial, Phase II ; Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1220066-9
    ISSN 1546-170X ; 1078-8956
    ISSN (online) 1546-170X
    ISSN 1078-8956
    DOI 10.1038/s41591-022-01956-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4212: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 39: Show issues

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