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  1. Article ; Online: Endosomal structure and APP biology are not altered in a preclinical mouse cellular model of Down syndrome.

    Cannavo, Claudia / Cleverley, Karen / Maduro, Cheryl / Mumford, Paige / Moulding, Dale / Fisher, Elizabeth M C / Wiseman, Frances K

    PloS one

    2022  Volume 17, Issue 5, Page(s) e0262558

    Abstract: Individuals who have Down syndrome (trisomy 21) are at greatly increased risk of developing Alzheimer's disease, characterised by the accumulation in the brain of amyloid-β plaques. Amyloid-β is a product of the processing of the amyloid precursor ... ...

    Abstract Individuals who have Down syndrome (trisomy 21) are at greatly increased risk of developing Alzheimer's disease, characterised by the accumulation in the brain of amyloid-β plaques. Amyloid-β is a product of the processing of the amyloid precursor protein, encoded by the APP gene on chromosome 21. In Down syndrome the first site of amyloid-β accumulation is within endosomes, and changes to endosome biology occur early in Alzheimer's disease. Here, we determine if primary mouse embryonic fibroblasts isolated from a mouse model of Down syndrome can be used to study endosome and APP cell biology. We report that in this cellular model, endosome number, size and APP processing are not altered, likely because APP is not dosage sensitive in the model, despite three copies of App.
    MeSH term(s) Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/genetics ; Amyloid beta-Protein Precursor/metabolism ; Animals ; Biology ; Down Syndrome/genetics ; Down Syndrome/metabolism ; Endosomes/metabolism ; Fibroblasts/metabolism ; Mice ; Plaque, Amyloid/metabolism
    Chemical Substances Amyloid beta-Peptides ; Amyloid beta-Protein Precursor
    Language English
    Publishing date 2022-05-11
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0262558
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Using mouse models to understand Alzheimer's disease mechanisms in the context of trisomy of chromosome 21.

    Cannavo, Claudia / Tosh, Justin / Fisher, Elizabeth M C / Wiseman, Frances K

    Progress in brain research

    2019  Volume 251, Page(s) 181–208

    Abstract: People who have Down syndrome are at significantly elevated risk of developing early onset Alzheimer's disease that causes dementia (AD-DS). Here we review recent progress in modeling the development of AD-DS in mouse models. These studies provide ... ...

    Abstract People who have Down syndrome are at significantly elevated risk of developing early onset Alzheimer's disease that causes dementia (AD-DS). Here we review recent progress in modeling the development of AD-DS in mouse models. These studies provide insight into mechanisms underlying Alzheimer's disease and generate new clinical research questions. In addition, they suggest potential new targets for disease prevention therapies.
    MeSH term(s) Alzheimer Disease/drug therapy ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Animals ; Disease Models, Animal ; Down Syndrome/drug therapy ; Down Syndrome/genetics ; Down Syndrome/metabolism ; Down Syndrome/pathology ; Mice
    Language English
    Publishing date 2019-11-29
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ISSN 1875-7855 ; 0079-6123
    ISSN (online) 1875-7855
    ISSN 0079-6123
    DOI 10.1016/bs.pbr.2019.10.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Opposing Roles of apolipoprotein E in aging and neurodegeneration.

    Hudry, Eloise / Klickstein, Jacob / Cannavo, Claudia / Jackson, Rosemary / Muzikansky, Alona / Gandhi, Sheetal / Urick, David / Sargent, Taylie / Wrobleski, Lauren / Roe, Allyson D / Hou, Steven S / Kuchibhotla, Kishore V / Betensky, Rebecca A / Spires-Jones, Tara / Hyman, Bradley T

    Life science alliance

    2019  Volume 2, Issue 1

    Abstract: Apolipoprotein E (APOE) effects on brain function remain controversial. Removal of APOE not only impairs cognitive functions but also reduces neuritic amyloid plaques in mouse models of Alzheimer's disease (AD). Can APOE simultaneously protect and impair ...

    Abstract Apolipoprotein E (APOE) effects on brain function remain controversial. Removal of APOE not only impairs cognitive functions but also reduces neuritic amyloid plaques in mouse models of Alzheimer's disease (AD). Can APOE simultaneously protect and impair neural circuits? Here, we dissociated the role of APOE in AD versus aging to determine its effects on neuronal function and synaptic integrity. Using two-photon calcium imaging in awake mice to record visually evoked responses, we found that genetic removal of APOE improved neuronal responses in adult APP/PSEN1 mice (8-10 mo). These animals also exhibited fewer neuritic plaques with less surrounding synapse loss, fewer neuritic dystrophies, and reactive glia. Surprisingly, the lack of APOE in aged mice (18-20 mo), even in the absence of amyloid, disrupted visually evoked responses. These results suggest a dissociation in APOE's role in AD versus aging: APOE may be neurotoxic during early stages of amyloid deposition, although being neuroprotective in latter stages of aging.
    MeSH term(s) Aging/physiology ; Alzheimer Disease/genetics ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/genetics ; Amyloidosis ; Animals ; Apolipoproteins E/genetics ; Disease Models, Animal ; Evoked Potentials, Visual/genetics ; Humans ; Loss of Function Mutation/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neuroglia/metabolism ; Neurons/metabolism ; Plaque, Amyloid/pathology ; Presenilin-1/genetics ; Regeneration/physiology ; Synapses/metabolism ; Visual Cortex/physiology
    Chemical Substances APP protein, human ; Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Apolipoproteins E ; PSEN1 protein, human ; Presenilin-1 ; apolipoprotein E (Arg61), mouse
    Language English
    Publishing date 2019-02-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2575-1077
    ISSN (online) 2575-1077
    DOI 10.26508/lsa.201900325
    Database MEDical Literature Analysis and Retrieval System OnLINE

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