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  1. Article: Rodent Modeling of Alzheimer's Disease in Down Syndrome:

    Farrell, Clíona / Mumford, Paige / Wiseman, Frances K

    Frontiers in neuroscience

    2022  Volume 16, Page(s) 909669

    Abstract: There are an estimated 6 million people with Down syndrome (DS) worldwide. In developed countries, the vast majority of these individuals will develop Alzheimer's disease neuropathology characterized by the accumulation of amyloid-β (Aβ) plaques and tau ... ...

    Abstract There are an estimated 6 million people with Down syndrome (DS) worldwide. In developed countries, the vast majority of these individuals will develop Alzheimer's disease neuropathology characterized by the accumulation of amyloid-β (Aβ) plaques and tau neurofibrillary tangles within the brain, which leads to the early onset of dementia (AD-DS) and reduced life-expectancy. The mean age of onset of clinical dementia is ~55 years and by the age of 80, approaching 100% of individuals with DS will have a dementia diagnosis. DS is caused by trisomy of chromosome 21 (Hsa21) thus an additional copy of a gene(s) on the chromosome must cause the development of AD neuropathology and dementia. Indeed, triplication of the gene
    Language English
    Publishing date 2022-06-07
    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.2022.909669
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Integrated analysis of transcriptomic and proteomic alterations in mouse models of ALS/FTD identify early metabolic adaptions with similarities to mitochondrial dysfunction disorders.

    Matveeva, Anna / Watters, Orla / Rukhadze, Ani / Khemka, Niraj / Gentile, Debora / Perez, Ivan Fernandez / Llorente-Folch, Irene / Farrell, Cliona / Lo Cacciato, Elide / Jackson, Joshua / Piazzesi, Antonia / Wischhof, Lena / Woods, Ina / Halang, Luise / Hogg, Marion / Muñoz, Amaya Garcia / Dillon, Eugène T / Matallanas, David / Arijs, Ingrid /
    Lambrechts, Diether / Bano, Daniele / Connolly, Niamh M C / Prehn, Jochen H M

    Amyotrophic lateral sclerosis & frontotemporal degeneration

    2024  Volume 25, Issue 1-2, Page(s) 135–149

    Abstract: Objective: Sporadic and familial amyotrophic lateral sclerosis (ALS) is a fatal progressive neurodegenerative disease that results in loss of motor neurons and, in some patients, associates with frontotemporal dementia (FTD). Apart from the accumulation ...

    Abstract Objective: Sporadic and familial amyotrophic lateral sclerosis (ALS) is a fatal progressive neurodegenerative disease that results in loss of motor neurons and, in some patients, associates with frontotemporal dementia (FTD). Apart from the accumulation of proteinaceous deposits, emerging literature indicates that aberrant mitochondrial bioenergetics may contribute to the onset and progression of ALS/FTD. Here we sought to investigate the pathophysiological signatures of mitochondrial dysfunction associated with ALS/FTD.
    Methods: By means of label-free mass spectrometry (MS) and mRNA sequencing (mRNA-seq), we report pre-symptomatic changes in the cortices of TDP-43 and FUS mutant mouse models. Using tissues from transgenic mouse models of mitochondrial diseases as a reference, we performed comparative analyses and extracted unique and common mitochondrial signatures that revealed neuroprotective compensatory mechanisms in response to early damage.
    Results: In this regard, upregulation of both Acyl-CoA Synthetase Long-Chain Family Member 3 (ACSL3) and mitochondrial tyrosyl-tRNA synthetase 2 (YARS2) were the most representative change in pre-symptomatic ALS/FTD tissues, suggesting that fatty acid beta-oxidation and mitochondrial protein translation are mechanisms of adaptation in response to ALS/FTD pathology.
    Conclusions: Together, our unbiased integrative analyses unveil novel molecular components that may influence mitochondrial homeostasis in the earliest phase of ALS.
    MeSH term(s) Mice ; Animals ; Humans ; Frontotemporal Dementia/metabolism ; Amyotrophic Lateral Sclerosis/pathology ; Proteomics ; Neurodegenerative Diseases ; Pick Disease of the Brain ; Mice, Transgenic ; Mitochondrial Diseases ; Gene Expression Profiling ; RNA, Messenger
    Chemical Substances RNA, Messenger
    Language English
    Publishing date 2024-01-23
    Publishing country England
    Document type Journal Article
    ZDB-ID 2705049-X
    ISSN 2167-9223 ; 2167-8421
    ISSN (online) 2167-9223
    ISSN 2167-8421
    DOI 10.1080/21678421.2023.2261979
    Database MEDical Literature Analysis and Retrieval System OnLINE

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