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    Network anatomy in logopenic variant of primary progressive aphasia
    (2023)
    Maria Luisa Mandelli
    ;
    Diego L. Lorca‐Puls
    ;
    Sladjana Lukic
    ;
    Maxime Montembeault
    ;
    GAJARDO VIDAL, ANDREA ELIZABETH  
    <jats:title>Abstract</jats:title><jats:p>The logopenic variant of primary progressive aphasia (lvPPA) is a neurodegenerative syndrome characterized linguistically by gradual loss of repetition and naming skills resulting from left posterior temporal and inferior parietal atrophy. Here, we sought to identify which specific cortical loci are initially targeted by the disease (epicenters) and investigate whether atrophy spreads through predetermined networks. First, we used cross‐sectional structural MRI data from individuals with lvPPA to define putative disease epicenters using a surface‐based approach paired with an anatomically fine‐grained parcellation of the cortical surface (i.e., HCP‐MMP1.0 atlas). Second, we combined cross‐sectional functional MRI data from healthy controls and longitudinal structural MRI data from individuals with lvPPA to derive the epicenter‐seeded resting‐state networks most relevant to lvPPA symptomatology and ascertain whether functional connectivity in these networks predicts longitudinal atrophy spread in lvPPA. Our results show that two partially distinct brain networks anchored to the left anterior angular and posterior superior temporal gyri epicenters were preferentially associated with sentence repetition and naming skills in lvPPA. Critically, the strength of connectivity within these two networks in the neurologically‐intact brain significantly predicted longitudinal atrophy progression in lvPPA. Taken together, our findings indicate that atrophy progression in lvPPA, starting from inferior parietal and temporoparietal junction regions, predominantly follows at least two partially nonoverlapping pathways, which may influence the heterogeneity in clinical presentation and prognosis.</jats:p>
    Scopus© Citations 10  2
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    Atrophic violaceous plaques as the first manifestation of a disorder of GNAS inactivation
    (2023)
    Marie‐Chantal Caussade
    ;
    Camila Downey
    ;
    Daniela Kramer
    ;
    Claudia Morales
      1
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      1Scopus© Citations 33  6
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    Síndrome de Mounier-Kuhn: reporte de caso y revisión de la literatura
    (2022)
    Israel Díaz
    ;
    Andrés Vicentela
    ;
    Bastián Lara
    ;
    Pablo González
    ;
    Fabián Villacrés
      25
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    Multimodal neurocognitive markers of naturalistic discourse typify diverse neurodegenerative diseases
    (2021)
    Agustina Birba
    ;
    Sol Fittipaldi
    ;
    Judith C Cediel Escobar
    ;
    Cecilia Gonzalez Campo
    ;
    Agustina Legaz
    <jats:title>Abstract</jats:title> <jats:p>Neurodegeneration has multiscalar impacts, including behavioral, neuroanatomical, and neurofunctional disruptions. Can disease-differential alterations be captured across such dimensions using naturalistic stimuli? To address this question, we assessed comprehension of four naturalistic stories, highlighting action, nonaction, social, and nonsocial events, in Parkinson’s disease (PD) and behavioral variant frontotemporal dementia (bvFTD) relative to Alzheimer’s disease patients and healthy controls. Text-specific correlates were evaluated via voxel-based morphometry, spatial (fMRI), and temporal (hd-EEG) functional connectivity. PD patients presented action–text deficits related to the volume of action–observation regions, connectivity across motor-related and multimodal-semantic hubs, and frontal hd-EEG hypoconnectivity. BvFTD patients exhibited social–text deficits, associated with atrophy and spatial connectivity patterns along social-network hubs, alongside right frontotemporal hd-EEG hypoconnectivity. Alzheimer’s disease patients showed impairments in all stories, widespread atrophy and spatial connectivity patterns, and heightened occipitotemporal hd-EEG connectivity. Our framework revealed disease-specific signatures across behavioral, neuroanatomical, and neurofunctional dimensions, highlighting the sensitivity and specificity of a single naturalistic task. This investigation opens a translational agenda combining ecological approaches and multimodal cognitive neuroscience for the study of neurodegeneration.</jats:p>
      2Scopus© Citations 39
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    Allostatic-Interoceptive Overload in Frontotemporal Dementia
    (2022)
    Agustina Birba
    ;
    Hernando Santamaría-García
    ;
    Pavel Prado
    ;
    Josefina Cruzat
    ;
    Agustín Sainz Ballesteros
    Scopus© Citations 54  1
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    Mapping Subcortical Brain Alterations in 22q11.2 Deletion Syndrome: Effects of Deletion Size and Convergence With Idiopathic Neuropsychiatric Illness
    (2020)
    Christopher R.K. Ching
    ;
    Boris A. Gutman
    ;
    Daqiang Sun
    ;
    Julio Villalon Reina
    ;
    Anjanibhargavi Ragothaman
    Scopus© Citations 44  8
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      1Scopus© Citations 3  2
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    High Fat Diet-Induced Skeletal Muscle Wasting Is Decreased by Mesenchymal Stem Cells Administration: Implications on Oxidative Stress, Ubiquitin Proteasome Pathway Activation, and Myonuclear Apoptosis
    (2016)
    Johanna Abrigo
    ;
    Juan Carlos Rivera
    ;
    Javier Aravena
    ;
    Daniel Cabrera
    ;
    Felipe Simon
    <jats:p>Obesity can lead to skeletal muscle atrophy, a pathological condition characterized by the loss of strength and muscle mass. A feature of muscle atrophy is a decrease of myofibrillar proteins as a result of ubiquitin proteasome pathway overactivation, as evidenced by increased expression of the muscle-specific ubiquitin ligases atrogin-1 and MuRF-1. Additionally, other mechanisms are related to muscle wasting, including oxidative stress, myonuclear apoptosis, and autophagy. Stem cells are an emerging therapy in the treatment of chronic diseases such as high fat diet-induced obesity. Mesenchymal stem cells (MSCs) are a population of self-renewable and undifferentiated cells present in the bone marrow and other mesenchymal tissues of adult individuals. The present study is the first to analyze the effects of systemic MSC administration on high fat diet-induced skeletal muscle atrophy in the tibialis anterior of mice. Treatment with MSCs reduced losses of muscle strength and mass, decreases of fiber diameter and myosin heavy chain protein levels, and fiber type transitions. Underlying these antiatrophic effects, MSC administration also decreased ubiquitin proteasome pathway activation, oxidative stress, and myonuclear apoptosis. These results are the first to indicate that systemically administered MSCs could prevent muscle wasting associated with high fat diet-induced obesity and diabetes.</jats:p>
      6Scopus© Citations 94
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    Scopus© Citations 18  1