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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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Analyzing Olfactory Neuron Precursors Non-Invasively Isolated through NADH FLIM as a Potential Tool to Study Oxidative Stress in Alzheimer’s Disease
(2021)
Laura Gómez-Virgilio
;
Alejandro Luarte
;
Daniela P. Ponce
;
Bárbara A. Bruna
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BEHRENS PELLEGRINO, MARIA ISABEL
<jats:p>Among all the proposed pathogenic mechanisms to understand the etiology of Alzheimer’s disease (AD), increased oxidative stress seems to be a robust and early disease feature where many of those hypotheses converge. However, despite the significant lines of evidence accumulated, an effective diagnosis and treatment of AD are not yet available. This limitation might be partially explained by the use of cellular and animal models that recapitulate partial aspects of the disease and do not account for the particular biology of patients. As such, cultures of patient-derived cells of peripheral origin may provide a convenient solution for this problem. Peripheral cells of neuronal lineage such as olfactory neuronal precursors (ONPs) can be easily cultured through non-invasive isolation, reproducing AD-related oxidative stress. Interestingly, the autofluorescence of key metabolic cofactors such as reduced nicotinamide adenine dinucleotide (NADH) can be highly correlated with the oxidative state and antioxidant capacity of cells in a non-destructive and label-free manner. In particular, imaging NADH through fluorescence lifetime imaging microscopy (FLIM) has greatly improved the sensitivity in detecting oxidative shifts with minimal intervention to cell physiology. Here, we discuss the translational potential of analyzing patient-derived ONPs non-invasively isolated through NADH FLIM to reveal AD-related oxidative stress. We believe this approach may potentially accelerate the discovery of effective antioxidant therapies and contribute to early diagnosis and personalized monitoring of this devastating disease.</jats:p>
7Scopus© Citations 9
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Moral Emotions and Their Brain Structural Correlates Across Neurodegenerative Disorders
(2023)
Sandra Baez
;
Catalina Trujillo-Llano
;
Leonardo Cruz de Souza
;
Patricia Lillo
;
Gonzalo Forno
<jats:p>Background: Although social cognition is compromised in patients with neurodegenerative disorders such as behavioral variant frontotemporal dementia (bvFTD) and Alzheimer’s disease (AD), research on moral emotions and their neural correlates in these populations is scarce. No previous study has explored the utility of moral emotions, compared to and in combination with classical general cognitive state tools, to discriminate bvFTD from AD patients. Objective: To examine self-conscious (guilt and embarrassment) and other-oriented (pity and indignation) moral emotions, their subjective experience, and their structural brain underpinnings in bvFTD (n = 31) and AD (n = 30) patients, compared to healthy controls (n = 37). We also explored the potential utility of moral emotions measures to discriminate bvFTD from AD. Methods: We used a modified version of the Moral Sentiment Task measuring the participants’ accuracy scores and their emotional subjective experiences. Results: bvFTD patients exhibited greater impairments in self-conscious and other-oriented moral emotions as compared with AD patients and healthy controls. Moral emotions combined with general cognitive state tools emerged as useful measures to discriminate bvFTD from AD patients. In bvFTD patients, lower moral emotions scores were associated with lower gray matter volumes in caudate nucleus and inferior and middle temporal gyri. In AD, these scores were associated with lower gray matter volumes in superior and middle frontal gyri, middle temporal gyrus, inferior parietal lobule and supramarginal gyrus. Conclusion: These findings contribute to a better understanding of moral emotion deficits across neurodegenerative disorders, highlighting the potential benefits of integrating this domain into the clinical assessment.</jats:p>
24Scopus© Citations 3
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Interoception Primes Emotional Processing: Multimodal Evidence from Neurodegeneration
(2021)
Paula C. Salamone
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Agustina Legaz
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Lucas Sedeño
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Sebastián Moguilner
;
Matías Fraile-Vazquez
7Scopus© Citations 80
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Classification of Alzheimer's disease and frontotemporal dementia using routine clinical and cognitive measures across multicentric underrepresented samples: A cross sectional observational study
(2023)
Marcelo Adrián Maito
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Hernando Santamaría-García
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Sebastián Moguilner
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Katherine L. Possin
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María E. Godoy
33Scopus© Citations 53
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Multimodal mechanisms of human socially reinforced learning across neurodegenerative diseases
(2021)
Agustina Legaz
;
Sofía Abrevaya
;
Martín Dottori
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Cecilia González Campo
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Agustina Birba
<jats:title>Abstract</jats:title> <jats:p>Social feedback can selectively enhance learning in diverse domains. Relevant neurocognitive mechanisms have been studied mainly in healthy persons, yielding correlational findings. Neurodegenerative lesion models, coupled with multimodal brain measures, can complement standard approaches by revealing direct multidimensional correlates of the phenomenon.</jats:p> <jats:p>To this end, we assessed socially reinforced and non-socially reinforced learning in 40 healthy participants as well as persons with behavioural variant frontotemporal dementia (n = 21), Parkinson’s disease (n = 31) and Alzheimer’s disease (n = 20). These conditions are typified by predominant deficits in social cognition, feedback-based learning and associative learning, respectively, although all three domains may be partly compromised in the other conditions. We combined a validated behavioural task with ongoing EEG signatures of implicit learning (medial frontal negativity) and offline MRI measures (voxel-based morphometry).</jats:p> <jats:p>In healthy participants, learning was facilitated by social feedback relative to non-social feedback. In comparison with controls, this effect was specifically impaired in behavioural variant frontotemporal dementia and Parkinson’s disease, while unspecific learning deficits (across social and non-social conditions) were observed in Alzheimer’s disease. EEG results showed increased medial frontal negativity in healthy controls during social feedback and learning. Such a modulation was selectively disrupted in behavioural variant frontotemporal dementia. Neuroanatomical results revealed extended temporo-parietal and fronto-limbic correlates of socially reinforced learning, with specific temporo-parietal associations in behavioural variant frontotemporal dementia and predominantly fronto-limbic regions in Alzheimer’s disease. In contrast, non-socially reinforced learning was consistently linked to medial temporal/hippocampal regions. No associations with cortical volume were found in Parkinson’s disease. Results are consistent with core social deficits in behavioural variant frontotemporal dementia, subtle disruptions in ongoing feedback-mechanisms and social processes in Parkinson’s disease and generalized learning alterations in Alzheimer’s disease. This multimodal approach highlights the impact of different neurodegenerative profiles on learning and social feedback.</jats:p> <jats:p>Our findings inform a promising theoretical and clinical agenda in the fields of social learning, socially reinforced learning and neurodegeneration.</jats:p>
2Scopus© Citations 28
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Systematic Review of the Diagnostic Validity of Brief Cognitive Screenings for Early Dementia Detection in Spanish-Speaking Adults in Latin America
(2020)
Nilton Custodio
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Lissette Duque
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Rosa Montesinos
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Carlos Alva-Diaz
;
Martin Mellado
2Scopus© Citations 45
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Alzheimer’s Disease or Behavioral Variant Frontotemporal Dementia? Review of Key Points Toward an Accurate Clinical and Neuropsychological Diagnosis
(2020)
Gada Musa
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Andrea Slachevsky
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Carlos Muñoz-Neira
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Carolina Méndez-Orellana
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Roque Villagra
29Scopus© Citations 73
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Neuroanatomical Comparison of the "Word" and "Picture" Versions of the Free and Cued Selective Reminding Test in Alzheimer's Disease
(2018)
Andrea Slachevsky
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Paulo Barraza
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Michael Hornberger
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Carlos Muñoz-Neira
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Emma Flanagan
14Scopus© Citations 21
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Tau Platelets Correlate with Regional Brain Atrophy in Patients with Alzheimer's Disease
(2017)
SLACHEVSKY CHONCHOL, ANDREA MARÍA
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Leonardo Guzmán-Martínez
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Carolina Delgado
;
Pablo Reyes
;
Gonzalo A. Farías
1Scopus© Citations 34 1

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