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Neural embedding of frailty in cognitively unimpaired aging and dementia across Latin America
(Wiley, 2026-04)
Joaquin Migeot
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Olivia Wen
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Raul Gonzalez‐Gomez
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Hernan Hernandez
;
David Aguillon
<jats:title>Abstract</jats:title> <jats:sec> <jats:title>INTRODUCTION</jats:title> <jats:p>Frailty influences dementia risk and severity. However, its role in differentiating dementia subtypes and associations with brain structural and functional alterations remain understudied, especially in Latin America.</jats:p> </jats:sec> <jats:sec> <jats:title>METHODS</jats:title> <jats:p>Multi‐Partner Consortium to Expand Dementia Research in Latin America data included 3461 participants (cognitively unimpaired [CU], Alzheimer's disease [AD], and frontotemporal lobar degeneration [FTLD]) from Latin America using a frailty index constructed from 32 health‐related variables. XGBoost‐logistic regression models tested group discrimination, and voxel‐based morphometry plus functional connectivity analyses explored neural correlates.</jats:p> </jats:sec> <jats:sec> <jats:title>RESULTS</jats:title> <jats:p>Frailty distinguished CU from AD (area under the curve [AUC] = 0.85) and CU from FTLD (AUC = 0.88) but not AD from FTLD (AUC = 0.59). Higher frailty was linked to widespread gray matter loss, with temporal involvement in CU and stronger frontotemporal effects in dementia, particularly FTLD. Connectivity analyses showed fronto‐temporo‐posterior reductions and increased connectivity across the frailty network.</jats:p> </jats:sec> <jats:sec> <jats:title>DISCUSSION</jats:title> <jats:p>Findings position frailty as a promising marker for identifying AD and FTLD relative to CU individuals, linked with brain health alterations in Latin American populations.</jats:p> </jats:sec>
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The exposome of brain aging across 34 countries
(Springer Science and Business Media LLC, 2026-04-03)
Agustina Legaz
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Sebastian Moguilner
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Pablo Barttfeld
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Jhosmary Cuadros Castro
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Dante Sebastián Galván Rial
Scopus© Citations 7 1
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Cardiovascular risk factors and the allostatic interoceptive network in dementia
(Oxford University Press (OUP), 2025-10)
Jessica L Hazelton
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Joaquín Migeot
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Raul Gonzalez-Gomez
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Florencia Altschuler
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Claudia Duran-Aniotz
2
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Dementia prevention requires moving beyond individual choice: the costs of effort and time intersect with social determinants of health
(Elsevier BV, 2025-11)
Joaquín Migeot
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Daniel Araya-Ríos
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Matias Montecinos
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Sandra Baez
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BEHRENS PELLEGRINO, MARIA ISABEL
Scopus© Citations 5 2
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Social exposome and brain health outcomes of dementia across Latin America
(Springer Science and Business Media LLC, 2025-09-11)
Joaquin Migeot
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Stefanie D. Pina-Escudero
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Hernan Hernandez
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Raul Gonzalez-Gomez
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Agustina Legaz
A multidimensional social exposome (MSE)—the combined lifespan measures of education, food insecurity, financial status, access to healthcare, childhood experiences, and more—may shape dementia risk and brain health over the lifespan, particularly in underserved regions like Latin America. However, the MSE effects on brain health and dementia are unknown. We evaluated 2211 individuals (controls, Alzheimer’s disease, and frontotemporal lobar degeneration) from a non-representative sample across six Latin American countries. Adverse exposomes associate with poorer cognition in healthy aging. In dementia, more complex exposomes correlate with lower cognitive and functional performance, higher neuropsychiatric symptoms, and brain structural and connectivity alterations in frontal-temporal-limbic and cerebellar regions. Food insecurity, financial resources, subjective socioeconomic status, and access to healthcare emerge as critical predictors. Cumulative exposome measures surpass isolated factors in predicting clinical-cognitive profiles. Multiple sensitivity analyses confirm our results. Findings highlight the need for personalized approaches integrating MSE across the lifespan, emphasizing prevention and interventions targeting social disparities.
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Heterogeneous factors influence social cognition across diverse settings in brain health and age-related diseases
(Springer Science and Business Media LLC, 2024-01-02)
Sol Fittipaldi
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Agustina Legaz
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Marcelo Maito
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Hernan Hernandez
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Florencia Altschuler
Aging diminishes social cognition, and changes in this capacity can indicate brain diseases. However, the relative contribution of age, diagnosis and brain reserve to social cognition, especially among older adults and in global settings, remains unclear when considering other factors. Here, using a computational approach, we combined predictors of social cognition from a diverse sample of 1,063 older adults across nine countries. Emotion recognition, mentalizing and overall social cognition were predicted via support vector regressions from various factors, including diagnosis (subjective cognitive complaints, mild cognitive impairment, Alzheimer’s disease and behavioral variant frontotemporal dementia), demographics, cognition/executive function, brain reserve and motion artifacts from functional magnetic resonance imaging recordings. Higher cognitive/executive functions and education ranked among the top predictors, outweighing age, diagnosis and brain reserve. Network connectivity did not show predictive values. The results challenge traditional interpretations of age-related decline, patient–control differences and brain associations of social cognition, emphasizing the importance of heterogeneous factors.
Scopus© Citations 31 1
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Alzheimer Disease as a Clinical-Biological Construct—An International Working Group Recommendation
(2024)
Bruno Dubois
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Nicolas Villain
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Lon Schneider
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Nick Fox
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Noll Campbell
<jats:sec id="ab-nsc240001-1"><jats:title>Importance</jats:title><jats:p>Since 2018, a movement has emerged to define Alzheimer disease (AD) as a purely biological entity based on biomarker findings. The recent revision of the Alzheimer’s Association (AA) criteria for AD furthers this direction. However, concerns about a purely biological definition of AD being applied clinically, the understanding of AD by society at large, and the translation of blood-based biomarkers into clinical practice prompt these International Working Group (IWG) updated recommendations.</jats:p></jats:sec><jats:sec id="ab-nsc240001-2"><jats:title>Objective</jats:title><jats:p>To consider the revised AA criteria and to offer an alternative definitional view of AD as a clinical-biological construct for clinical use. The recommendations of the 2021 IWG diagnostic criteria are updated for further elaborating at-risk and presymptomatic states.</jats:p></jats:sec><jats:sec id="ab-nsc240001-3"><jats:title>Evidence Review</jats:title><jats:p>PubMed was searched for articles published between July 1, 2020, and March 1, 2024, using the terms “biomarker” OR “amyloid” OR “tau” OR “neurodegeneration” OR “preclinical” OR “CSF” OR “PET” OR “plasma” AND “Alzheimer’s disease.” The references of relevant articles were also searched.</jats:p></jats:sec><jats:sec id="ab-nsc240001-4"><jats:title>Findings</jats:title><jats:p>In the new AA diagnostic criteria, AD can be defined clinically as encompassing cognitively normal people having a core 1 AD biomarker. However, recent literature shows that the majority of biomarker-positive cognitively normal individuals will not become symptomatic along a proximate timeline. In the clinical setting, disclosing a diagnosis of AD to cognitively normal people with only core 1 AD biomarkers represents the most problematic implication of a purely biological definition of the disease.</jats:p></jats:sec><jats:sec id="ab-nsc240001-5"><jats:title>Conclusions and Relevance</jats:title><jats:p>The ultimate aim of the field was to foster effective AD treatments, including preventing symptoms and dementia. The approach of diagnosing AD without a clinical and biological construct would be unwarranted and potentially concerning without a clear knowledge of when or whether symptoms will ever develop. It is recommended that those who are amyloid-positive only and, more generally, most biomarker-positive cognitively normal individuals, should not be labeled as having AD. Rather, they should be considered as being at risk for AD. The expansion of presymptomatic AD is viewed as a better diagnostic construct for those with a specific pattern of biomarkers, indicating that they are proximate to the expression of symptoms in the near future.</jats:p></jats:sec>
Scopus© Citations 73 2
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Author Correction: Brain clocks capture diversity and disparities in aging and dementia across geographically diverse populations
(2024)
Sebastian Moguilner
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Sandra Baez
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Hernan Hernandez
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Joaquín Migeot
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Agustina Legaz
9Scopus© Citations 1
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Brain clocks capture diversity and disparities in aging and dementia across geographically diverse populations
(2024)
Sebastian Moguilner
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Sandra Baez
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Hernan Hernandez
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Joaquín Migeot
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Agustina Legaz
<jats:title>Abstract</jats:title><jats:p>Brain clocks, which quantify discrepancies between brain age and chronological age, hold promise for understanding brain health and disease. However, the impact of diversity (including geographical, socioeconomic, sociodemographic, sex and neurodegeneration) on the brain-age gap is unknown. We analyzed datasets from 5,306 participants across 15 countries (7 Latin American and Caribbean countries (LAC) and 8 non-LAC countries). Based on higher-order interactions, we developed a brain-age gap deep learning architecture for functional magnetic resonance imaging (2,953) and electroencephalography (2,353). The datasets comprised healthy controls and individuals with mild cognitive impairment, Alzheimer disease and behavioral variant frontotemporal dementia. LAC models evidenced older brain ages (functional magnetic resonance imaging: mean directional error = 5.60, root mean square error (r.m.s.e.) = 11.91; electroencephalography: mean directional error = 5.34, r.m.s.e. = 9.82) associated with frontoposterior networks compared with non-LAC models. Structural socioeconomic inequality, pollution and health disparities were influential predictors of increased brain-age gaps, especially in LAC (<jats:italic>R</jats:italic>² = 0.37, <jats:italic>F</jats:italic>² = 0.59, r.m.s.e. = 6.9). An ascending brain-age gap from healthy controls to mild cognitive impairment to Alzheimer disease was found. In LAC, we observed larger brain-age gaps in females in control and Alzheimer disease groups compared with the respective males. The results were not explained by variations in signal quality, demographics or acquisition methods. These findings provide a quantitative framework capturing the diversity of accelerated brain aging.</jats:p>
Scopus© Citations 33 2
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Environmental–genetic interactions in ageing and dementia across Latin America
(2024)
Agustin Ibanez
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SLACHEVSKY CHONCHOL, ANDREA MARÍA
17Scopus© Citations 6

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