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Can Frontal Assessment Battery Discriminate between Patients with Alzheimer’s and Frontotemporal Dementia?
(Oxford University Press (OUP), 2025-08-29)
Fabrissio Grandi
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Loreto Olavarría
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Mario A Parra
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David Martínez-Pernía
;
Cesar Serey
Objectives: The Frontal Assessment Battery (FAB) is a widely used tool for assessing executive function. However, its ability to distinguish between Alzheimer's disease dementia (ADD) and behavioural variant frontotemporal dementia (bvFTD) remains under debate. This study assessed the diagnostic utility of the Chilean version of the FAB (FAB-Ch) in differentiating ADD from bvFTD and used data-driven cluster analysis to explore dysexecutive profiles. Method: A total of 288 participants were recruited: 45 with ADD, 33 with bvFTD, and 208 cognitively unimpaired controls (CU). Mean FAB-Ch total scores were compared across groups. Receiver operating characteristic (ROC) curves evaluated the instrument's ability to distinguish (i) dementia from no dementia, (ii) ADD from bvFTD, and (iii) executive dysfunction. Hierarchical cluster analysis was conducted to identify executive profiles among dementia patients. Results: FAB-Ch scores were significantly lower in individuals with dementia compared to controls (p < .001). However, there were no significant differences between ADD and bvFTD groups (p = .59). The FAB-Ch showed strong discriminatory power between dementia and controls (AUC = 0.882; sensitivity = 0.731; specificity = 0.885), but poor discrimination between ADD and bvFTD (AUC = 0.465; p = .59). Cluster analysis among patients with dementia revealed three distinct executive profiles corresponding to different levels of cognitive impairment (p < .001). Conclusion: The FAB-Ch effectively differentiates individuals with dementia from cognitively unimpaired controls but does not distinguish between ADD and bvFTD. Nevertheless, it is sensitive to executive dysfunction and can aid in the clinical characterization of dementia severity and heterogeneity.
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Advancements in dementia research, diagnostics, and care in Latin America: Highlights from the 2023 Alzheimer's Association International conference satellite symposium in Mexico City
(2024)
Ana Luisa Sosa
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Sonia MD Brucki
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Lucia Crivelli
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Francisco Javier Lopera
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Daisy M Acosta
<jats:title>Abstract</jats:title><jats:sec><jats:title>INTRODUCTION</jats:title><jats:p>While Latin America (LatAm) is facing an increasing burden of dementia due to the rapid aging of the population, it remains underrepresented in dementia research, diagnostics, and care.</jats:p></jats:sec><jats:sec><jats:title>METHODS</jats:title><jats:p>In 2023, the Alzheimer's Association hosted its eighth satellite symposium in Mexico, highlighting emerging dementia research, priorities, and challenges within LatAm.</jats:p></jats:sec><jats:sec><jats:title>RESULTS</jats:title><jats:p>Significant initiatives in the region, including intracountry support, showcased their efforts in fostering national and international collaborations; genetic studies unveiled the unique genetic admixture in LatAm; researchers conducting emerging clinical trials discussed ongoing culturally specific interventions; and the urgent need to harmonize practices and studies, improve diagnosis and care, and use affordable biomarkers in the region was highlighted.</jats:p></jats:sec><jats:sec><jats:title>DISCUSSION</jats:title><jats:p>The myriad of topics discussed at the 2023 AAIC satellite symposium highlighted the growing research efforts in LatAm, providing valuable insights into dementia biology, genetics, epidemiology, treatment, and care.</jats:p></jats:sec>
Scopus© Citations 6 1
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Neural basis of speech and grammar symptoms in non-fluent variant primary progressive aphasia spectrum
(2023)
Diego L Lorca-Puls
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GAJARDO VIDAL, ANDREA ELIZABETH
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Maria Luisa Mandelli
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Ignacio Illán-Gala
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Zoe Ezzes
The non-fluent/agrammatic variant of primary progressive aphasia (nfvPPA) is a neurodegenerative syndrome primarily defined by the presence of apraxia of speech (AoS) and/or expressive agrammatism. In addition, many patients exhibit dysarthria and/or receptive agrammatism. This leads to substantial phenotypic variation within the speech-language domain across individuals and time, in terms of both the specific combination of symptoms as well as their severity. How to resolve such phenotypic heterogeneity in nfvPPA is a matter of debate. ‘Splitting’ views propose separate clinical entities: ‘primary progressive apraxia of speech’ when AoS occurs in the absence of expressive agrammatism, ‘progressive agrammatic aphasia’ (PAA) in the opposite case, and ‘AOS + PAA’ when mixed motor speech and language symptoms are clearly present. While therapeutic interventions typically vary depending on the predominant symptom (e.g. AoS versus expressive agrammatism), the existence of behavioural, anatomical and pathological overlap across these phenotypes argues against drawing such clear-cut boundaries. In the current study, we contribute to this debate by mapping behaviour to brain in a large, prospective cohort of well characterized patients with nfvPPA (n = 104). We sought to advance scientific understanding of nfvPPA and the neural basis of speech-language by uncovering where in the brain the degree of MRI-based atrophy is associated with inter-patient variability in the presence and severity of AoS, dysarthria, expressive agrammatism or receptive agrammatism.</jats:p> <jats:p>Our cross-sectional examination of brain-behaviour relationships revealed three main observations. First, we found that the neural correlates of AoS and expressive agrammatism in nfvPPA lie side by side in the left posterior inferior frontal lobe, explaining their behavioural dissociation/association in previous reports. Second, we identified a ‘left-right’ and ‘ventral-dorsal’ neuroanatomical distinction between AoS versus dysarthria, highlighting (i) that dysarthria, but not AoS, is significantly influenced by tissue loss in right-hemisphere motor-speech regions; and (ii) that, within the left hemisphere, dysarthria and AoS map onto dorsally versus ventrally located motor-speech regions, respectively. Third, we confirmed that, within the large-scale grammar network, left frontal tissue loss is preferentially involved in expressive agrammatism and left temporal tissue loss in receptive agrammatism.</jats:p> <jats:p>Our findings thus contribute to define the function and location of the epicentres within the large-scale neural networks vulnerable to neurodegenerative changes in nfvPPA. We propose that nfvPPA be redefined as an umbrella term subsuming a spectrum of speech and/or language phenotypes that are closely linked by the underlying neuroanatomy and neuropathology.
10Scopus© Citations 19
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Multidimensional inhibitory signatures of sentential negation in behavioral variant frontotemporal dementia
(2022)
Mariano N Díaz-Rivera
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Agustina Birba
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Sol Fittipaldi
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Débora Mola
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Yurena Morera
<jats:title>Abstract</jats:title> <jats:sec> <jats:title>Background</jats:title> <jats:p>Processing of linguistic negation has been associated to inhibitory brain mechanisms. However, no study has tapped this link via multimodal measures in patients with core inhibitory alterations, a critical approach to reveal direct neural correlates and potential disease markers.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p>Here we examined oscillatory, neuroanatomical, and functional connectivity signatures of a recently reported Go/No-go negation task in healthy controls and behavioral variant frontotemporal dementia (bvFTD) patients, typified by primary and generalized inhibitory disruptions. To test for specificity, we also recruited persons with Alzheimer's disease (AD), a disease involving frequent but nonprimary inhibitory deficits.</jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p>In controls, negative sentences in the No-go condition distinctly involved frontocentral delta (2–3 Hz) suppression, a canonical inhibitory marker. In bvFTD patients, this modulation was selectively abolished and significantly correlated with the volume and functional connectivity of regions supporting inhibition (e.g. precentral gyrus, caudate nucleus, and cerebellum). Such canonical delta suppression was preserved in the AD group and associated with widespread anatomo-functional patterns across non-inhibitory regions.</jats:p> </jats:sec> <jats:sec> <jats:title>Discussion</jats:title> <jats:p>These findings suggest that negation hinges on the integrity and interaction of spatiotemporal inhibitory mechanisms. Moreover, our results reveal potential neurocognitive markers of bvFTD, opening a new agenda at the crossing of cognitive neuroscience and behavioral neurology.</jats:p> </jats:sec>
Scopus© Citations 18 4
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Multimodal mechanisms of human socially reinforced learning across neurodegenerative diseases
(2021)
Agustina Legaz
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Sofía Abrevaya
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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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Multimodal neurocognitive markers of naturalistic discourse typify diverse neurodegenerative diseases
(2021)
Agustina Birba
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Sol Fittipaldi
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Judith C Cediel Escobar
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Cecilia Gonzalez Campo
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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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