The research team set out to characterize what neuropsychologists call dysexecutive behavioral changes, a term that describes disruptions in the suite of behaviors orchestrated by the frontal systems of the brain. Executive functions encompass the ability to initiate activity, sustain effort toward goals, inhibit inappropriate impulses, organize sequences of actions, and adapt behavior to changing circumstances. When these systems falter, the consequences show up not as failures on a laboratory puzzle but as changes in daily life: a person may become apathetic and lose the drive to begin tasks, may struggle to organize and complete multi-step activities, or may find themselves saying and doing things that a previously well-regulated sense of social restraint would have suppressed. The study’s central premise is that capturing these changes requires a multidimensional behavioral assessment, complementing the cognitive testing that has dominated much of the post-COVID literature to date.

To do this, the researchers conducted a cross-sectional study of 69 participants, dividing them into two groups according to their clinical trajectory after infection. Forty-five participants had a history of acute COVID-19, meaning they had been infected and had experienced the acute illness, while 24 participants had post-COVID-19 syndrome, the condition in which symptoms persist well beyond the acute phase. The instrument at the heart of the study was the Frontal Systems Behavior Scale, known in the field as the FrSBe. This standardized questionnaire is designed to quantify behaviors associated with damage or dysfunction in frontal brain systems, and it yields scores along three well-characterized dimensions: apathy, executive dysfunction, and disinhibition. Crucially, the scale asks respondents to rate behavior both before and after the event of interest, which in this case was SARS-CoV-2 infection, allowing each participant to serve as their own baseline for comparison.

The three dimensions measured by the FrSBe map onto distinct aspects of frontal-lobe function. Apathy reflects a loss of motivation, initiative, and emotional engagement, and it is classically associated with damage to medial frontal regions and their connections to deep brain circuits involved in drive and reward. Executive dysfunction captures difficulties with planning, organization, working memory in the service of action, and the flexible shifting of strategies when circumstances change. Disinhibition, by contrast, reflects a failure of inhibitory control, manifesting as impulsivity, socially inappropriate behavior, and difficulty restraining emotional or appetitive responses. Because these dimensions can be affected independently, a profile-based assessment can reveal patterns that a single global measure of cognitive impairment would obscure. This is precisely the kind of granularity the Spanish team sought in comparing the two post-infection groups.

The findings were consistent in one broad respect and revealing in another. Across both groups, the mean standardized scores, expressed as z-scores, for the FrSBe behavioral dimensions increased in the period after infection compared with participants’ retrospective ratings of their own pre-infection functioning. In other words, on average, people in both the acute COVID-19 group and the post-COVID-19 syndrome group reported more dysexecutive behaviors after their infection than before it. This uniform direction of change suggests that SARS-CoV-2 infection, regardless of the subsequent clinical course, may be associated with perceived alterations in behaviors that depend on frontal systems, a conclusion that aligns with the broader literature documenting neuropsychological alterations, particularly executive dysfunction, as frequently reported consequences of the infection.

The differences between the groups, however, were where the study’s most clinically interesting signal emerged. Participants with post-COVID-19 syndrome showed significant increases in all three dysexecutive symptom dimensions, and their post-infection scores reached the range of clinical difficulty on the apathy and disinhibition dimensions. This means that individuals living with the persistent form of the illness not only noticed changes in their capacity for organized, goal-directed activity but also reported meaningful losses of motivation and initiative alongside weakened behavioral inhibition. For a condition whose day-to-day burden is often described in terms of fatigue and cognitive fog, the finding that apathy, a motivational rather than purely cognitive construct, features prominently offers a potentially important reframing: some of what patients experience as exhaustion or loss of drive may be measurable as a distinct frontal-systems behavioral syndrome.

The acute COVID-19 group presented a subtler picture. These participants, who had been infected but had not developed the persistent syndrome, exhibited slight perceived behavioral changes on the executive dysfunction dimension, and more marked changes on the dimension of disinhibition. The prominence of disinhibition in this group is noteworthy because it suggests that even people whose infection resolves without a chronic syndrome may perceive changes in impulse control and behavioral regulation. The authors’ interpretation, as reflected in their reported results, is that the two trajectories carry distinct patterns of self-reported alteration: a broader and clinically elevated profile in post-COVID-19 syndrome, and a narrower, milder profile dominated by disinhibitory features in those with a history of acute infection alone.

From these observations, the researchers draw two practical conclusions. First, they propose that SARS-CoV-2 infection may be associated with perceived changes in dysexecutive behavior, with distinct patterns across individuals on different post-infection trajectories. Second, they suggest that the Frontal Systems Behavior Scale may be a useful tool for identifying behavioral alterations across the different clinical spectra of the disease. The second point has real methodological weight. Much of the post-COVID assessment literature relies on neuropsychological batteries that measure cognitive performance under structured testing conditions, which can miss changes that manifest primarily in spontaneous, real-world behavior. A validated behavioral instrument with established norms and a built-in pre-post comparison offers clinicians and researchers a complementary lens, one that may be particularly sensitive to the motivational and inhibitory changes that patients themselves notice but that standard testing may not capture.

The authors are careful, appropriately, to frame their conclusions as exploratory. The study is a cross-sectional comparison with a modest sample size, and the FrSBe’s pre-infection ratings are retrospective, which means they depend on participants’ memory and self-perception of how they functioned before falling ill. Retrospective self-report is vulnerable to bias, particularly in a population experiencing fatigue, low mood, or cognitive complaints, and the design cannot establish that the behavioral changes were caused by the infection itself rather than by illness-related stress, lifestyle disruption, or other confounding factors. The researchers explicitly state that these exploratory findings should be interpreted with caution and justify further research using a more robust methodological approach, a caveat that responsible readers should take seriously. Larger longitudinal studies, ideally with pre-infection behavioral data collected prospectively, would be needed to confirm and extend the reported patterns.

Even with those limitations, the study makes a contribution that fits into a growing scientific effort to understand the full neurological and psychological footprint of SARS-CoV-2. Executive dysfunction has been widely reported after infection, but behavioral dimensions such as apathy and disinhibition have received less systematic attention. By showing that these dimensions can be measured, that they change in self-reported terms after infection, and that their profiles differ between acute and persistent clinical courses, Becerra-García and Laval provide a template for how behavioral neuropsychology can sharpen the characterization of post-COVID conditions. The work was funded by the Universidad Internacional de La Rioja’s call for grants for scientific publication, was approved by the institution’s research ethics commission, and is published open access, making the full report available to clinicians, researchers, and patients alike. As the field moves toward more rigorous designs, instruments like the FrSBe may help ensure that the behavioral consequences of COVID-19, not just its cognitive ones, are neither overlooked nor underestimated.

Subject of Research: Perceived dysexecutive behavioral changes after SARS-CoV-2 infection in acute COVID-19 versus post-COVID-19 syndrome

Article Title: Characterizing perceived dysexecutive behavioral changes following SARS-CoV-2 infection in individuals with different clinical trajectories

Article References: Becerra-García, J. A., & Laval, M. D. F. (2026). Characterizing perceived dysexecutive behavioral changes following SARS-CoV-2 infection in individuals with different clinical trajectories. Discover Psychology. https://doi.org/10.1007/s44202-026-00933-y

Image Credits: AI Generated

DOI: 10.1007/s44202-026-00933-y

Keywords: SARS-CoV-2, post-COVID-19 syndrome, dysexecutive behavior, executive dysfunction, apathy, disinhibition, Frontal Systems Behavior Scale, neuropsychology, behavioral assessment, frontal lobes, COVID-19, mental health

A new study published in the Journal of Neurology by Electra Chatzidimitriou of the University of California, San Francisco and Aristotle University of Thessaloniki, together with colleagues including Howard Rosen, Maria Luisa Gorno-Tempini, William Seeley, Bruce Miller, and Katherine Rankin, set out to answer that question with unusual rigor. The team had previously developed an integrative model of functional decline in a small Greek cohort of 26 patients with bvFTD, combining cognitive, behavioral, personality, and brain imaging variables. Now they have tested whether that model holds up in a much larger and completely independent sample: 146 individuals with mild-stage bvFTD evaluated at the UCSF Memory and Aging Center. This kind of external validation is a critical but underused step in dementia research, because it determines whether relationships observed in one cohort are robust enough to generalize across clinical settings, demographics, and cultures.

The participants all met the international consortium criteria for at least possible bvFTD, and only patients scoring above 18 on the Mini-Mental State Examination were included, ensuring the analyses focused on early disease rather than advanced neurodegeneration. Each patient underwent structural magnetic resonance imaging on 3 Tesla scanners, a comprehensive neuropsychological battery, and informant-based assessments of behavior, personality, and daily functioning. Because patients with bvFTD frequently lack self-awareness, the researchers relied on knowledgeable informants, such as close relatives, to rate personality with the Big Five Inventory and behavior with the Neuropsychiatric Inventory. The primary outcome was the Functional Activities Questionnaire, an informant report covering ten domains of instrumental daily living, from balancing a checkbook to preparing meals and keeping track of current events.

On the analytical side, the study combined two complementary statistical approaches. First, the team used penalized Least Absolute Shrinkage and Selection Operator regression, a machine learning technique that shrinks the coefficients of uninformative predictors to zero, allowing the strongest correlates of functional status to emerge even when candidate variables are highly correlated. The regularization parameter was tuned through ten-fold cross-validation, and the data were split into training and test sets to evaluate predictive performance. Second, structural equation modeling was used to map the directional pathways among the surviving variables, testing how brain structure, cognition, behavior, and personality interconnect to produce functional disability.

The LASSO analysis delivered a striking result: the two strongest predictors of functional impairment were not cognitive measures at all, but personality and behavior. Reduced conscientiousness, as rated by informants, carried the largest coefficient, followed closely by apathy. Only then came global cognition on the MMSE, executive performance on a modified Trail Making Test, the ability to detect sarcasm on the Awareness of Social Inference Test, and semantic verbal fluency. Together these six variables explained roughly 39 percent of the variance in functional scores. Variables that often preoccupy clinicians, including inhibitory control on the Stroop test, visuoconstructional skills, disinhibition, and even the volume of the right superior frontal gyrus, were shrunk out of the model, indicating that they contributed no independent predictive information once the stronger correlates were accounted for.

The path model then revealed how these predictors relate to one another, and it fit the data exceptionally well, with a nonsignificant chi-square, a Comparative Fit Index of 1.000, a Root Mean Square Error of Approximation of zero, and a standardized residual below 0.05. Three brain-to-cognition pathways emerged from the volume of the right superior frontal gyrus, a prefrontal region involved in executive control, attentional regulation, and the initiation of goal-directed behavior. Smaller gray matter volume in this region was associated with slower executive performance, which in turn predicted worse daily functioning. A parallel pathway linked the same region to global cognition and, through it, to disability. A third, more hierarchical pathway showed that executive dysfunction feeds into broader global cognitive decline, consistent with the characteristic trajectory of bvFTD, in which early frontal network disruption progressively erodes multiple cognitive domains.

Alongside this neural-cognitive cascade, the model identified a partially independent behavioral-personality pathway. Apathy was associated with functional impairment both directly and indirectly, through its relationship with reduced conscientiousness. In other words, the motivational collapse that defines bvFTD appears to undermine daily life in two ways: patients stop initiating activities altogether, and the erosion of goal-directed behavior manifests as disorganization, unreliability, and an inability to plan and complete multistep tasks. Notably, this pathway appeared relatively independent of the neural-cognitive pathways, hinting that motivational and personality changes in bvFTD are mediated by partially distinct neural systems, such as medial frontal and limbic circuits, rather than being mere downstream consequences of executive dysfunction.

One intriguing nuance concerned semantic verbal fluency. In the larger American cohort, fluency was strongly connected to the superior frontal gyrus, executive performance, and global cognition, but it no longer showed a direct path to functional status, unlike in the original smaller Greek study. The authors interpret this through the framework of controlled semantic cognition, which holds that retrieving and deploying conceptual knowledge depends on both a semantic representational system and an executive control system. In a larger sample, the shared variance that fluency once captured across executive and global domains was more precisely disentangled, positioning semantic fluency as an intermediate cognitive marker rather than an independent driver of disability.

The clinical implications are substantial. Because behavioral and personality variables outperformed cognitive tests as predictors of everyday function, the authors argue that assessing bvFTD with cognitive screening alone fundamentally misses the point. Comprehensive evaluation should integrate neurocognitive, behavioral, socioemotional, and personality domains, and care planning should be tailored to each patient’s profile. Patients dominated by apathy and reduced conscientiousness may benefit most from structured environmental support, external cueing, routine-based interventions, and caregiver-mediated behavioral activation, whereas those with prominent executive inefficiency may need targeted training in task sequencing, planning, and goal management. Many patients will require combined approaches.

The study is not without limitations. Variable selection was partly guided by the earlier Greek findings, the neuroimaging analysis focused on a single prefrontal region, and some assessment instruments differed between cohorts, requiring conceptual rather than exact measurement equivalence. The cross-sectional design also precludes causal inference. Still, the convergence of findings across two countries, two healthcare systems, and a fivefold larger sample provides compelling evidence that disability in early bvFTD emerges from the dynamic interplay of two complementary processes: frontal neurodegeneration eroding the cognitive machinery of independence, and motivational and personality changes directly dismantling the will and organization needed to engage with daily life. Recognizing both streams, the authors conclude, is essential for optimizing clinical care and preserving quality of life for patients and families facing this devastating disease.

Subject of Research: Functional impairment and its neural, cognitive, behavioral, and personality determinants in early-stage behavioral variant frontotemporal dementia

Article Title: External validation of an integrative model of functional impairment in early-stage behavioral variant frontotemporal dementia (bvFTD)

Article References: Chatzidimitriou, E., Moraitou, D., Ioannidis, P., Aretouli, E., Chen, Y., Rosen, H. J., Gorno-Tempini, M. L., Seeley, W. W., Miller, B. L., & Rankin, K. P. (2026). External validation of an integrative model of functional impairment in early-stage behavioral variant frontotemporal dementia (bvFTD). Journal of Neurology, 273(10), Article 642. https://doi.org/10.1007/s00415-026-14182-5

Image Credits: AI Generated

DOI: 10.1007/s00415-026-14182-5

Keywords: bvFTD, frontotemporal dementia, functional impairment, apathy, conscientiousness, executive function, superior frontal gyrus, LASSO regression, structural equation modeling, neuropsychology, neuroimaging, dementia

The research team, led by Tao Chen, Qingyu Sun, and senior author Muireann Irish, analysed data from 432 people diagnosed with clinically probable frontotemporal lobar degeneration (FTLD) or Alzheimer’s disease between 2008 and 2025 at the Brain and Mind Centre in Sydney. Of these, 358 individuals had complete carer burden data and formed the primary analytic cohort, comprising 230 people in the FTLD group and 128 in the Alzheimer’s disease group. The FTLD group spanned the full clinical spectrum, including behavioural variant frontotemporal dementia, left- and right-sided semantic dementia, progressive nonfluent aphasia, progressive supranuclear palsy, and corticobasal syndrome, while the Alzheimer’s group included typical presentations and logopenic progressive aphasia. Diagnoses were reached by multidisciplinary consensus using internationally recognised criteria, and all participants scored at least 40 out of 100 on a standard cognitive screening battery at baseline.

The methodological design of the study is what sets it apart from earlier work. Rather than relying on the Neuropsychiatric Inventory, the instrument used in most previous caregiver studies, the team turned to the Cambridge Behavioural Inventory—Revised, a carer-reported questionnaire whose broader coverage captures behavioural domains that other tools routinely miss. Chief among these is behavioural rigidity, an umbrella term encompassing stereotypies such as excessive hand rubbing, compulsions like relentless hand washing, stereotyped catchphrases, impulsive acts including pathological gambling, hoarding, restricted interests, insistence on sameness, and ritualistic routines. Carer burden itself was measured with the widely used 12-item Zarit Burden Interview, which quantifies the emotional, physical, and role-related demands of caregiving on a scale from 0 to 48.

The statistical approach was equally rigorous. Multivariate regression models predicted carer burden from seven behavioural and psychological symptom domains, adjusting for patient age, sex, education, disease duration, disease severity, and diagnostic category. Missing data were handled through multiple imputation by chained equations, and the team complemented standardised regression coefficients with relative importance metrics based on the Lindeman–Merenda–Gold method, which partitions explained variance among correlated predictors. This dual strategy allowed the researchers to distinguish symptoms that independently drive burden from those that contribute through shared, synergistic effects with co-occurring behaviours, a nuance that single-coefficient analyses cannot capture.

The headline finding is striking in its clarity. Across the entire dementia cohort, two symptoms emerged as significant predictors of carer burden: behavioural rigidity, with a standardised coefficient of 0.15, and apathy, indexed by the motivation subscale, with a coefficient of 0.14. Both were modest in absolute terms but statistically robust, with confidence intervals excluding zero. Crucially, global cognition, measured by the Addenbrooke’s Cognitive Examination, showed no significant association with carer burden whatsoever. This dissociation is particularly provocative in Alzheimer’s disease, where cognitive decline is conventionally assumed to be the primary engine of carer distress. The data suggest instead that it is the disruption of motivation, behaviour, and daily routine, not the erosion of memory, that most corrodes carer wellbeing.

When the analyses were run separately within diagnostic groups, a syndrome-specific pattern emerged. In the FTLD group, behavioural rigidity was the strongest and most important predictor of carer burden, with a standardised coefficient of 0.18 and the largest relative importance score of 0.137. This finding held even when the researchers excluded participants with behavioural variant frontotemporal dementia, the syndrome most obviously associated with rigid behaviour, indicating that the effect extends across the broader FTLD spectrum. The authors propose a compelling mechanistic account: rigid behaviours are typically high-frequency and resistant to change, forcing carers to organise entire days around accommodating rituals and rules. Over time, this does not merely add to the caregiving workload; it fundamentally reconfigures the carer’s own life, constraining the timing, sequencing, and nature of everyday activities at the expense of efficiency and shared decision-making.

In the Alzheimer’s group, the picture shifted. Here, apathy and abnormal behaviour were the significant predictors, each with a standardised coefficient of 0.26, and apathy carried the largest relative importance value of 0.232. The findings align with qualitative research suggesting that apathy imposes its toll through a subtle but relentless reconfiguration of the caregiving relationship. When a person with dementia loses the drive to initiate activity, responsibility for starting and sustaining every part of daily life falls to the carer, who must navigate the tension between gently steering engagement and preserving the person’s remaining autonomy. That balancing act, the literature suggests, breeds frustration, guilt, and a gradual, painful acceptance of diminished reciprocity in the relationship.

Perhaps the most forward-looking element of the study is its longitudinal component. In 172 participants assessed at baseline and again roughly one year later, the researchers examined how within-person changes in symptoms related to changes in carer burden over the same interval. A single domain stood out: mood-related symptoms, including irritability and agitation, were the only significant longitudinal predictor of increasing carer burden across the combined cohort, with a standardised coefficient of 0.24. No significant longitudinal predictors emerged within either diagnostic group alone, likely reflecting the modest sample sizes and heterogeneous progression rates of individual syndromes. The transdiagnostic pattern, however, is clinically meaningful. Mood-related symptoms fluctuate with situational demands and are notoriously difficult to anticipate, and experience-sampling research has shown that unpredictable and uncontrollable events are potent drivers of negative affect in dementia carers. Even infrequent episodes of agitation, previous work has demonstrated, impose disproportionately high levels of stress, because each episode forces carers to abandon coping strategies that had been working and reallocate their emotional resources.

The clinical implications are direct and actionable. The authors argue that routine screening for behavioural rigidity and apathy should be considered in all patients with dementia, with psychoeducation at the point of diagnosis preparing carers, particularly in Alzheimer’s disease, for apathy as a prominent and burdensome feature rather than a secondary annoyance. In the absence of effective disease-modifying therapies, symptom-focused management may offer the greatest realistic potential for reducing carer burden. Given the well-documented dysfunction of serotonergic and dopaminergic systems in FTLD, and their established links to cognitive flexibility, pharmacological modulation of these pathways may eventually help alleviate rigidity and repetitive behaviours, though current guidelines recommend prioritising non-pharmacological approaches whenever symptoms are mild and pose minimal risk. The study is not without limitations: carer-side factors such as personality, coping style, social support, and hours of care were not modelled, pathological confirmation of diagnosis was unavailable, and the functional rating scale used to index severity has not been validated across every syndrome included. Larger, multi-centre samples with extended follow-up will be needed to refine these syndrome-specific relationships. Yet the core message stands firm. What determines whether a carer buckles under the strain is not how far memory has faded, but whether rigid routines have colonised the household, whether motivation has drained away, and whether mood disturbances are flaring without warning. Recognising these targets, and treating them as the primary clinical outcomes they truly are, may be the most effective way to protect the people who hold dementia care together.

Subject of Research: Behavioural and psychological symptom determinants of carer burden in frontotemporal lobar degeneration and Alzheimer's disease

Article Title: Behavioural and psychological symptom determinants of carer burden across clinical syndromes associated with frontotemporal lobar degeneration and Alzheimer’s disease: a transdiagnostic analysis

Article References: Chen, T., Sun, Q., Foxe, D., Narasimhan, M., Teng, C., Cheung, S. C., Carrick, J., Burrell, J. R., Hwang, Y. T., Ahmed, R. M., Piguet, O., & Irish, M. (2026). Behavioural and psychological symptom determinants of carer burden across clinical syndromes associated with frontotemporal lobar degeneration and Alzheimer’s disease: a transdiagnostic analysis. Journal of Neurology, 273(10), Article 592. https://doi.org/10.1007/s00415-026-14132-1

Image Credits: AI Generated

DOI: 10.1007/s00415-026-14132-1

Keywords: carer burden, dementia, frontotemporal lobar degeneration, Alzheimer's disease, behavioural rigidity, apathy, behavioural and psychological symptoms, Zarit Burden Interview, Cambridge Behavioural Inventory-Revised, caregiving, longitudinal analysis, neuropsychiatry