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LCBC forskning bidrar til menneskelig kognitiv nevrovitenskap nasjonalt og internasjonalt ved publisering av resultater i vitenskapelige tidsskrifter enten som åpen tilgang eller ved deponering på fortrykkstjenere. LCBC publiserer også sine koder og metoder i samsvar med FAIR-prinsippene.
R-pakker fra LCBC:
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Kransberg, Jonas Moe; Bråthen, Anne Cecilie Sjøli; Falch, Emilie Sogn; Øverbye, Knut Eiliv Ødegård; Garrido, Pablo F. & Fjell, Anders Martin
[Vis alle 10 forfattere av denne artikkelen]
(2026).
Failure to detect entorhinal grid-like signals in a passive navigation human fMRI study.
Imaging Neuroscience.
4.
doi:
10.1162/imag.a.1196.
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Abstract Grid cells in the human entorhinal cortex (EC) play a critical role in spatial navigation and memory. The EC is also one of the first regions affected by ageing and Alzheimer’s disease. This pre-registered functional magnetic resonance imaging (fMRI) study aimed to detect grid-cell-like signals (GLS) in a passive virtual navigation task. Contrary to our hypotheses and previous findings, we did not observe significant GLS at a population level, even in younger participants. Further exploratory analyses investigated the impact of task-engagement, as inferred from object-location memory performance, and showed no relationship with GLS magnitude. We also examined potential influences of a confounding one-fold directional signal and various data-processing choices but observed no consistent patterns. Our findings, consistent with recent null results from similar studies, suggest that passive navigation paradigms may be insufficient for reliably eliciting grid-like signals in human fMRI.
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Roe, James Michael; J., Jagust, William; M., Landau, Susan; M., Harrison, Theresa; Grydeland, Håkon & Slivka, Maksim
[Vis alle 19 forfattere av denne artikkelen]
(2026).
Cortical thickness changes precede high levels of amyloid by at least 7 years | Nature Neuroscience.
Nature Neuroscience.
ISSN 1097-6256.
doi:
10.1038/s41593-026-02363-4.
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Alzheimer’s disease is now defined by underlying pathology, with elevated amyloid-beta (Aβ) sufficient for diagnosis in the absence of cognitive symptoms. We combined longitudinal magnetic resonance imaging and Aβ positron emission tomography data from three cognitively healthy cohorts to examine cortical thickness trajectories in individuals who later converted to Aβ-positive status, using magnetic resonance images acquired years before conversion. Individuals who subsequently developed elevated Aβ showed a thicker cortex and reduced cortical thinning, detectable up to 7 years before conversion. Many effects persisted after accounting for quantitative Aβ levels, suggesting some cortical thickness changes may be partly independent of Aβ. Differences in cortical thickness and its change showed moderate spatial correspondence with Aβ deposition patterns, and the timing of thickness changes tracked the progression of Aβ accumulation. These findings indicate that cortical thickness alterations can precede positron emission tomography-detectable amyloid positivity by several years, suggesting high amyloid burden may not represent the earliest imaging marker of Alzheimer’s disease. Longitudinal MRI reveals that the cortex becomes relatively thicker years before amyloid positivity is detected on PET, providing insight into the earliest brain changes and potential consequences of amyloid accumulation in Alzheimer’s disease.
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Walhovd, Kristine B; Bråthen, Anne Cecilie Sjøli; Øverbye, Knut Eiliv Ødegård; Kransberg, Jonas Moe; Sørensen, Øystein & Garrido, Pablo F.
[Vis alle 19 forfattere av denne artikkelen]
(2026).
Feature-specific environmental contributions to human cortical architecture revealed by twin brainprints.
Communications Biology.
doi:
10.1038/s42003-026-10707-w.
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Abstract How environmental variation shapes the human cerebral cortex remains incompletely understood. Here we compare cortical brainprints – individual profiles of regional cortical morphology – in 210 twins (age 16-78 years) to distinguish prenatal, adult naturalistic and experimentally induced environmental variation from genetic contributions. Monozygotic twins showed higher brainprint similarity than dizygotic twins, consistent with genetic effects. Lasting influences of early environment were evident in lower brainprint similarity in monozygotic twin-pairs with greater birthweight discordances, driven by surface area across the cortical ribbon. In contrast, within-pair differences in adult weight and lifestyle had minimal influence. Still, a 10-week virtual-reality navigation intervention revealed training-induced changes in the gray-white interface, with curvature and area changes supported by microstructural reconfigurations. Relative brainprint similarity increased in monozygotic but diverged in dizygotic pairs following training. These findings show that distinct environmental influences acting at prenatal and adult stages are reflected in different features of the human cerebral cortex.
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Pineiro, Didac Vidal; Sørensen, Øystein; Strømstad, Marie Lorentsen; Amlien, Inge; Baaré, William & Bartrés-Faz, David
[Vis alle 74 forfattere av denne artikkelen]
(2025).
Vulnerability to memory decline in aging revealed by a mega-analysis of structural brain change.
Nature Communications.
16(1).
doi:
10.1038/s41467-025-66354-y.
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Brain atrophy is a key factor behind episodic memory loss in aging, but the nature and ubiquity of this relationship remains poorly understood. This study leverages 13 longitudinal datasets, including 3737 cognitively healthy adults (10,343 MRI scans; 13,460 memory assessments), to determine whether brain change-memory change associations are more pronounced with age and genetic risk for Alzheimer’s Disease. Both factors are associated with accelerated brain decline, yet it remains unclear whethermemory loss is exacerbated beyond what atrophy alone would predict. Additionally, we assess whether memory decline aligns with a global pattern of atrophy or stems from distinct regional contributions. Our mega-analysis reveals a nonlinear relationship between memory decline and brain atrophy, primarily affecting individuals with above-average brain structural decline. The associations are stronger in the hippocampus but also spread across diverse cortical and subcortical regions. The associations strengthen with age, reachingmoderate associations in participants in their eighties. While APOE ε4 carriers exhibit steeper brain and memory loss, genetic risk has no effect on the change-change associations. These findings support the presence of common biological macrostructural substrates underlying memory function in older age which are vulnerable to multiple age-related factors, even in the absence of overt pathological changes.
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Krogsrud, Stine Kleppe; Nordeng, Hedvig Marie Egeland; Roe, James Michael; Torkildsen, Janne von Koss; Wood, Mollie Elizabeth & Ystrøm, Eivind
(2025).
Associations between prenatal paracetamol exposure and brain development from ages 4–16: A longitudinal MRI study.
Developmental Cognitive Neuroscience.
ISSN 1878-9293.
78.
doi:
10.1016/j.dcn.2025.101667.
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Research has raised concerns regarding the potential impact of prenatal paracetamol exposure on fetal neurodevelopment. This is the first longitudinal study to investigate whether such exposure is related to structural brain development and cognitive abilities during childhood and adolescence. The sample includes 447 children aged 4.1–16.2 years with 905 MRI scans. The study is based on The Norwegian Mother, Father and Child Study (MoBa), and uses data from the Medical Birth Registry of Norway. The exposure variable is mothers’ self-reported use of paracetamol from prenatal and postnatal questionnaires. Among 447 children (229 girls; mean age 8.38 years), 193 (43.2 %) were prenatally exposed. Days of exposure range from 1 to 128 (mean 8.2). Vertex-wise linear mixed effect models showed that exposed children (n = 193; 393 scans) had slightly smaller cortical surface area and volume in some regions compared to non-exposed children. These results were seemingly driven by long-term exposed children (≥14 days in utero; n = 35; 72 scans, and exposed in all three trimesters, n = 21; 44 scans). However, group differences in brain structure were small with largely overlapping distributions, and the observational design and risk of unmeasured confounding preclude causal inference. Thus, the clinical significance remains uncertain. For cognitive abilities, results were reassuring showing no significant effect of prenatal paracetamol exposure on working memory capacity or IQ scores.
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Ravndal, Anne; Fjell, Anders Martin; Vidal-Piñeiro, Didac; Sørensen, Øystein; Falch, Emilie Sogn & Kropiunig, Julia
[Vis alle 21 forfattere av denne artikkelen]
(2025).
Sex differences in healthy brain aging are unlikely to explain higher Alzheimer’s disease prevalence in women.
Proceedings of the National Academy of Sciences of the United States of America (PNAS).
ISSN 0027-8424.
122(42).
doi:
10.1073/pnas.2510486122.
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As Alzheimer’s disease (AD) is diagnosed more frequently in women, understanding the role of sex has become a key priority in AD research. However, despite aging being the primary risk factor for AD, it remains unclear whether men and women differ in the extent of brain decline with age. Using 12,638 longitudinal brain MRIs from 4,726 participants aged 17 to 95 y across 14 cohorts, we examined sex differences in structural brain changes over time, controlling for differences in head size. Men showed greater cortical thickness (CT) decline in the cuneus, lingual, parahippocampal, and pericalcarine regions; surface area decline in the fusiform and postcentral regions; and in older adults, greater subcortical decline in the caudate, nucleus accumbens, putamen, and pallidum. In contrast, women only showed greater surface area decline in the banks of the superior temporal sulcus and greater ventricular expansion in older adults. These results suggest that sex differences in age-related brain decline are unlikely to contribute to the higher AD diagnosis prevalence in women, necessitating research into alternative explanations.
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Vidal-Piñeiro, Didac; Sørensen, Øystein; Strømstad, Marie Lorentsen; Amlien, Inge; Anderson, Micael & Baaré, William F.C.
[Vis alle 25 forfattere av denne artikkelen]
(2025).
Reliability of structural brain change in cognitively healthy adult samples.
Imaging Neuroscience.
3,
s. 1–25.
doi:
10.1162/imag_a_00547.
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In neuroimaging research, tracking individuals over time is key to understanding the interplay between brain changes and genetic, environmental, or cognitive factors across the lifespan. Yet, the extent to which we can estimate the individual trajectories of brain change over time with precision remains uncertain. In this study, we estimated the reliability of structural brain change in cognitively healthy adults from multiple samples and assessed the influence of follow-up time and number of observations. Estimates of cross-sectional measurement error and brain change variance were obtained using the longitudinal FreeSurfer processing stream. Our findings showed, on average, modest longitudinal reliability with 2 years of follow-up. Increasing the follow-up time was associated with a substantial increase in longitudinal reliability, while the impact of increasing the number of observations was comparatively minor. On average, 2-year follow-up studies require ≈2.7 and ≈4.0 times more individuals than designs with follow-ups of 4 and 6 years to achieve comparable statistical power. Subcortical volume exhibited higher longitudinal reliability than cortical area, thickness, and volume. The reliability estimates were comparable with those estimated from empirical data. The reliability estimates were affected by both the cohort’s age where younger adults had lower reliability of change and the preprocessing pipeline where the FreeSurfer’s longitudinal stream was notably superior than the cross-sectional stream. Suboptimal reliability inflated sample size requirements and compromised the ability to distinguish individual trajectories of brain aging. This study underscores the importance of long-term follow-ups and the need to consider reliability in longitudinal neuroimaging research.
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Tungesvik, Helene Melsom; Padrela, Beatriz; Groote, Inge Rasmus; Bjørnerud, Atle; Geier, Oliver Marcel & Hisdal, Jonny
[Vis alle 8 forfattere av denne artikkelen]
(2025).
Imaging cerebral circulation in long-term anabolic-androgenic steroid users and non-using weightlifters.
Drug and Alcohol Dependence.
ISSN 0376-8716.
275,
s. 112829–112829.
doi:
10.1016/j.drugalcdep.2025.112829.
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Background: Anabolic-androgenic steroids (AAS) are commonly used by recreational weightlifters for performance enhancement, despite associated health risks, including cardiovascular and brain effects. This study investigates the cerebrovascular effects of prolonged AAS use in male weightlifters, focusing on cerebral blood flow (CBF) and other indicators of cerebrovascular health.
Methods: Eighty-six males were included, with 41 current consumers of AAS and 45 non-using weightlifting controls. Cerebrovascular health was evaluated using magnetic resonance imaging (MRI) pseudo-continuous arterial spin labeling (PCASL) derivatives to measure CBF and spatial coefficient of variation (sCoV) of CBF in gray matter. Additionally, MRI T2-weighted fluid-attenuated inversion recovery (FLAIR) sequences were used to analyze white matter hyperintensities as a marker of small-vessel disease.
Results: AAS consumers had significantly higher sCoV than weightlifting controls (p = 0.001). Further, sCoV in total gray matter correlated with testosterone/epitestosterone ratio and total years of AAS use. No significant differences were found in CBF or white matter hyperintensity volume.
Conclusion: These findings indicate that long-term AAS use may impact cerebrovascular health, evidenced by increased sCoV. Although cerebral perfusion was unaffected, elevated sCoV suggest that AAS use may pose a risk for cerebrovascular pathology later in life.
Keywords: Anabolic androgenic steroids; Arterial spin labeling (ASL) perfusion MRI; Cerebral blood flow; Spatial coefficient of variation; Substance misuse.
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Andrew, Silberfeld; Roe, James Michael; Jacob, Ellegood; Jason, Lerch; Lily, Qiu & Yongsoo, Kim
[Vis alle 11 forfattere av denne artikkelen]
(2025).
Left-Right Brain-Wide Asymmetry of Neuroanatomy in the Mouse Brain.
NeuroImage.
ISSN 1053-8119.
307.
doi:
10.1016/j.neuroimage.2025.121017.
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Left-right asymmetry of the human brain is widespread through its anatomy and function. However, limited microscopic understanding of it exists, particularly for anatomical asymmetry where there are few well-established animal models. In humans, most brain regions show subtle, population-average regional asymmetries in thickness or surface area, alongside a macro-scale twisting called the cerebral petalia in which the right hemisphere protrudes past the left. Here, we ask whether neuroanatomical asymmetries can be observed in mice, leveraging 6 mouse neuroimaging cohorts from 5 different research groups (∼3,500 animals). We found an anterior-posterior pattern of volume asymmetry with anterior regions larger on the right and posterior regions larger on the left. This pattern appears driven by similar trends in surface area and positional asymmetries, with the results together indicating a small brain-wide twisting pattern, similar to the human cerebral petalia. Furthermore, the results show no apparent relationship to known functional asymmetries in mice, emphasizing the complexity of the structure-function relationship in brain asymmetry. Our results recapitulate and extend previous patterns of asymmetry from two published studies as well as capture well-established, bilateral male-female differences in the mouse brain as a positive control. By establishing a signature of anatomical brain asymmetry in mice, we aim to provide a foundation for future studies to probe the mechanistic underpinnings of brain asymmetry seen in humans – a feature of the brain with extremely limited understanding.
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Etholm, Lars; Ivanovic, Jugoslav; Larsen, Vilde Stangebye; Sneve, Markus Handal; Lossius, Morten Ingvar & Alfstad, Kristin Åshild
(2024).
Localizing value of disturbances of self-integration, depersonalization, and forced thinking: A systematic review.
Epileptic disorders.
ISSN 1294-9361.
s. 1–15.
doi:
10.1002/epd2.20317.
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We performed a systematic review of the localizational value of disturbances of self-integration, depersonalization and forced thinking in focal epilepsy with the aim to summarize the state-of-the-art anatomo-clinical correlations in the field and help guide interpretation of ictal semiology within the framework of pre-surgical evaluation. The review was performed using a PRISMA- and QUADAS2-based approach. Three separate PubMed and EMBASE searches were undertaken using the keywords self-integration, depersonalization and forced thinking, along with synonyms, in combination with terms to identify epileptogenic zone as defined by surgical outcome, MRI-findings or intracranially recorded EEG. Studies published in peer-reviewed journals with an abstract available, limited to English, French, German, Spanish, or Italian were included for review. Abstracts from scientific meetings were included if precise data on semiology in addition to either localization or surgical outcome was presented. Cases were regarded as eligible if data informing on anatomo-clinical correlations were sufficient to allow determination of an epileptogenic zone and evaluate its level of confidence. For disturbances of self-integration, the search identified 18 publications containing 23 eligible cases, with 10 additional cases identified in the literature. For depersonalization, a single case from a two patient study fulfilled inclusion criteria. For forced thinking, the search identified two publications containing four eligible cases, with six additional cases identified through literature searches. The retrieved cases suggest that disturbances of self-integration often reflect an epileptogenic zone centered around the temporoparietal region, where neighboring areas in the parietal lobe, the posterior insula, and likely depending on the type of disturbance also the adjoining occipital lobe, the anterior and middle cingulum, premotor and supplementary motor in addition to medial temporal structures could be involved. When present, lateralized symptomatology reflects a contralateral focus. Depersonalization, as a localizing ictal phenomenon was quite elusive. Forced thinking either pointed to premotor frontal or temporal epileptogenic zones. Currently, outlined epileptogenic zones of ictal disturbances of self-integration and forced thinking are quite widespread and should be regarded with a low-to-moderate degree of reliability. A focus on such rarer ictal phenomena, in combination with improved imaging techniques and increased use of SEEG, will hopefully lead to an accumulation of cases with better defined epileptogenic zones.
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Warren, José Luis Alatorre & Sneve, Markus Handal
(2026).
Navigation training alters twin cortical similarity at the gray–white matter boundary.
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Walhovd, Kristine B; Kransberg, Jonas Moe; Krogsrud, Stine Kleppe & Fjell, Anders Martin
(2025).
Hippocampal Volume in Childhood Predicts Navigation Performance 6–16 Years Later.
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Poster presentation at Flux Congress
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Padrela, Beatriz; Mahroo, Amnah; Tee, Mervin; Sneve, Markus Handal; Moyaert, Paulien & Geier, Oliver
[Vis alle 43 forfattere av denne artikkelen]
(2024).
Developing blood-brain barrier arterial spin labelling as a non-invasive early biomarker of Alzheimer's disease (DEBBIE-AD): a prospective observational multicohort study protocol.
BMJ Open.
14(3).
doi:
10.1136/bmjopen-2023-081635.
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Introduction Loss of blood-brain barrier (BBB) integrity is hypothesised to be one of the earliest microvascular signs of Alzheimer’s disease (AD). Existing BBB integrity imaging methods involve contrast agents or ionising radiation, and pose limitations in terms of cost and logistics. Arterial spin labelling (ASL) perfusion MRI has been recently adapted to map the BBB permeability non-invasively. The DEveloping BBB-ASL as a non-Invasive Early biomarker (DEBBIE) consortium aims to develop this modified ASL-MRI technique for patient-specific and robust BBB permeability assessments. This article outlines the study design of the DEBBIE cohorts focused on investigating the potential of BBB-ASL as an early biomarker for AD (DEBBIE-AD). Methods and analysis DEBBIE-AD consists of a multicohort study enrolling participants with subjective cognitive decline, mild cognitive impairment and AD, as well as age-matched healthy controls, from 13 cohorts. The precision and accuracy of BBB-ASL will be evaluated in healthy participants. The clinical value of BBB-ASL will be evaluated by comparing results with both established and novel AD biomarkers. The DEBBIE-AD study aims to provide evidence of the ability of BBB-ASL to measure BBB permeability and demonstrate its utility in AD and AD-related pathologies. Ethics and dissemination Ethics approval was obtained for 10 cohorts, and is pending for 3 cohorts. The results of the main trial and each of the secondary endpoints will be submitted for publication in a peer-reviewed journal.
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Garrido, Pablo F.; Bråthen, Anne Cecilie Sjøli; Falch, Emilie Sogn; Kransberg, Jonas; Sørensen, Øystein & Walhovd, Kristine B
(2024).
A novel analysis approach to Mirror Tracing Task performance to detect fine-grained age-related differences.
Alzheimer's & Dementia.
ISSN 1552-5260.
20,
s. e092273–e092273.
doi:
10.1002/alz.092273.
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Publisert 10. jan. 2024 14:22
- Sist endret 1. juni 2026 09:40