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A better understanding of practice-induced functional and structural changes in our brains can help us design more effective learning environments that provide better outcomes. Although there is growing evidence from human neuroimaging that experience-dependent brain plasticity is expressed in measurable brain changes that are correlated with behavioural performance, the relationship between behavioural performance and structural or functional brain changes, and particularly the time course of these changes, is not well characterised. To understand the link between neuroplastic changes and behavioural performance, 15 healthy participants in this study followed a systematic eye movement training programme for 30 min daily at home, 5 days a week and for 6 consecutive weeks. Behavioural performance statistics and eye tracking data were captured throughout the training period to evaluate learning outcomes. Imaging data (DTI and fMRI) were collected at baseline, after two and six weeks of continuous training, and four weeks after training ended. Participants showed significant improvements in behavioural performance (faster task completion time, lower fixation number and fixation duration). Spatially overlapping reductions in microstructural diffusivity measures (MD, AD and RD) and functional activation increases (BOLD signal) were observed in two main areas: extrastriate visual cortex (V3d) and the frontal part of the cerebellum/Fastigial Oculomotor Region (FOR), which are both involved in visual processing. An increase of functional activity was also recorded in the right frontal eye field. Behavioural, structural and functional changes were correlated. Microstructural change is a better predictor for long-term behavioural change than functional activation is, whereas the latter is superior in predicting instantaneous performance. Structural and functional measures at week 2 of the training programme also predict performance at week 6 and 10, which suggests that imaging data at an early stage of training may be useful in optimising practice environments or rehabilitative training programmes.

Glaucoma, the world's leading cause of irreversible blindness, is a condition for which elevated intraocular pressure is currently the only modifiable risk factor. However, the disorder can continue to progress even at reduced intraocular pressure. This indicates additional key factors that contribute to the etiopathogenesis. There has been a growing amount of literature suggesting glaucoma as a neurodegenerative disease of the visual system. However, it remains debatable whether the observed pathophysiological conditions are causes or consequences. This review summarizes recent in vivo imaging studies that helped advance the understanding of early glaucoma involvements and disease progression in the brains of humans and experimental animal models. In particular, we focused on the non-invasive detection of early structural and functional brain changes before substantial clinical visual field loss in glaucoma patients; the eye-brain interactions across disease severity; the metabolic changes occurring in the brain's visual system in glaucoma; and, the widespread brain involvements beyond the visual pathway as well as the potential behavioral relevance. If the mechanisms of glaucomatous brain changes are reliably identified, novel neurotherapeutics that target parameters beyond intraocular pressure lowering can be the promise of the near future, which would lead to reduced prevalence of this irreversible but preventable disease.

The notion of notable anatomical, biochemical, and behavioral distinctions within male and female brains has been a contentious topic of interest within the scientific community over several decades. Advancements in neuroimaging and molecular biological techniques have increasingly elucidated common mechanisms characterizing brain aging while also revealing disparities between sexes in these processes. Variations in cognitive functions; susceptibility to and progression of neurodegenerative conditions, notably Alzheimer’s and Parkinson’s diseases; and notable disparities in life expectancy between sexes, underscore the significance of evaluating aging within the framework of gender differences. This comprehensive review surveys contemporary literature on the restructuring of brain structures and fundamental processes unfolding in the aging brain at cellular and molecular levels, with a focus on gender distinctions. Additionally, the review delves into age-related cognitive alterations, exploring factors influencing the acceleration or deceleration of aging, with particular attention to estrogen’s hormonal support of the central nervous system.

INTRODUCTION We quantified the association of mild (ie, involving one or two body systems) and complex (ie, involving ≥3 systems) multimorbidity with structural brain changes in older adults. METHODS We included 390 dementia‐free participants aged 60+ from the Swedish National Study on Aging and Care in Kungsholmen who underwent brain magnetic resonance imaging at baseline and after 3 and/or 6 years. Using linear mixed models, we estimated the association between multimorbidity and changes in total brain tissue, ventricular, hippocampal, and white matter hyperintensities volumes. RESULTS Compared to non‐multimorbid participants, those with complex multimorbidity showed the steepest reduction in total brain (β*time −0.03, 95% CI −0.05, −0.01) and hippocampal (β*time −0.05, 95% CI −0.08, −0.03) volumes, the greatest ventricular enlargement (β*time 0.03, 95% CI 0.01, 0.05), and the fastest white matter hyperintensities accumulation (β*time 0.04, 95% CI 0.01, 0.07). DISCUSSION Multimorbidity, particularly when involving multiple body systems, is associated with accelerated structural brain changes, involving both neurodegeneration and vascular pathology. Highlights Multimorbidity accelerates structural brain changes in cognitively intact older adults These brain changes encompass both neurodegeneration and cerebrovascular pathology The complexity of multimorbidity is associated with the rate of brain changes’ progression

Background Disruption of the default‐mode network (DMN) in healthy elders has been reported in many studies. Methods In a group of 51 participants (25 young, 26 elder) we examined DMN connectivity in subjects' native space. In the native space method, subject‐specific regional masks (obtained independently for each subject) are used to extract regional fMRI times series. This approach substitutes the spatial normalization and subsequent smoothing used in prevailing methods, affords more accurate spatial localization, and provides the power to examine connectivity separately in the two hemispheres instead of averaging regions across hemispheres. Results The native space method yielded new findings which were not detectable by the prevailing methods. The most reliable and robust disruption in elders' DMN connectivity were found between supramarginal gyrus and superior‐frontal cortex in the right hemisphere only. The mean correlation between these two regions in young participants was about 0.5, and dropped significantly to 0.04 in elders (P = 2.1 × 10−5). In addition, the magnitude of functional connectivity between these regions in the right hemisphere correlated with memory (P = 0.05) and general fluid ability (P = 0.01) in elder participants and with speed of processing in young participants (P = 0.008). These relationships were not observed in the left hemisphere. Conclusion These findings suggest that analysis of DMN connectivity in subjects' native space can improve localization and power and that it is important to examine connectivity separately in each hemisphere. This manuscript is examining the effects of normal aging on the functional connectivity between the default‐mode network's nodes. Extensive atrophy in the brains of older adults makes spatial normalization a very challenging task. By analyzing the fMRI data in a subject's native space, we have been able to circumvent problems related to spatial normalization and we detected important unilateral age‐related brain changes which were not possible using prevailing methods. In addition, the strength of the functional connectivity between the detected nodes was correlated with cognitive performance.

Background Brain age is a biomarker that predicts chronological age using neuroimaging features. Deviations of this predicted age from chronological age is considered a sign of age-related brain changes, or commonly referred to as brain ageing. The aim of this systematic review is to identify and synthesize the evidence for an association between lifestyle, health factors and diseases in adult populations, with brain ageing. Methods This systematic review was undertaken in accordance with the PRISMA guidelines. A systematic search of Embase and Medline was conducted to identify relevant articles using search terms relating to the prediction of age from neuroimaging data or brain ageing. The tables of two recent review papers on brain ageing were also examined to identify additional articles. Studies were limited to adult humans (aged 18 years and above), from clinical or general populations. Exposures and study design of all types were also considered eligible. Results A systematic search identified 52 studies, which examined brain ageing in clinical and community dwelling adults (mean age between 21 to 78 years, ~ 37% were female). Most research came from studies of individuals diagnosed with schizophrenia or Alzheimer’s disease, or healthy populations that were assessed cognitively. From these studies, psychiatric and neurologic diseases were most commonly associated with accelerated brain ageing, though not all studies drew the same conclusions. Evidence for all other exposures is nascent, and relatively inconsistent. Heterogenous methodologies, or methods of outcome ascertainment, were partly accountable. Conclusion This systematic review summarised the current evidence for an association between genetic, lifestyle, health, or diseases and brain ageing. Overall there is good evidence to suggest schizophrenia and Alzheimer’s disease are associated with accelerated brain ageing. Evidence for all other exposures was mixed or limited. This was mostly due to a lack of independent replication, and inconsistency across studies that were primarily cross sectional in nature. Future research efforts should focus on replicating current findings, using prospective datasets. Trial registration A copy of the review protocol can be accessed through PROSPERO, registration number CRD42020142817 .

[This corrects the article DOI: 10.3389/fnagi.2025.1550319.].

This study focuses on the structural brain changes, alterations in Apparent Diffusion Coefficient (ADC) values, and the morphological characteristics of distal intracranial arteries in chronic alcohol consumption. A total of 50 chronic alcoholics and 43 non-alcoholics were recruited from neurology inpatient and outpatient services. Using the Brainnetome Atlas to segment the brain into 246 regions, ADC values were observed to be consistently higher in alcoholics, with statistically significant differences in 134 of these regions. This number is far greater than the number of brain regions where changes in gray matter volume were observed. The alcohol group exhibited lower mean arterial density, mean arterial radius, and mean arterial tortuosity, along with higher mean arterial flexibility, though mean arterial length did not differ significantly between groups. But correlation analysis revealed a negative relationship between alcohol consumption and mean arterial density and mean arterial length. Gray matter volume was positively correlated with mean arterial length, density, and radius. White matter volume also showed a positive correlation with mean arterial length and density. Conversely, cerebrospinal fluid volume was negatively correlated with mean arterial length and density. These results suggest that the diffusion of water molecules in the brains of alcoholics is altered before observable changes in gray matter structure occur. Changes in cerebrovascular morphology are a contributing factor to the structural brain changes observed in chronic alcoholics.

IntroductionSeveral neuroimaging studies on psychosis spectrum have been published in the last decades, most of them based on schizophrenia. In the context of neuroanatomical dysfunctions, clinical and prognosis implications have been reported. Nevertheless, only a few studies have been focused on delusional disorder (DD).ObjectivesTo present the case of a patient diagnosed with DD who suffered from two cerebrovascular events after the onset of the psychiatric disease. Our aim is to elucidate potential implications of those lesions on the course of DD. We also reviewed the literature to assess evidence for specific changes in DD on brain structures and functions.MethodsCase report and non-systematic narrative review in PubMed (2000-2020).ResultsCase report: A 66-year-old female with DD presenting, during the course of the disease, general atrophy and consecutive ischemic lesions on parietal, occipital and cerebellar areas. Clinical stabilization was achieved 12-16 months after risperidone 1.5mg/day treatment. Review: 19 studies were included: Structural brain data (n=15), Functional data (n=13). Most of the structural neuroimaging studies reported white and gray matter abnormalities, particularly in temporal, parietal and frontal lobes, and in limbic structures. Functional neuroimaging studies pointed to temporal and parietal lobes, as well as basal ganglia and limbic related structures.ConclusionsTemporal, parietal, frontal, basal ganglia and limbic-related structures, as well as dysfunctions in other specific brain regions, may be implicated in the core symptoms of DD. These findings might be further investigated as potential neuroimaging markers of prognosis, such as partial or delayed response to antipsychotic treatment, as presented in our case.

Lung diseases induce changes in brain structure and function, leading to a range of cognitive, emotional, and motor deficits. The concept of the lung-brain axis has been proposed through neuroanatomy, endocrine, and immune pathway, while a considerable number of studies also explored the existence of the lung-brain axis from a neuroimaging perspective. This survey summarizes studies exploring the relationship between lung disease and brain structure and function from neuroimaging perspective, particular in magnetic resonance imaging (MRI). We have collated existing lung diseases studies and categorized them into four types: chronic obstructive pulmonary disease (COPD), coronavirus disease 2019 (COVID-19), lung cancer and other lung diseases. The observed structural and functional changes in the brain and cognitive dysfunction induced by lung diseases are discussed. We also present distinct pattern of brain changes in various lung diseases. Neuroimaging changes in COPD are concentrated in the frontal lobes, including gray matter atrophy, white matter damage, and reduced perfusion. Patients with COVID-19 exhibit extensive microhemorrhages and neuroinflammation, brain regions functionally connected to the primary olfactory cortex show greater changes. For lung cancer patients, brain changes are mainly attributed to the neurotoxicity of radiotherapy and chemotherapy, with damage concentrated in subcortical structures, patients with cancer pain demonstrate hyperconnectivity in motor and visual networks. The survey also discusses the pathological mechanisms revealed in neuroimaging studies and clinical significance of current studies. Finally, we analyzed current limitations, mainly in terms of small sample size, non-standardized criteria, reliance on correlation analyses, lack of longitudinal studies, and absence of reliable biomarkers. We suggest future research directions should include leveraging artificial intelligence for biomarker development, conducting longitudinal and multicenter studies, and investigating the systemic effects of lung disease on the brain and neuromodulation strategies.