Explore the vast range of titles available.

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.

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.

Diffusion tensor imaging (DTI) and diffusion kurtosis imaging (DKI) can quantify indices related to brain structure and their change in pathology. However, only few studies have applied these techniques to spinal cord injury (SCI), and subtle microstructural changes in the brain of SCI individuals are not well understood. Our goal was to investigate structural changes in the brain using DTI (fractional anisotropy, FA; mean diffusivity, MD) and DKI parameters (kurtosis anisotropy, KA; mean kurtosis, MK) in subacute SCI and to study whether these changes were associated with clinical outcomes. Twenty-eight individuals with SCI underwent brain MRI 3 months post-injury, alongside 20 healthy controls. Imaging included a multi-shell diffusion protocol, from which DTI and DKI metrics (FA, MD, KA and MK) were derived. Group comparisons were conducted for each metric across 17 brain regions selected based on their relevance to SCI from previous studies. Multiple comparison corrections were applied per metric to account for the number of examined regions. Effect sizes were calculated using Cohen's . For regions showing significant group differences, Spearman correlations were performed to assess associations between imaging metrics and clinical outcomes, including neurological status (ISNCSCI) and functional independence (SCIM III), with correction for multiple comparisons. MD was significantly higher in the right genu of the corpus callosum in the SCI group (adjusted  = 0.021). In this region, MD negatively correlated with SCIM scores (  = -0.51,  = 0.022), whereas MK showed a positive correlation (  = 0.482,  = 0.038). Structural changes in the corpus callosum may reflect impaired interhemispheric communication, linked to reduced functional independence after SCI. DTI and DKI could serve as complementary tools for identifying brain-based biomarkers, potentially informing recovery trajectories.

Subjective Cognitive Decline (SCD) can progress to mild cognitive impairment (MCI) and Alzheimer's disease (AD) dementia and thus may represent a preclinical stage of the AD continuum. However, evidence about structural changes observed in the brain during SCD remains inconsistent. This cross-sectional study aimed to evaluate, in subjects recruited from the CompAS project, neurocognitive and neurostructural differences between a group of forty-nine control subjects and forty-nine individuals who met the diagnostic criteria for SCD and exhibited high levels of subjective cognitive complaints (SCCs). Structural magnetic resonance imaging was used to compare neuroanatomical differences in brain volume and cortical thickness between both groups. Relative to the control group, the SCD group displayed structural changes involving frontal, parietal, and medial temporal lobe regions of critical importance in AD etiology and functionally related to several cognitive domains, including executive control, attention, memory, and language. Despite the absence of clinical deficits, SCD may constitute a preclinical entity with a similar (although subtle) pattern of neuroanatomical changes to that observed in individuals with amnestic MCI or AD dementia.

Introduction Studies have recognized that the loss of the blood–brain barrier (BBB) integrity is a major structural biomarker where neurodegenerative disease potentially begins. Using a combination of high‐quality neuroimaging techniques, we investigated potential subtle differences in BBB permeability in mid‐age healthy people, comparing carriers of the apolipoprotein E epsilon‐4 (APOEε4) genotype, the biggest risk factor for late onset, non‐familial AD (LOAD) with APOEε3 carriers, the population norm. Methods Forty‐one cognitively healthy mid‐age participants (42–59) were genotyped and pseudo‐randomly selected to participate in the study by a third party. Blind to genotype, all participants had a structural brain scan acquisition including gadolinium‐based dynamic contrast‐enhanced magnetic resonance imaging acquired using a T1‐weighted 3D vibe sequence. A B1 map and T1 map were acquired as part of the multi‐parametric mapping acquisition. Results Non‐significant, but subtle differences in blood–brain barrier permeability were identified between healthy mid‐age APOEε4 and APOEε3 carriers, matched on age, education, and gender. Discussion This study demonstrated a tendency toward BBB permeability in APOEε4 participants emerging from mid‐age, with quantitative differences observable on a number of the measures. While the differences did not reach a statistical significance, the results from this study hint at early changes in ε4 carrier BBB that may help identify at‐risk populations and facilitate the development of early interventions to change the trajectory of decline. This study demonstrated a tendency towards BBB permeability in APOEε4 participants emerging from mid‐age, with quantitative differences observable on a number of the measures. Results from this study may help identify at‐risk populations at an early stage which will be crucial in facilitating the development of early interventions to change the trajectory of decline. To our knowledge, the BBB/APOEε4/healthy mid‐age human studies have not yet been established at the novel age range (45‐59).

Dyslexia is a neurodevelopmental disorder that presents a deficit in accuracy and/or fluency while reading or spelling that is not expected given the level of cognitive functioning. Research indicates brain structural changes mainly in the left hemisphere, comprising arcuate fasciculus (AF) and corona radiata (CR). The purpose of this systematic review is to better understand the possible methods for analyzing Diffusion Tensor Imaging (DTI) data while accounting for the characteristics of dyslexia in the last decade of the literature. Among 124 articles screened from PubMed and Scopus, 49 met inclusion criteria, focusing on dyslexia without neurological or psychiatric comorbidities. Article selection involved paired evaluation, with a third reviewer resolving discrepancies. The selected articles were analyzed using two topics: (1) a demographic and cognitive assessment of the sample and (2) DTI acquisition and analysis. Predominantly, studies centered on English-speaking children with reading difficulties, with preserved non-verbal intelligence, attention, and memory, and deficits in reading tests, rapid automatic naming, and phonological awareness. Structural differences were found mainly in the left AF in all ages and in the bilateral superior longitudinal fasciculus for readers-children and adults. A better understanding of structural brain changes of dyslexia and neuroadaptations can be a guide for future interventions.

One of the central features of brain aging is the accumulation of multiple age-related structural changes, which occur heterogeneously in individuals and can have immediate or potential clinical consequences. Each of these deficits can coexist and interact, producing both independent and additive impacts on brain health. Many of the changes can be visualized using MRI. To collectively assess whole-brain structural changes, the MRI-based Brain Atrophy and Lesion Index (BALI) has been developed. In this study, we validate this whole-brain health assessment approach using several clinical MRI examinations. Data came from three independent studies: the Alzheimer's Disease Neuroimaging Initiative Phase II (n=950; women =47.9%; age =72.7±7.4 years); the National Alzheimer's Coordinating Center (n=722; women =55.1%; age =72.7±9.9 years); and the Tianjin Medical University General Hospital Research database on older adults (n=170; women =60.0%; age =62.9±9.3 years). The 3.0-Tesla MRI scans were evaluated using the BALI rating scheme on the basis of T1-weighted (T1WI), T2-weighted (T2WI), T2-weighted fluid-attenuated inversion recovery (T2-FLAIR), and T2*-weighted gradient-recalled echo (T2*GRE) images. Atrophy and lesion changes were commonly seen in each MRI test. The BALI scores based on different sequences were highly correlated (Spearman >0.69; <0.00001). They were associated with age ( >0.29; <0.00001) and differed by cognitive status ( >26.48, <0.00001). T2-FLAIR revealed a greater level of periventricular ( =29.09) and deep white matter ( =26.65, <0.001) lesions than others, but missed revealing certain dilated perivascular spaces that were seen in T2WI ( <0.001). Microhemorrhages occurred in 15.3% of the sample examined and were detected using only T2*GRE. The T1WI- and T2WI-based BALI evaluations consistently identified the burden of aging and dementia-related decline of structural brain health. Inclusion of additional MRI tests increased lesion differentiation. Further research is to integrate MRI tests for a clinical tool to aid the diagnosis and intervention of brain aging.

Chronic kidney disease (CKD) leads to profound metabolic and hemodynamic changes, which damage other organs, such as heart and brain. The brain abnormalities and cognitive deficit progress with the severity of the CKD and are mostly expressed among hemodialysis patients. They have great socio-economic impact. In this review, we present the current knowledge of involved mechanisms.

Anorexia nervosa (AN) is a severe psychiatric disorder with high mortality and, to a large extent, unknown pathophysiology. Structural brain differences, such as global or focal reductions in grey or white matter volumes, as well as enlargement of the sulci and the ventricles, have repeatedly been observed in individuals with AN. However, many of the documented aberrances normalize with weight recovery, even though some studies show enduring changes. To further explore whether AN is associated with neuronal damage, we analysed the levels of neurofilament light chain (NfL), a marker reflecting ongoing neuronal injury, in plasma samples from females with AN, females recovered from AN (AN-REC) and normal-weight age-matched female controls (CTRLS). We detected significantly increased plasma levels of NfL in AN vs CTRLS (medianAN = 15.6 pg/ml, IQRAN = 12.1–21.3, medianCTRL = 9.3 pg/ml, IQRCTRL = 6.4–12.9, and p < 0.0001), AN vs AN-REC (medianAN-REC = 11.1 pg/ml, IQRAN-REC = 8.6–15.5, and p < 0.0001), and AN-REC vs CTRLS (p = 0.004). The plasma levels of NfL are negatively associated with BMI overall samples (β (±se) = −0.62 ± 0.087 and p = 6.9‧10−12). This indicates that AN is associated with neuronal damage that partially normalizes with weight recovery. Further studies are needed to determine which brain areas are affected, and potential long-term sequelae.

This chapter looks at the neurobiological aspects of how physical activity (PA) and physical exercise (PEx) change the human brain in its structure and functionality on a short‐ and long‐term level. It reviews findings related to brain structure, connectivity, blood perfusion, as well as results on growth factors and metabolic changes that occur instantly as well as over longer time periods. Brain plasticity related to motor practice and learning is also covered. As an additional aspect, the chapter considers different populations such as the elderly, children, or athletes, and how those inform about the changes PA/PEx/motor practice can induce in the structure and functioning of the brain. It summarizes changes in the athlete's brain that are related to the acquisition of perceptual‐cognitive processing expertise in interactive sport games.