The use of the diffusion tensor imaging (DTI) is rapidly growing in the neuroimaging field. Nevertheless, rigorously performed quantitative validation of DTI pathologic metrics remains very limited owing to the difficulty in co-registering quantitative histology findings with magnetic resonance imaging. The aim of this review is to summarize the existing state-of-the-art knowledge with respect to axial (λ_║) and radial (λ_┴) diffusivity as DTI markers of axonal and myelin damage, respectively. First, we provide technical background for DTI and briefly discuss the specific organization of white matter in bundles of axonal fibers running in parallel; this is the natural target for imaging based on diffusion anisotropy. Second, we discuss the four seminal studies that paved the way for considering axial (λ_║) and radial (λ_┴) diffusivity as potential in vivo surrogate markers of axonal and myelin damage, respectively. Then, we present difficulties in interpreting axial (λ_║) and radial (λ_┴) diffusivity in clinical conditions associated with inflammation, edema, and white matter fiber crossing. Finally, future directions are highlighted. In summary, DTI can reveal strategic information with respect to white matter tracts, disconnection mechanisms, and related symptoms. Axial (λ_║) and radial (λ_┴) diffusivity seem to provide quite consistent information in healthy subjects, and in pathological conditions with limited edema and inflammatory changes. DTI remains one of the most promising non-invasive diagnostic tools in medicine.

In this narrative review, a theoretical framework on the crosstalk between physical exercise and blood-brain barrier (BBB) permeability is presented. We discuss the influence of physical activity on the factors affecting BBB permeability such as systemic inflammation, the brain renin-angiotensin and noradrenergic systems, central autonomic function and the kynurenine pathway. The positive role of exercise in multiple sclerosis and Alzheimer’s disease is described. Finally, the potential role of conditioning as well as the effect of exercise on BBB tight junctions is outlined. There is a body of evidence that regular physical exercise diminishes BBB permeability as it reinforces antioxidative capacity, reduces oxidative stress and has anti-inflammatory effects. It improves endothelial function and might increase the density of brain capillaries. Thus, physical training can be emphasised as a component of prevention programs developed for patients to minimise the risk of the onset of neuroinflammatory diseases as well as an augmentation of existing treatment. Unfortunately, despite a sound theoretical background, it remains unclear as to whether exercise training is effective in modulating BBB permeability in several specific diseases. Further research is needed as the impact of exercise is yet to be fully elucidated.

Context The review summarizes key studies assessing epidemiology, mechanisms, and consequences of cognitive dysfunction (CD) in type 1 diabetes (DM1). Evidence Synthesis In a number of studies, the severity of CD in DM1 was affected by the age of onset and diabetes duration, the presence of proliferative retinopathy and autonomic neuropathy. Diabetes-related CD has been observed not only in adults but also in children and adolescents. Most neuroimaging studies in DM1 did not show any differences in whole brain volumes, however, they did reveal selective deficits in grey matter volume or density within the frontal, posterior and temporal cortex, subcortical grey matter. Studies of middle-aged adults with long-standing DM1 using diffusion tensor imaging have demonstrated partial lesions of white matter and decreased fractional anisotropy in posterior brain regions. The mechanisms underlying diabetes-related CD are very complex and include factors related to diabetes per se and to diabetes-related cardiovascular disease and microvascular dysfunction: chronic hyperglycemia, hypoglycemia, macro- and microvascular disease, increased expression of inflammatory cytokines. The above mechanisms may contribute to the development and progression of both vascular dementia and Alzheimer disease. Conclusions Higher rates of CD and its faster progression in DM1 can be explained by both the direct effects of altered glucose metabolism on the brain and diabetes-related cardiovascular disease. Since the presence and progression of CD significantly worsens the quality of life of diabetic patients, further multidisciplinary studies based on the recent progress in both neuroimaging and type 1 diabetes management are warranted to tackle this problem.

Our study aimed at exploring structural and functional differences in the brain during higher cognitive processing between middle-aged hypertensive patients and controls matched for sex, age and years of education. Two groups of 20 patients took part in MRI examinations. This article reports the results of functional MRI during a Stroop color interference task and structural evaluations based on a modified Fazekas scale. No intergroup differences were found in regards to the severity of white matter lesions (Mann–Whitney U test = 150.5, P > 0.1), nor from the task performance in the scanner (t(35) = 0.2, P > 0.1). However, brain activation patterns between patients and controls varied. Hypertensive patients involved significantly more cerebral areas during the processing, regardless of the task difficulty. Differences were found in 26 diverse regions of both primary and associative cortices (with a peak voxel located in the cuneus, Z = 6.94, P < 0.05 family-wise error corrected at voxel level). Our findings provide an insight into the brain mechanisms related to essential hypertension and suggest a functional reorganization (neuroplasticity) early in the course of the disease.

Background: Frontal aslant tract (FAT) is a white matter bundle connecting the pre-supplementary motor area (pre-SMA) and the supplementary motor area (SMA) with the inferior frontal gyrus (IFG). The purpose of the present study was to evaluate the anatomical variability of FAT. Materials and methods: Total number of fibres and the lateralisation index (LI) were calculated. We attempted to find factors contributing to the diversity of FAT regarding IFG terminations to the pars opercularis (IFG-Op) and to the pars triangularis (IFG-Tr). Magnetic resonance imaging of adult patients with diffusion tensor imaging (DTI) with total number of 98 hemispheres composed a cohort. V-shaped operculum was the most common (60.5%). Results: Total number of FAT fibres had widespread and unimodal distribution (6 to 1765; median: 160). Left lateralisation was noted in 64.3% of cases and was positively correlated with total number of FAT fibres and the bundle projecting to IFG-Op (p < 0.01). LI correlated with total number of FAT fibres (r = 0.43, p < 0.01). FAT projected predominantly to IFG-Op (88.9%; 88 of 99). Only in 3 (3.1%) cases more fibres terminated in IFG-Tr than in IFG-Op. Total number of FAT fibres and number of fibres terminating at IFG-Op did not correlate with the ratio of fibre numbers: FAT/IFG-Op, FAT/IFG-Tr and IFG-Op/IFG-Tr (p > 0.05). The greater total number of fibres to IFG-Tr was, the higher were the ratios of IFG-Tr/ /FAT (r = 0.57, p < 0.01) and IFG-Tr/IFG-Op (r = 0.32, p = 0.04). Conclusions: Among the IFG, the major termination of FAT is IFG-Op. Whereas the IFG-Tr projection seems to be related to the expansion of the entire FAT bundle regardless of side, domination and handedness. Nevertheless, FAT features a significant anatomical variability which cannot be explained in terms of DTI findings. Background: Frontal aslant tract (FAT) is a white matter bundle connecting the pre-supplementary motor area (pre-SMA) and the supplementary motor area (SMA) with the inferior frontal gyrus (IFG). The purpose of the present study was to evaluate the anatomical variability of FAT. Materials and methods: Total number of fibres and the lateralisation index (LI) were calculated. We attempted to find factors contributing to the diversity of FAT regarding IFG terminations to the pars opercularis (IFG-Op) and to the pars triangularis (IFG-Tr). Magnetic resonance imaging of adult patients with diffusion tensor imaging (DTI) with total number of 98 hemispheres composed a cohort. V-shaped operculum was the most common (60.5%). Results: Total number of FAT fibres had widespread and unimodal distribution (6 to 1765; median: 160). Left lateralisation was noted in 64.3% of cases and was positively correlated with total number of FAT fibres and the bundle projecting to IFG-Op (p < 0.01). LI correlated with total number of FAT fibres (r = 0.43, p < 0.01). FAT projected predominantly to IFG-Op (88.9%; 88 of 99). Only in 3 (3.1%) cases more fibres terminated in IFG-Tr than in IFG-Op. Total number of FAT fibres and number of fibres terminating at IFG-Op did not correlate with the ratio of fibre numbers: FAT/IFG-Op, FAT/IFG-Tr and IFG-Op/IFG-Tr (p > 0.05). The greater total number of fibres to IFG-Tr was, the higher were the ratios of IFG-Tr/ /FAT (r = 0.57, p < 0.01) and IFG-Tr/IFG-Op (r = 0.32, p = 0.04). Conclusions: Among the IFG, the major termination of FAT is IFG-Op. Whereas the IFG-Tr projection seems to be related to the expansion of the entire FAT bundle regardless of side, domination and handedness. Nevertheless, FAT features a significant anatomical variability which cannot be explained in terms of DTI findings.

Electron-scattering cross sections have been determined for the furan (C${}_4$H${}_4$O) molecule, both experimentally and theoretically. An absolute total cross section (TCS) has been measured over energies from 0.6 to 400 eV using a linear electron-transmission method. The TCS energy function is dominated with a very broad enhancement, between 1.2 and 9 eV; on the low-energy side, some resonant structures are visible. Integral elastic (ECS) and ionization (ICS) cross sections have been also calculated up to 4 keV in the additivity rule approximation and the binary-encounter-Bethe approach, respectively. Their sum, ECS$+$ICS, is in a very good agreement with the measured TCS above 70 eV. DOI: http://dx.doi.org/10.1103/PhysRevA.82.032701 © 2010 The American Physical Society