Acer truncatum Bunge seed oil ameliorates cuprizone-induced cognitive decline and brain white matter impairment by improving sphingomyelin metabolism and neuroinflammation via activation of the TREM2 signaling pathway.

Human T-cell leukemia virus type 1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) patients may have brain white matter (WM) lesions, but the association of these lesions with disease activity is poorly understood. We retrospectively evaluated the brain WM lesions of 22 HAM/TSP patients (male 4: female 18) including 5 rapid progressors, 16 slow progressors, and 1 very slow progressor. The severity of WM brain lesions on axial Fluid Attenuated Inversion Recovery images was evaluated utilizing the Fazekas scale, cerebrospinal fluid biomarkers, and proviral load in peripheral blood mononuclear cells. Imaging and biological data were compared at the first visit and a subsequent visit more than 4 years later. Patients with comorbidities including adult T-cell leukemia–lymphoma and cerebrovascular disease were excluded. The results revealed that brain WM lesions in the rapid progressors group were more pronounced than those in slow progressors. In patients with HAM/TSP, severe and persistent inflammation of the spinal cord may cause brain WM lesions.

Marchiafava–Bignami disease (MBD) is an uncommon alcoholism‐related neuropsychiatric disorder, featured with symmetrical demyelination of part or whole corpus callosum (CC). Previous studies reported follow‐up neuroimaging changes with necrosis, cystic degeneration, and atrophy of the CC after the diagnosis of MBD, but it is unclear whether the white matter is damaged before MBD. We report a case of alcoholic MBD whose magnetic resonance imaging revealed structural lesions in the white matter before the typical demyelination of CC during MBD, which support the prior hypothesis that chronic hazardous drinking may initially lead to microstructure abnormalities of the white matter and CC through some possible mechanisms, then microstructure lesions in the CC, and white matter deterioration into extensive demyelination, that is MBD. In future clinical practice, when patients with chronic alcoholism seek treatment for neuropsychiatric disorders, they may need to undergo repeated MRI scans to reveal progressive neuroimaging features before and after MBD.

Remyelination of lesions in the central nervous system contributes to neural repair following clinical relapses in multiple sclerosis. Remyelination is initiated by recruitment and differentiation of oligodendrocyte progenitor cells (OPCs) into myelinating oligodendrocytes. Simvastatin, a blood-brain barrier-permeable statin in multiple sclerosis clinical trials, has been shown to impact the in vitro processes that have been implicated in remyelination. Animals were fed a cuprizone-supplemented diet for 6 weeks to induce localized demyelination in the corpus callosum; subsequent return to normal diet for 3 weeks stimulated remyelination. Simvastatin was injected intraperitoneally during the period of coincident demyelination and OPC maturation (weeks 4 to 6), throughout the entire period of OPC responses (weeks 4 to 9), or during the remyelination-only phase (weeks 7 to 9). Simvastatin treatment (weeks 4 to 6) caused a decrease in myelin load and both Olig2(strong) and Nkx2.2(strong) OPC numbers. Simvastatin treatment (weeks 4 to 9 and 7 to 9) caused a decrease in myelin load, which was correlated with a reduction in Nkx2.2(strong) OPCs and an increase in Olig2(strong) cells, suggesting that OPCs were maintained in an immature state (Olig2(strong)/Nkx2.2(weak)). NogoA+ oligodendrocyte numbers were decreased during all simvastatin treatment regimens. Our findings suggest that simvastatin inhibits central nervous system remyelination by blocking progenitor differentiation, indicating the need to monitor effects of systemic immunotherapies that can access the central nervous system on brain tissue-repair processes.

To investigate the effects of variability in self-measured systolic blood pressure at home on the progression of cognitive impairment and white matter lesions in the oldest old. Between April 2009 and October 2009, 248 oldest old aged 80 years or older were eligibly enrolled from geriatric practices and community-dwelling areas of Shandong, China. Self-measured blood pressure at home (HBP) was measured for 7 consecutive days at the baseline, and the Mini-Mental State Examination (MMSE) score and brain white matter hyperintensities (WMH) were assessed at the baseline and during the final follow-up visit. Variability in systolic HBP was evaluated using coefficient of variation (CV) in serial daily systolic HBP measurements of the last 6 consecutive days. After an average of 2.3 years of follow-up visits, 232 oldest old were included in and 16 were excluded from the analysis. The MMSE score declined -4.76 (interquartile ranges: -10.71, -0.83) %, the periventricular WMH, deep WMH, total WMH and WMH fraction increased 16.46 (s.d.: 6.72)%, 10.05 (s.d.: 6.40)%, 14.69 (s.d.: 6.07)% and 15.95 (s.d.: 6.32)%, respectively, in the total oldest old. A declined percentage of the MMSE score and increased percentages of the periventricular WMH, deep WMH, total WMH and WMH fraction in the high group divided by tertile of the CV of the systolic HBP at baseline were greater than those in the low group (P<0.05). The significant differences were retained after adjusting for covariates, including the MMSE score, periventricular WMH, deep WMH and WMH fraction at the baseline (P<0.05). Excessive variability in self-measured systolic HBP exacerbates the progression of cognitive impairment and brain white matter lesions in the oldest old.

Background and ObjectivesThere is currently no consensus about the extent of gray matter (GM) atrophy that can be attributed to secondary changes after white matter (WM) lesions or the temporal and spatial relationships between the 2 phenomena. Elucidating this interplay will broaden the understanding of the combined inflammatory and neurodegenerative pathophysiology of multiple sclerosis (MS), and separating atrophic changes due to primary and secondary neurodegenerative mechanisms will then be pivotal to properly evaluate treatment effects, especially if these treatments target the different processes individually. To untangle these complex pathologic mechanisms, this systematic review provides an essential first step: an objective and comprehensive overview of the existing in vivo knowledge of the relationship between brain WM lesions and GM atrophy in patients diagnosed with MS. The overall aim was to clarify the extent to which WM lesions are associated with both global and regional GM atrophy and how this may differ in the different disease subtypes.MethodsWe searched MEDLINE (through PubMed) and Embase for reports containing direct associations between brain GM and WM lesion measures obtained by conventional MRI sequences in patients with clinically isolated syndrome and MS. No restriction was applied for publication date. The quality and risk of bias in included studies were evaluated with the Quality Assessment Tool for observational cohort and cross-sectional studies (NIH, Bethesda, MA). Qualitative and descriptive analyses were performed.ResultsA total of 90 articles were included. WM lesion volumes were related mostly to global, cortical and deep GM volumes, and those significant associations were almost without exception negative, indicating that higher WM lesion volumes were associated with lower GM volumes or lower cortical thicknesses. The most consistent relationship between WM lesions and GM atrophy was seen in early (relapsing) disease and less so in progressive MS.DiscussionThe findings suggest that GM neurodegeneration is mostly secondary to damage in the WM during early disease stages while becoming more detached and dominated by other, possibly primary neurodegenerative disease mechanisms in progressive MS.

Experimentally induced intrauterine infection causes fetal brain white matter lesions in rabbits

Molecular forms of acetylcholinesterase present in the white and grey matter of pig brain

Quantifying the effects of normal ageing on white matter structure using unsupervised tract shape modelling

Silent brain infarcts and white matter lesions are associated with an increased risk of subsequent stroke in minor stroke patients. In healthy elderly people, silent brain infarcts and white matter lesions are common, but little is known about their relevance. We examined the risk of stroke associated with these lesions in the general population. The Rotterdam Scan Study is a population-based prospective cohort study among 1077 elderly people. The presence of silent brain infarcts and white matter lesions was scored on cerebral MRI scans obtained from 1995 to 1996. Participants were followed for stroke for on average 4.2 years. We estimated the risk of stroke in relation to presence of brain lesions with Cox proportional hazards regression analysis. Fifty-seven participants (6%) experienced a stroke during follow-up. Participants with silent brain infarcts had a 5 times higher stroke incidence than those without. The presence of silent brain infarcts increased the risk of stroke >3-fold, independently of other stroke risk factors (adjusted hazard ratio 3.9, 95% CI 2.3 to 6.8). People in the upper tertile of the white matter lesion distribution had an increased stroke risk compared with those in the lowest tertile (adjusted hazard ratio for periventricular lesions 4.7, 95% CI 2.0 to 11.2 and for subcortical lesions 3.6, 95% CI 1.4 to 9.2). Silent brain infarcts and severe white matter lesions increased the stroke risk independently of each other. Elderly people with silent brain infarcts and white matter lesions are at a strongly increased risk of stroke, which could not be explained by the major stroke risk factors.

Excessive Lowering of Blood Pressure Is Not Beneficial for Progression of Brain White Matter Hyperintensive and Cognitive Impairment in Elderly Hypertensive Patients: 4-Year Follow-Up Study

Micro-structural white matter abnormalities and cognitive impairment in asymptomatic carotid plaque patients: A DTI study using TBSS analysis

Accurate quantification of brain tissues is a very challenging problem in neuroimaging, such as quantification of gray matter (GM), white matter (WM) and cerebrospinal fluid (CSF), and white matter lesions (WMLs). However, on many cases brain tissues and white matter lesions cannot be segmented and separated simultaneously by current techniques. Recently, a TRIO algorithm (TRIOA) is proposed to integrate three algorithms, Independent Component Analysis (ICA), Support Vector Machine (SVM) and Fisher's Linear Discriminant Analysis (FLDA) (ICA+SVM+IFLDA) which can effectively classify GM, WM and CSF by considering MR images as multispectral images in the native coordinate space. This paper further extends TRIOA in conjunction with Band Expansion Process (BEP), called Extended TRIOA (ETRIOA), to classify brain tissues as well as WMLs simultaneously. The accuracy assessment of the ETRIOA was evaluated by using the similarity index. The conducted experimental results demonstrate the clinical applicability of ETRIOA in simultaneous classification of GM, WM, CSF and WMLs.

Osteopontin (OPN) is a proinflammatory marker produced by systemic immune and central nervous system (CNS) resident cells. We examined, if the level of OPN in the cerebrospinal fluid (CSF) and blood is associated with late-time regional brain volumes and white matter (WM) lesion load in MS. Concentrations of OPN in blood and CSF were related to MRI findings 10.1 ± 2.0 years later in 46 patients with MS. OPN concentration was measured by ELISA, while regional brain volumes and lesion load was assessed by magnetic resonance imaging (MRI) using 3D MPRAGE sequence and automated MR volumetry. OPN measured in the CSF was associated with several regional brain volumes and WM lesion load measured 10.1 ± 2.0 years later. CSF OPN concentration correlated with long-term enlargement of lateral- and inferior lateral ventricles and the elevation of gross CSF volume, in conjunction with the reduction of several cortical/subcortical gray matter and WM volumes. Serum OPN showed no long-term association with regional brain volumes. OPN measured from the CSF but not from the serum was associated with lower regional brain volumes measured a decade later, indicating the primary role of inflammation within the CNS in developing long-term brain related alterations.

A COMPARATIVE STUDY OF ACETYLCHOLINESTERASE PRESENT IN THE WHITE AND GREY MATTER OF PIG BRAIN

This work investigated the feasibility and utility of using T2-weighted or dual spin-echo data to provide volume and T2 relaxation time for regional and global gray and white matter using standardized brain templates and anatomically labeled atlases. A total of 130 healthy males and females (age range 15-59 years) were included. Dual echo magnetic resonance imaging data were acquired and analyzed using standardized International Consortium for Human Brain Mapping atlas-based tissue segmentation procedures implemented in the statistical parametric mapping toolbox to obtain the age trajectories of volume and corresponding T2 relaxation time in whole brain white and gray matter, in the caudate nucleus and in the anterior limb of internal capsule. Whole brain gray matter and caudate nucleus volumes linearly decreased with age while whole brain white matter and anterior limb internal capsule volume increased slowly with age bilaterally in males and females. The relation between T2 relaxation time and age of whole brain gray and white matter, and caudate nucleus and anterior limb internal capsule followed a quadratic U-curve. The T2 relaxation times of the human brain followed a U curve both globally and regionally in both white and gray matter.