Herein, we studied histopathological and molecular changes in brain lesions of the Eker rat model carrying germline mutation of the tsc2 gene, predisposed to multiple neoplasias.
Episodic relapses of the disease which lead to brain lesions and irreversible neurological dysfunctions could be decreased by the interferon-beta (IFN-β) therapy in most of the MS patients.
Multivariable analyses were adjusted for pretreatment ECOG PS, age, sex, race, smoking status, histology, count of prior treatments, PDL1 expression, serum LDH levels, and the presence of liver, lung, or brain lesions.
Kaplan-Meier survival analysis demonstrated that STAT3 phosphorylation, IL-10 expression and multiple brain lesions were significantly associated with PFS in PCNSL (P = 0.009, P = 0.030 and P = 0.040, respectively).
Thus, our data suggest that dysfunction of supraspinal bladder control due to cerebral lesions may contribute to the pathophysiology of urinary incontinence in MS.
STAT3 phosphorylation and IL-10 expression were associated with the presence of multiple brain lesions (P = 0.004 and P = 0.027, respectively), suggesting that STAT3 activation may enhance the intracranial spread of tumors in PCNSL.
To verify the utility of brain lesion distribution criteria in distinguishing multiple sclerosis (MS) from aquaporin-4 (AQP4)-immunoglobulin G (IgG)-positive/-negative neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein IgG-associated encephalomyelitis (MOG-EM) in the Chinese population.
We aimed to evaluate the utility of the recently described brain lesion distribution criteria to differentiate multiple sclerosis (MS) from aquaporin-4 immunoglobulin G-positive neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein immunoglobulin G-associated encephalomyelitis (MOG-EM) at disease onset in an Asian cohort.
All the patients showed disseminated lesions in the subcortical region to deep white matter, which were different from those found in MS and AQP4-Ab-positive NMOSD and were consistent with the characteristics of brain lesions in MOG-Ab-positive ADS, including other disease types.
<b>Conclusions:</b> Seizures and encephalopathy are not rare in MOG encephalomyelitis, and are commonly associated with cortical and subcortical brain lesions.
Our cases suggest that we need to differentiate anti-MOG antibody-associated encephalitis from probable NBD because both disorders can present with brainstem or cerebral lesions, CSF pleocytosis, and elevated levels of CSF IL-6 and respond to steroid treatment.
In a stochastic mouse model of TSC1brain lesions, complete loss of <i>Tsc1</i> is achieved in homozygous <i>Tsc1-</i>floxed mice in a subpopulation of neural cells in the brain by intracerebroventricular (i.c.v.) injection at birth of an adeno-associated virus (AAV) vector encoding Cre recombinase.
Various neurodegenerative diseases, including Alzheimer's disease (AD), are related to abnormal hyperphosphorylated microtubule-associated protein tau accumulation in brain lesions.
Brain lesions in Alzheimer's disease (AD) include amyloid plaques made of Aβ peptides and neurofibrillary tangles composed of hyperphosphorylated tau protein with synaptic and neuronal loss and neuroinflammation.
<b>Conclusions:</b> IL-6 interfering with synaptic plasticity mechanisms may impair the ability to compensate the clinical manifestation of new brain lesions in RR-MS patients.
Children with ADS MOG+ and macaques with EAE induced with rhMOG, present a similar cytokine signature in the CSF and a comparable aspect of brain lesions indicating analogous pathophysiological processes.
To assess the role of PKR in an AD in vivo model, we crossed 5xFAD transgenic mice with PKR knockout (PKRKO) mice and we explored the contribution of PKR on cognition and brain lesions in the 5xFAD mouse model of AD as well as in neuron-microglia co-cultures exposed to the innate immunity activator lipopolysaccharide (LPS).
In contrast to plasminogen activator inhibitor-1 (PAI-1), PAI-2 plays a limited role for brain lesion formation and does not influence blood-brain barrier integrity.
Multimodal in vivo imaging involved a combination of 3 modalities: (1) magnetic resonance imaging by T2-weighted scans to assess brain lesion size, (2) bioluminescence imaging of Gap43-luc/gfp transgenic mice to visualize the axonal remodeling, and (3) caged-luciferin bioluminescence imaging of DEVD-luciferin allowing for visualization of caspase 3 and 7 activity in Gap43-luc/gfp mice.
We confirmed this finding for SIRT1 protein expression and were able to localize upregulated SIRT1 in nuclei of NG2<sup>+</sup> or PDGFRα<sup>+</sup> OPCs in demyelinated brain lesions.