The crucial role of gadolinium-enhanced MRI in a case of amaurosis fugax - a case report and literature review.

Optic perineuritis is the inflammation of the optic nerve sheath. This affliction can lead to visual field impairment and other signs and symptoms related to the orbital space, such as pain, disc edema, ophthalmoplegia, proptosis. However, not all patients present with such suggestive symptoms, requiring a thorough assessment. We report the case of a young male admitted to our hospital for recurrent episodes of monocular blindness. Amaurosis fugax is a well-known presentation of transient ischemic attacks (TIA) and it was ruled out. Gadolinium-enhanced MRI revealed a typical aspect of optic perineuritis. It was mandatory to consider all possible causes of secondary optic perineuritis as they all represent serious clinical conditions, even if the idiopathic form is more frequent. The clinical and paraclinical evaluation of the patient excluded an underlying disease and primary optic perineuritis was diagnosed. Corticosteroid therapy is usually curative and a course of methylprednisolone was initiated for our patient with good outcome. However, response to treatment is not diagnostic as both primary and secondary optic perineuritis are normally responsive, hence thorough differential diagnosis is necessary.

Risk factors for the outcome after thrombolysis in acute ischemic stroke - the prominent role of kidney dysfunction: A retrospective cohort observational study.

A complex interplay of factors reflecting the general biological, cardiovascular, neurological, renal, and metabolic status of patients influences the outcome of thrombolysis in stroke patients. This is a retrospective cohort observational study aimed to determine the importance of kidney dysfunction among these factors. Data (demographic, lifestyle, physical examination, laboratory, imaging, including metabolic and cardiovascular risk factors and comorbidities, neurological scores, and outcomes) of all stroke patients who underwent thrombolysis have been registered since January 1, 2016, in an online database. A total of 296 patients registered until December 31, 2020, were included in the study. The National Institutes of Health Stroke Scale, modified Rankin scale, Barthel index, percentage of hemorrhagic transformation, and in hospital death were used to evaluate the neurological status and outcomes of the patients. Regression analysis, Mann-Whitney test, Fisher exact test, logistic regression, and multivariate analysis were used for statistical analysis. Kidney dysfunction, as reflected by the estimated glomerular filtration rate, was associated with in hospital death and all but one of the neurological scores. Other risk factors most frequently associated with neurological scores were age, international normalized ratio, and cognitive decline. Multivariate analysis revealed estimated glomerular filtration rate (as determined by chronic kidney disease-EPI equation) as a determinant for all but one of these scores, and as the most important determinant for most of them, except for those reflecting the pre-intervention neurological status of the patient. Kidney dysfunction seems to be the most important determinant of the outcome of thrombolysed stroke patients, a result obtained by no other study.

Behaviour testing in two different knockout mouse strains related to chronic inflammation and oxidative stress.

CD36, a fatty acid translocator and NRF2, a transcription factor, are two important players in inflammation and oxidative stress, including in the central nervous system. Both were associated with neurodegeneration as tilting arms of a balance: while activation of CD36 participates in neuroinflammation, activation of NRF2 seems to protect against oxidative stress and neuroinflammation. This study aimed to establish whether tilting the balance one way or the other, by knocking out either of them (NRF2-/- or CD36-/-), would show that one holds higher weight over the other in the cognitive behaviour of mice. We tested both young and old knockout animals in a long-term testing protocol (over one month), using the 8-arm radial maze,. Young NRF2-/- mice exhibited a sustained anxious-like behaviour, which was not recapitulated in old mice nor CD36 -/- mice of either age. Neither knockout strain exhibited cognitive alterations, although CD36 -/- mice showed some improvement over WT littermates. In conclusion, NRF2-/- seems to affect behaviour of mice early in life, and could be considered a vulnerability factor for neurocognition, while CD36 impact on cognitive protection of the aging brain requires more investigation.

Low-Concentrations of Fatty Acids Induce an Early Increase in IL-8 Levels in Normal Human Astrocytes.

Fatty acids (FAs) have been shown to exhibit a pro-inflammatory response in various cell types, but astrocytes have been mostly overlooked. FAs, both saturated and unsaturated, have previously been shown to induce pro-inflammatory responses in astrocytes at high concentrations of hundreds of µg/mL. SSO (Sulfo-N-succinimidyl Oleate sodium), an inhibitor of FA translocase CD36, has been shown to prevent inflammation in the mouse brain by acting on local microglia and infiltrating monocytes. Our hypothesis was that SSO treatment would also impact astrocyte pro-inflammatory response to FA. In order to verify our assumption, we evaluated the expression of pro- and anti-inflammatory cytokines in normal human astrocyte cell culture pre-treated (or not) with SSO, and then exposed to low concentrations of both saturated (palmitic acid) and unsaturated (oleic acid) FAs. As a positive control for astrocyte inflammation, we used fibrillary amyloid. Neither Aß 1-42 nor FAs induced CD36 protein expression in human astrocytes in cell culture At low concentrations, both types of FAs induced IL-8 protein secretion, and this effect was specifically inhibited by SSO pre-treatment. In conclusion, low concentrations of oleic acid are able to induce an early increase in IL-8 expression in normal human astrocytes, which is specifically downregulated by SSO.

Fatty Acids, CD36, Thrombospondin-1, and CD47 in Glioblastoma: Together and/or Separately?

Glioblastoma (GBM) is one of the most aggressive tumors of the central nervous system, characterized by a wide range of inter- and intratumor heterogeneity. Accumulation of fatty acids (FA) metabolites was associated with a low survival rate in high-grade glioma patients. The diversity of brain lipids, especially polyunsaturated fatty acids (PUFAs), is greater than in all other organs and several classes of proteins, such as FA transport proteins (FATPs), and FA translocases are considered principal candidates for PUFAs transport through BBB and delivery of PUFAs to brain cells. Among these, the CD36 FA translocase promotes long-chain FA uptake as well as oxidated lipoproteins. Moreover, CD36 binds and recognizes thrombospondin-1 (TSP-1), an extracellular matrix protein that was shown to play a multifaceted role in cancer as part of the tumor microenvironment. Effects on tumor cells are mediated by TSP-1 through the interaction with CD36 as well as CD47, a member of the immunoglobulin superfamily. TSP-1/CD47 interactions have an important role in the modulation of glioma cell invasion and angiogenesis in GBM. Separately, FA, the two membrane receptors CD36, CD47, and their joint ligand TSP-1 all play a part in GBM pathogenesis. The last research has put in light their interconnection/interrelationship in order to exert a cumulative effect in the modulation of the GBM molecular network.

CD36 in Alzheimer's Disease: An Overview of Molecular Mechanisms and Therapeutic Targeting.

CD36 is a membrane protein with wide distribution in the human body, is enriched in the monocyte-macrophage system and endothelial cells, and is involved in the cellular uptake of long chain fatty acids (LCFA) and oxidized low-density lipoproteins. It is also a scavenger receptor, binding hydrophobic amyloid fibrils found in the Alzheimer's disease (AD) brain. In neurobiology research, it has been mostly studied in relationship with chronic ischemia and stroke, but it was also related to amyloid clearance by microglial phagocytosis. In AD animal models, amyloid binding to CD36 has been consistently correlated with a pro-inflammatory response. Therapeutic approaches have two main focuses: CD36 blockade with monoclonal antibodies or small molecules, which is beneficial in terms of the inflammatory milieu, and upregulation of CD36 for increased amyloid clearance. The balance of the two approaches, centered on microglia, is poorly understood. Furthermore, CD36 evaluation in AD clinical studies is still at a very early stage and there is a gap in the knowledge regarding the impact of LCFA on AD progression and CD36 expression and genetic phenotype. This review summarizes the role played by CD36 in the pathogenic amyloid cascade and explore the translatability of preclinical data towards clinical research.

Aortic Dissection: An Easily Missed Diagnosis when Pain Doesn't Hold the Stage.

BACKGROUND Type A aortic dissection (AD) is a rare disease, with a high mortality rate. Its most common symptom is thoracic pain, which is nevertheless absent in about 6% of cases. Neurologic complications are extremely rare and include ischemic stroke and ischemic neuropathy (which are the most common as presenting symptoms), spinal cord ischemia, and hypoxic encephalopathy. These rare neurological presentations can often be missed at initial clinical examination. CASE REPORT We report 2 cases of patients presenting with seemingly mild neurological symptoms. However, diagnostic tests revealed acute type A AD, and further steps were taken. CONCLUSIONS Although it is a rare cause of transient stroke or peripheral nerve ischemia, AD should be quickly recognized as a potential cause of new-onset neurological manifestations.

Multiple acute ischemic strokes as the onset manifestation of acute promyelocytic leukemia.

Acute promyelocytic leukemia often manifests with hemorrhagic diathesis, thrombotic events being much rarer. This is the case of a 59-year-old patient with thrombotic cerebro-vascular complications as the onset manifestation of acute promyelocytic leukemia.