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Category: neuroscience – Page 80

Blood–Brain Barrier Permeability Dynamics and Mediation of Triglyceride–Glucose Index on Acute Ischemic Stroke Outcomes

In acute ischemic stroke, insulin resistance worsens outcomes by increasing blood-brain barrier permeability in the ischemic core.

Acute large‐vessel occlusion of head and neck severely affect quality of life. One of the critical pathological events associated with prognosis of acute ischemic stroke (AIS) is the disruption of the blood–brain barrier (BBB), a highly selective barrier maintaining the brain’s microenvironment.1 Ischemia causes BBB dysfunction,2 exacerbated by peripheral immune cell infiltration,3 leading to increased parenchymal injury, hemorrhage,4 and edema.4, 5 Therefore, accurately determining the evolution and severity of BBB permeability are crucial for prognostic evaluation in patients with AIS.

Research on BBB disruption in patients with AIS primarily focuses on pathological mechanisms and imaging evaluations. Numerous studies use animal models and cell culture experiments to elucidate the physiological and molecular bases of BBB disruption.2, 5, 6, 7, 8 Additionally, imaging techniques like magnetic resonance imaging are widely used to assess evolution of BBB permeability1, 9, 10, 11, 12 and demonstrate correlations between BBB damage, cerebral edema, hemorrhagic transformation, and poor prognosis. Despite significant advances, several issues remain unresolved. First, differences between animal models and human disease limit clinical applicability. Second, while magnetic resonance imaging is widely used to provide quantitative data on BBB disruption, they still face the limitations of being time consuming and inconvenient in the clinical environment. However, BBB disruption in patients with AIS based on computed tomography perfusion (CTP) needs further study.

Insulin resistance (IR) is linked to adverse cardiovascular13, 14 and metabolic outcomes.15, 16 Therefore, identifying patients with IR aids early risk stratification and management. The triglyceride–glucose (TyG) index, which combines fasting triglyceride and glucose levels, has been proposed as a marker of IR. Currently, research on the TyG index primarily focuses on type 2 diabetes,17 obesity,18 and cardiovascular diseases.19 Recent studies have found that an elevated TyG index is associated with higher stroke recurrence,19, 20 functional deterioration,21, 22 and death.23 However, whether the underlying mechanisms involved in the association of IR with stroke outcomes have not been fully understood. IR exacerbated vascular inflammation and endothelial dysfunction,24, 25, 26 which were critical contributors to BBB disruption in AIS. Previous studies have shown that metabolic dysregulation, including hypertriglyceridemia27 and hyperglycemia,28 aggravates BBB permeability by triggering oxidative stress and inflammatory pathways.29, 30 Specifically, IR leads to the generation of reactive oxygen species and the activation of NADPH oxidase, which contribute to oxidative stress and endothelial damage.30, 31 Inflammatory cytokines such as tumor necrosis factor‐α, interleukin‐1β, and interleukin‐6 are also elevated in the insulin‐resistant state, activating nuclear factor‐κB and Janus kinase signaling pathways that further compromise endothelial tight junction proteins such as occludin, claudin‐5, and zonula occludens‐1, crucial for BBB integrity.29, 32 These mechanisms are known to increase BBB permeability, facilitating the entry of harmful substances into the brain and contributing to worsened stroke outcomes. These findings indicated that the relationship between IR and stroke outcomes may be mediated by increased BBB permeability. However, the TyG index’s relationship with BBB disruption and outcomes in patients with AIS is not well studied.

Potential biomarker linked to multiple sclerosis progression and brain inflammation

A new University of Toronto-led study has discovered a possible biomarker linked to multiple sclerosis (MS) disease progression that could help identify patients most likely to benefit from new drugs.

The findings were published today in Nature Immunology and validated in both mouse models and humans.

“We think we have uncovered a potential biomarker that signals a patient is experiencing so-called ‘compartmentalized inflammation’ in the central nervous system, a phenomenon which is strongly linked to MS progression,” says Jen Gommerman, a professor and chair of immunology at U of T’s Temerty Faculty of Medicine. “It’s been really hard to know who is progressing and who isn’t.”

Temporary retinal inactivation reverses effects of long-term monocular deprivation in visual cortex by induction of burst mode firing in the thalamus

Deprivation amblyopia can be reversed by the temporary inactivation of one eye after the critical period. Here, Echevarri-Leet et al. show that this is caused by increased burst firing in the neurons that relay information from the retina to the visual cortex. Even inactivation of the amblyopic eye can drive recovery.

Nanoparticle therapy reprograms tumor immune cells to attack cancer from within

Within tumors in the human body, there are immune cells (macrophages) capable of fighting cancer, but they have been unable to perform their roles properly due to suppression by the tumor. A KAIST research team led by Professor Ji-Ho Park of the Department of Bio and Brain Engineering have overcome this limitation by developing a new therapeutic approach that directly converts immune cells inside tumors into anticancer cell therapies.

In their approach, when a drug is injected directly into a tumor, macrophages already present in the body absorb it, produce CAR (a cancer-recognizing device) proteins on their own, and are converted into anticancer immune cells known as “CAR-macrophages.” The paper is published in the journal ACS Nano.

Solid tumors —such as gastric, lung, and liver cancers—grow as dense masses, making it difficult for immune cells to infiltrate tumors or maintain their function. As a result, the effectiveness of existing immune cell therapies has been limited.

Forget Transistors: This New “Intelligent” Material Computes Like a Human Brain

Tiny molecules that can think, remember, and learn may be the missing link between electronics and the brain. For more than half a century, researchers have looked for ways to move past silicon by building electronics from molecules. The idea sounded simple and beautiful, but real devices turned

Neuralink plans ‘high-volume’ brain implant production by 2026, Musk says

Elon Musk’s brain implant company Neuralink will start “high-volume production” of brain-computer interface devices and move to an entirely automated surgical procedure in 2026, Musk said in a post on the social media platform X on Wednesday.

A molecular gatekeeper that controls protein synthesis

Current smoking was linked to a higher risk for all-cause dementia, especially vascular dementia, with the strongest effects seen in those younger than 85 years and women. It was not significantly associated with the risk for Alzheimer’s dementia. Former smoking was associated with an increased risk for vascular dementia only in men, particularly those younger than 85 years.

Current smoking is associated with an elevated risk for all-cause dementia, particularly vascular dementia, with the strongest associations seen in participants younger than 85 years.

Parkinson Disease SNCA Risk Variants Are Associated With Higher Asymmetric Putamen Dopaminergic Dysfunction

This study assessed the endophenotypic potential of striatal dopamine transporter uptake in carriers of Parkinson disease–associated SNCA genetic risk variants.

ObjectivesThe aim of this study was to investigate the endophenotypic potential of striatal dopamine transporter (DAT) uptake in carriers of Parkinson disease (PD)–associated SNCA genetic risk variants. MethodsWe analyzed 381 patients with de novo PD from the Parkinson’s Progression Markers Initiative (PPMI). The genotype of previously identified PD-related SNCA risk variants was extracted and used to compute an individual PD-specific SNCA genetic risk score (GRS). Striatal DAT uptake was quantified using 123 I‐FP‐CIT SPECT and assessed at baseline and 24-month follow-up. Mixed models were applied to explore the relationship between striatal 123 I‐FP‐CIT SPECT specific binding ratios (SBRs) and PD SNCA risk variants.

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