Publications by authors named "Ronen Weiss"
Article Synopsis
- Antiphospholipid syndrome (APS) impacts the brain through both abnormal blood clotting and immune responses, related to specific autoantibodies affecting proteins like beta-2-glycoprotein I (β2-GPI) and annexin A2 (ANXA2).
- In a study using mouse models, teriflunomide—a drug for multiple sclerosis—showed potential in reducing anxiety-like behaviors early on and alleviating some neuroinflammation effects in mice with ANXA2-related APS, although later tests indicated depression-like behaviors.
- While teriflunomide did not lower overall serum autoantibody levels in the mice, it did help normalize IgG levels in the brain associated with ANXA2,
Article Synopsis
- Antiphospholipid syndrome (APS) is an autoimmune disorder that increases the risk of thrombosis, recurrent miscarriages, and stroke due to the presence of antiphospholipid antibodies, particularly anti-β glycoprotein I and anti-Annexin A2 (ANXA2) antibodies.
- In a study involving mice, researchers induced the production of anti-ANXA2 antibodies and assessed stroke severity using a cerebral artery occlusion model, comparing outcomes between the immunized mice and controls.
- The findings revealed that anti-ANXA2 antibodies worsened stroke severity, indicating their potential role as an independent risk factor for cerebral thrombosis, leading to recommendations for increased screening for these antibodies in patients with
Article Synopsis
- This study investigates antibody responses in a patient with active tuberculosis (TB) to understand if protective antibodies are produced against Mycobacterium tuberculosis (Mtb) antigens.
- Researchers generated monoclonal antibodies from the patient's memory B cells, identifying that some antibodies target the PstS1 protein, which is a part of Mtb's phosphate transporter system.
- The identified antibodies have shown promise in reducing Mtb levels in lab tests and in animal models, indicating that these anti-PstS1 responses could play a protective role during active TB infection.
Article Synopsis
- Increased plasmin activity is observed in the brains of male mice after ischemic stroke, peaking at 3, 6, and 24 hours post-stroke compared to healthy controls.
- The research established a method to quantify plasmin activity in brain slices and found higher levels in ischemic areas correlated with larger infarct volumes.
- The study suggests that while tPA is commonly used to treat stroke, the rise in plasmin suggests a need for caution and potential targeting of plasmin inhibition as a therapy in acute ischemic stroke.
Article Synopsis
- Antiphospholipid syndrome (APS) is an autoimmune disease that can cause blood clots and cognitive dysfunctions, often without visible brain damage.
- In a study using mice with induced APS, researchers found a significant decrease in cell proliferation in a specific area of the brain (hippocampus), which may relate to cognitive impairments.
- Despite reduced cell growth, the overall structure of white matter remained unchanged, suggesting that while neurogenesis is affected, the integrity of white matter might not be impacted in APS.
Vascular dementia (VD) comes second after Alzheimer's disease (AD) as a cause of impaired cognition. VD is not a specific nosological entity, but rather a syndrome encompassing a number of diseases caused by impaired supply of blood to the brain. Systemic autoimmune disorders such as systemic lupus erythematosus, rheumatoid arthritis, vasculitis and antiphospholipid syndrome (APS) can be associated with dementia.
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- The study investigated how thrombin and activated protein C (aPC) interact with protease-activated receptor 1 (PAR1) in Schwann glial cells, revealing the potential for both protective and harmful signaling during nerve injury.
- Elevated levels of thrombin were observed in injured sciatic nerves, peaking at one day post-injury, significantly higher than in uninjured nerves, indicating a rapid response to nerve damage.
- The endothelial protein C receptor (EPCR) was found to increase significantly in Schwann cells following nerve injury, particularly distal to the damage site, suggesting its role in mediating responses during nerve degeneration and healing.
Article Synopsis
- Vaccine adjuvants, like aluminum, may lead to autoimmune and inflammatory reactions, which the study investigates using the HPV vaccine Gardasil in female mice.
- The study found that mice injected with Gardasil and aluminum adjuvant spent more time floating in the forced swimming test, indicative of depressive behavior rather than locomotor issues.
- Additionally, evidence showed that antibodies produced in response to Gardasil reacted with brain proteins, suggesting potential neuroinflammation and autoimmune responses linked to behavioral changes.
This article has been withdrawn at the request of the Editor-in-Chief due to serious concerns regarding the scientific soundness of the article. Review by the Editor-in-Chief and evaluation by outside experts, confirmed that the methodology is seriously flawed, and the claims that the article makes are unjustified. As an international peer-reviewed journal we believe it is our duty to withdraw the article from further circulation, and to notify the community of this issue.
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- The text discusses the introduction of a nuclear neutron-proton contact, building on previous work by Tan, and evaluates it using experiments related to nuclear photodisintegration.
- It reformulates the quasideuteron model to connect the Levinger constant with this neutron-proton contact, allowing for experimental values to be used for extraction.
- Lastly, it suggests that assuming isospin symmetry could enable the evaluation of neutron-neutron contact by measuring correlations in photonuclear spin between neutron-proton pairs.
Article Synopsis
- - The study investigates how TGF-β1 influences insulin-degrading enzyme (IDE) activity, linking it to cerebrovascular amyloidosis (CA) and cognitive decline, particularly in Alzheimer's disease.
- - Researchers found that TGF-β1 reduces IDE expression and activity in brain endothelial cells, leading to increased cerebrovascular pathology in mice lacking IDE compared to TGF-β1 only mice.
- - Early reductions in synaptophysin protein levels in TGF-β1/IDE(-/-) mice suggest that TGF-β1 may contribute to cognitive impairment before significant age-related changes occur, highlighting potential therapeutic targets for cerebrovascular diseases.
Article Synopsis
- Cerebrovascular amyloidosis, caused by amyloid buildup in blood vessel walls, can result in hemorrhagic strokes and cognitive decline, starting from as early as 7 months in genetically modified mice.
- Researchers found that scavenger receptor A (SRA) on macrophages is crucial for clearing cerebrovascular amyloid, as SRA-deficient mice showed symptoms at just 3 months of age, compared to 7 months in normal mice.
- This study highlights the potential of targeting SRA in future treatments for conditions like cerebral amyloid angiopathy, emphasizing its role in managing amyloid-related vascular issues.
Article Synopsis
- Cerebrovascular amyloidosis involves the buildup of amyloid in blood vessel walls, leading to issues like stroke and cognitive decline, particularly in Alzheimer's disease (AD).
- Research shows that higher levels of TGF-β1 are linked to more amyloid deposition and are elevated near blood vessels in AD cases.
- A study found that a nasally administered proteosome-based adjuvant can activate macrophages, reduce vascular amyloid, prevent brain damage, and enhance cognitive function in mice.
Astrocyte-endothelial cell (EC) interactions play a major role in the function of the neurovascular unit. Dysfunction in these interactions may lead to amyloid accumulation in blood vessels and may cause microhemorrhage and cognitive impairment. Transforming growth factor-β1 (TGF-β1) expression levels positively correlate with the degree of cerebrovascular amyloid in Alzheimer's disease (AD) cases.
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