Publications by authors named "Elisa Nicoloso Simoes-Pires"

Article Synopsis
  • Alzheimer's disease (AD) is characterized by protein aggregates, inflammation, and issues with blood vessels, including a damaged blood-brain barrier that allows harmful proteins like fibrinogen to enter the brain.
  • Fibrinogen interacts negatively with amyloid-beta (Aβ) peptides, worsening blood flow and clotting issues associated with AD.
  • Lecanemab, an FDA-approved treatment for AD, helps remove Aβ plaques and prevents negative interactions between Aβ and fibrinogen, potentially slowing disease progression.
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Article Synopsis
  • Alzheimer's disease (AD) is characterized by protein-rich brain inclusions, neuroinflammation, and problems with blood vessels, which includes a weakened blood-brain barrier that allows blood proteins like fibrinogen to enter the brain.
  • Fibrinogen interacts negatively with the amyloid-beta (Aβ) peptide, worsening blood clotting issues and blood flow in AD.
  • Lecanemab, an FDA-approved antibody for AD, shows potential to reduce Aβ levels and slow cognitive decline by blocking the harmful interaction between Aβ and fibrinogen, preventing further damage in the brain.
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Cerebral ischemia constitutes the most frequent type of cerebrovascular disease. The reduction of blood supply to the brain initiates the ischemic cascade starting from ionic imbalance to subsequent glutamate excitotoxicity, neuroinflammation and oxidative stress, eventually causing neuronal death. Previously, the authors have demonstrated the in vitro cytoprotective and antioxidant effects of a new arylidene malonate derivative, KM-34, against oxidizing agents like hydrogen peroxide, glutamate or Fe/ascorbate.

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Stroke is frequently associated with severe neurological decline and mortality, and its incidence is expected to increase due to aging population. The only available pharmacological treatment for cerebral ischemia is thrombolysis, with narrow therapeutic windows. Efforts aimed to identify new therapeutics are crucial.

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Cerebral ischemia is the third most common cause of death and a major cause of disability worldwide. Beyond a shortage of essential metabolites, ischemia triggers many interconnected pathophysiological events, including excitotoxicity, oxidative stress, inflammation and apoptosis. Here, we investigated the neuroprotective mechanisms of JM-20, a novel synthetic molecule, focusing on the phosphoinositide-3-kinase (PI3K)/Akt survival pathway and glial cell response as potential targets of JM-20.

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We previously showed that JM-20, a novel 1,5-benzodiazepine fused to a dihydropyridine moiety, possessed an anxiolytic profile similar to diazepam and strong neuroprotective activity in different cell models relevant to cerebral ischemia. Here, we investigated whether JM-20 protects against ischemic neuronal damage in vitro and in vivo. The effects of JM-20 were evaluated on hippocampal slices subjected to oxygen and glucose deprivation (OGD).

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Berberine is an alkaloid derived from herb the Berberis sp. and has long-term use in Oriental medicine. Studies along the years have demonstrated its beneficial effect in various neurodegenerative and neuropsychiatric disorders.

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Objective: Accumulating evidence indicates that curcumin potently protects against beta-amyloid (Abeta) due to its oxygen free radicals scavenging and anti-inflammatory properties. However, cellular mechanisms that may underlie the neuroprotective effect of curcumin in Abeta-induced toxicity are not fully understood yet. The present study was undertaken to investigate the mechanisms involved in neuroprotective effects of curcumin, particularly involving Wnt/beta-catenin and PI3K pathways.

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