Publications by authors named "A Muona"

Article Synopsis
  • Prostate cancer is a serious problem for men, being a leading cause of cancer deaths worldwide.
  • Many treatments, like enzalutamide, often stop working over time, so new options are needed.
  • A new drug called ADA-308 has shown promise by effectively blocking cancer growth and working even when other treatments fail.
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Lipid peroxidation-initiated ferroptosis is an iron-dependent mechanism of programmed cell death taking place in neurological diseases. Here we show that a condensed benzo[b]thiazine derivative small molecule with an arylthiazine backbone (ADA-409-052) inhibits tert-Butyl hydroperoxide (TBHP)-induced lipid peroxidation (LP) and protects against ferroptotic cell death triggered by glutathione (GSH) depletion or glutathione peroxidase 4 (GPx4) inhibition in neuronal cell lines. In addition, ADA-409-052 suppresses pro-inflammatory activation of BV2 microglia and protects N2a neuronal cells from cell death induced by pro-inflammatory RAW 264.

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Cerebral ischemia is a risk factor for Alzheimer's disease (AD). Moreover, recent evidence indicates that it is a two-way street as the incidence rate of stroke is significantly higher in AD patients than those without the disease. Here we investigated the interaction of ischemic brain insults and AD in 9-month-old ApdE9 mice, which show full-blown accumulation of Aβ deposits and microgliosis in the brain.

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Accumulation of amyloid β (Aβ) is a major hallmark in Alzheimer's disease (AD). Bone marrow derived monocytic cells (BMM) have been shown to reduce Aβ burden in mouse models of AD, alleviating the AD pathology. BMM have been shown to be more efficient phagocytes in AD than the endogenous brain microglia.

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Article Synopsis
  • The Schwann cell basement membrane (BM) is crucial for the proper differentiation of Schwann cells, but the specific function of certain collagens, particularly collagen XV, in nerve development is not well understood.
  • The absence of collagen XV in mice results in improperly organized axons in C-fibers and compromised myelination, especially when combined with the lack of laminin α4, which leads to more severe nerve injury and abnormal nerve structure even after a year.
  • Observations show that the absence of these components affects sensory nerve function, resulting in slower conduction speeds and changes in myelin structure, highlighting the importance of collagen XV and laminin α4 in the maturation of peripheral nerves and C-fiber formation.
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