Publications by authors named "Annabel Maes"

Article Synopsis
  • The study reviews multiple CRISPR-Cas screenings that identify host factors influencing influenza A virus, but a comprehensive overview was lacking, prompting a systematic review and meta-analysis.
  • Two ranked gene lists were created based on 15 proviral and 4 antiviral screens, revealing significant pathways and raising questions about the roles of specific genes, like endosomal ion channels and kinases.
  • The findings highlight that host-virus interactions involve lesser-known pathways that require more research, providing insight for future host-directed antiviral drug development against influenza.
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Background: CCL-11 (eotaxin) is a chemokine with an important role in allergic conditions. Recent evidence indicates that CCL-11 plays a role in brain disorders as well. This paper reviews the associations between CCL-11 and aging, neurodegenerative, neuroinflammatory and neuropsychiatric disorders.

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Background: Primary deficit schizophrenia (DS) is characterized by enduring negative symptoms and represents a qualitatively different disease entity with respect to non-deficit schizophrenia (NDS). No studies investigated the association between the enzyme paraoxonase 1 (PON1) and DS and its phenomenology.

Methods: In this case-control study, Thai women and men, aged 18 to 65 years, were divided in DS (n = 40) and NDS (n = 40) and were compared to controls (n = 40).

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Accumulating evidence suggests that TNF-α-mediated immune-neurotoxicity contributes to cognitive impairments and the overall severity of schizophrenia (OSOS). There are no data whether peripheral IL-6 and IL-4 may affect the phenome of schizophrenia above and beyond the effects of TNF-α and whether those cytokines are regulated by lowered natural IgM to malondialdehyde (MDA) and paraoxonase 1 enzyme activity. We assessed the aforementioned biomarkers in a cross-sectional study that enrolled schizophrenia patients with (n = 40) and without (n = 40) deficit schizophrenia and 40 healthy controls.

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