Publications by authors named "P FORT"

HSPB4 and HSPB5 (α-crystallins) have shown increasing promise as neuroprotective agents, demonstrating several anti-apoptotic and protective roles in disorders such as multiple sclerosis and diabetic retinopathy. HSPs are highly regulated by post-translational modification, including deamidation, glycosylation, and phosphorylation. Among them, T148 phosphorylation has been shown to regulate the structural and functional characteristics of HSPB4 and underlie, in part, its neuroprotective capacity.

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Diabetes can lead to cell type-specific responses in the retina, including vascular lesions, glial dysfunction, and neurodegeneration, all of which contribute to retinopathy. However, the molecular mechanisms underlying these cell type-specific responses, and the cell types that are sensitive to diabetes have not been fully elucidated. Using single-cell transcriptomics, we profiled the transcriptional changes induced by diabetes in different retinal cell types in rat models as the disease progressed.

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Article Synopsis
  • A major challenge in treating neurodegenerative diseases is the lack of accurate models that simulate human disease processes, particularly concerning neuromelanin accumulation with aging.
  • Researchers developed a transgenic mouse model, tgNM, that mimics the distribution of neuromelanin in human brains, specifically in catecholamine-producing neurons.
  • This model exhibits age-related neuronal dysfunction and degeneration, presenting symptoms similar to early stages of neurodegenerative diseases, thus offering new opportunities for research in brain aging and neurodegeneration.
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Article Synopsis
  • This study looked at how a protein called α-crystallin helps protect special cells in the eye (called photoreceptors) when the retina gets separated from its layers.
  • Researchers tested this using rat and mouse eyes and found out that α-crystallin levels increase quickly when the retina gets detached.
  • They discovered that αA-crystallin not only helps keep photoreceptors alive but also works with another protein called FAIM2 to do this job better, especially when αA-crystallin is changed in a certain way (phosphorylation).
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Alteration of motor control during rapid eye movements (REM) sleep has been extensively described in sleep disorders, in particular in isolated REM sleep behavior disorder (iRBD) and narcolepsy type 1 (NT1). NT1 is caused by the loss of orexin/hypocretin (ORX) neurons. Unlike in iRBD, the RBD comorbid symptoms of NT1 are not associated with alpha-synucleinopathies.

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