Publications by authors named "Judith Leyh"

Plant sterols (PSs) cannot be synthesized in mammals and are exclusively diet-derived. PSs cross the blood-brain barrier and may have anti-neuroinflammatory effects. Obesity is linked to lower intestinal uptake and blood levels of PSs, but its effects in terms of neuroinflammation-if any-remain unknown.

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Obesity arising from excessive dietary fat intake is a risk factor for cognitive decline, dementia and neurodegenerative diseases, including Alzheimer's disease. Here, we studied the effect of long-term high-fat diet (HFD) (24 weeks) and return to normal diet (ND) on behavioral features, microglia and neurons in adult male C57BL/6J mice. Consequences of HFD-induced obesity and dietary changes on general health (coat appearance, presence of vibrissae), sensory and motor reflexes, learning and memory were assessed by applying a phenotypic assessment protocol, the Y maze and Morris Water Maze test.

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Microglia are the brain's immunocompetent macrophages with a unique feature that allows surveillance of the surrounding microenvironment and subsequent reactions to tissue damage, infection, or homeostatic perturbations. Thereby, microglia's striking morphological plasticity is one of their prominent characteristics and the categorization of microglial cell function based on morphology is well established. Frequently, automated classification of microglial morphological phenotypes is performed by using quantitative parameters.

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Polyunsaturated fatty acids (PUFAs) and eicosanoids are important mediators of inflammation. The functional role of eicosanoids in metabolic-syndrome-related diseases has been extensively studied. However, their role in neuroinflammation and the development of neurodegenerative diseases is still unclear.

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Article Synopsis
  • Sporadic Alzheimer's disease (AD) has a long preclinical phase where patients don't show symptoms but exhibit underlying pathology, including tau degeneration and Aβ deposits.
  • In a study of 66 nondemented individuals aged 42-93, all showed neurofibrillary degeneration, 35% had Aβ deposits, and only 8% had activated microglia, indicating localized neuroinflammation linked to Aβ plaques.
  • The findings suggest that tau pathology occurs first, followed by Aβ formation and microglial activation, with neuroinflammation potentially serving as a critical turning point towards symptomatic Alzheimer's disease.
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