Publications by authors named "R Guevara-Guzman"

Microglia are highly dynamic cells that have been mainly studied under pathological conditions. The present review discusses the possible implication of microglia as modulators of neuronal electrical responses in physiological conditions and hypothesizes how these cells might modulate hypothalamic circuits in health and during obesity. Microglial cells studied under physiological conditions are highly diverse, depending on the developmental stage and brain region.

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Seizure-mediated oxidative stress is a crucial mechanism in the pathophysiology of epilepsy. This study evaluated the antioxidant effects of daytime-restricted feeding (DRF) and the role of the Nrf2 signaling pathway in a lithium-pilocarpine model seizure model that induces status epilepticus (SE). We performed a lipoperoxidation assay and dihydroethidium fluorescence to measure oxidative stress markers in the hippocampus (malondialdehyde and reactive oxygen species).

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Sucrose consumption impairs behavioral and cognitive functions that correlate with decreased neurogenesis in animal models. When consumed during early adolescence, this disaccharide promotes anxious and depressive behaviors, along with a reduction in the generation of new neurons in the dentate gyrus of the hippocampus. Data concerning sucrose consumption during late adolescence are lacking, and the effect of sucrose intake on the ventral dentate gyrus of the hippocampus (which modulates anxiety and depression) remains elusive.

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Article Synopsis
  • Diabetes mellitus type 2 (T2D) can lead to brain damage, increasing the risk of neurodegenerative diseases and early signs like olfactory dysfunction (OD), which is common in diabetic patients.
  • Research shows that while the inflammatory marker IL-1β decreases over time in T2D, OD persists and is linked to changes in dopaminergic markers, particularly tyrosine hydroxylase and ERK1/2 phosphorylation.
  • Since dopaminergic neurons are vulnerable in conditions like Parkinson's disease, additional studies are needed to explore how these neurons and ERK1/2 signaling contribute to olfactory impairment in T2D.
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