Publications by authors named "Florent Sauve"

Article Synopsis
  • The arcuate nucleus (ARH) in the hypothalamus is crucial for energy balance, as it detects metabolic hormones in the blood, but only a few neurons in this area can sense these signals due to a barrier involving the median eminence (ME).
  • The study found that the proteoglycan aggrecan, produced by certain ARH neurons, establishes a diffusion gradient that limits the entry of these metabolic signals into the ARH, particularly during fasting when more aggrecan is deposited.
  • Disrupting aggrecan deposits allows more blood-borne molecules to enter the ARH, leading to uncontrolled food intake, highlighting the importance of this diffusion barrier in the brain's metabolism regulation.
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Background: Estrogen secretion by the ovaries regulates the hypothalamic-pituitary-gonadal axis during the reproductive cycle, influencing gonadotropin-releasing hormone (GnRH) and luteinizing hormone (LH) secretion, and also plays a role in regulating metabolism. Here, we establish that hypothalamic tanycytes-specialized glia lining the floor and walls of the third ventricle-integrate estrogenic feedback signals from the gonads and couple reproduction with metabolism by relaying this information to orexigenic neuropeptide Y (NPY) neurons.

Methods: Using mouse models, including mice floxed for Esr1 (encoding estrogen receptor alpha, ERα) and those with Cre-dependent expression of designer receptors exclusively activated by designer drugs (DREADDs), along with viral-mediated, pharmacological and indirect calorimetric approaches, we evaluated the role of tanycytes and tanycytic estrogen signaling in pulsatile LH secretion, cFos expression in NPY neurons, estrous cyclicity, body-weight changes and metabolic parameters in adult females.

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Alzheimer disease has a sex bias, with women twice as likely as men to be affected. Studies have linked elevated follicle-stimulating hormone (FSH) levels to worsened Alzheimer disease pathology and cognitive decline in mice. FSH interacts with APOE4, uncovering new aspects of Alzheimer disease.

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Article Synopsis
  • Recent research links loss of gonadotropin-releasing hormone (GnRH) to cognitive decline, suggesting a similar mechanism may underlie neurological symptoms in post-COVID patients.
  • Investigations revealed persistent low testosterone levels in some men post-COVID could indicate hypothalamic impact, connecting hormonal changes to cognitive issues.
  • Dysfunction of GnRH neurons and certain brain cells due to SARS-CoV-2 could lead to reproductive, metabolic, and mental health problems, potentially increasing risks for neurological disorders across all ages.
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Older age is one of the strongest risk factors for severe COVID-19. In this study, we determined whether age-associated cellular senescence contributes to the severity of experimental COVID-19. Aged golden hamsters accumulate senescent cells in the lungs, and the senolytic drug ABT-263, a BCL-2 inhibitor, depletes these cells at baseline and during SARS-CoV-2 infection.

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Article Synopsis
  • * Results showed a median serum AMH of 43.5 pmol/L and identified significant correlations between AMH levels, sperm concentration, and various reproductive hormones, indicating AMH's role in male fertility.
  • * The research also discovered the expression of AMH type II receptors in sperm and pituitary cells, suggesting new potential roles for AMH in influencing sperm motility and hormone secretion in men.
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Article Synopsis
  • - COVID-19 can harm small blood vessels in the brain, leading to various neurological symptoms and structural changes in patients.
  • - Researchers found that SARS-CoV-2 infection leads to empty basement membrane tubes, known as string vessels, indicating capillary loss, and that the virus infects brain endothelial cells.
  • - The study proposes that targeting RIPK, a key molecule involved in cell death, could be a new treatment strategy to combat the brain damage associated with COVID-19.
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Hypothalamic glucose sensing enables an organism to match energy expenditure and food intake to circulating levels of glucose, the main energy source of the brain. Here, we established that tanycytes of the arcuate nucleus of the hypothalamus, specialized glia that line the wall of the third ventricle, convert brain glucose supplies into lactate that they transmit through monocarboxylate transporters to arcuate proopiomelanocortin neurons, which integrate this signal to drive their activity and to adapt the metabolic response to meet physiological demands. Furthermore, this transmission required the formation of extensive connexin-43 gap junction-mediated metabolic networks by arcuate tanycytes.

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Alzheimer's disease (AD) is a neurodegenerative disorder characterized by synaptic loss that leads to the development of cognitive deficits. Synapses are neuronal structures that play a crucial role in memory formation and are known to consume most of the energy used in the brain. Interestingly, AMP-activated protein kinase (AMPK), the main intracellular energy sensor, is hyper-activated in degenerating neurons in several neurodegenerative diseases, including AD.

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Long-term memory formation depends on the expression of immediate early genes (IEGs). Their expression, which is induced by synaptic activation, is mainly regulated by the 3',5'-cyclic AMP (cAMP)-dependent protein kinase/cAMP response element binding protein (cAMP-dependent protein kinase (PKA)/ cAMP response element binding (CREB)) signaling pathway. Synaptic activation being highly energy demanding, neurons must maintain their energetic homeostasis in order to successfully induce long-term memory formation.

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