The acute effects of two industrial substances were studied in mice, rats, rabbits and guinea pigs: - lethal concentration 50 (L.D. 50) in mice and rats after intraperitoneal and oral administration; - investigation of cell growth inhibition (Hela cells), I.D.50 = inhibitory dose 50%; - neuropharmacological effects Histopathological investigations and biochemical analysis pointed out hepatic and renal damages; besides hematological disturbances were found. Both products had mild irritant effects on rabbits skin and eyes. They produced skin sensitization in guinea pigs.
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PLoS One
January 2025
Medical Faculty, Department of Neurology, Otto von Guericke University, Magdeburg, Germany.
For the last 38 years, all neuroprotective agents for patients with ischemic stroke have failed in clinical trials. The innate immune system, particularly microglia, is a much-discussed target for neuroprotective agents. Promising results for neuroprotection by inhibition of integrins with drugs such as natalizumab in animal stroke models have not been translated into clinical practice.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
HOSPITAL UNIVERSITARIO FUNDACION ALCORCON, MADRID, Spain.
Background: Lamin A is barely expressed in human brain neurons or in murine models such as mice and rats. However, in Alheimer´s disease (AD) brains, neurons in the hippocampus and entorhinal cortex abnormally express lamina A from the initial stages of the disease, being a biomarker together with phosphorylated Tau of the nuclear pathology of AD. Constipation and mesenteric neuronal loss are related to aging and neurodegenerative diseases such as AD.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Neurology, University of Colorado Alzheimer's and Cognition Center, and the Linda Crnic Institute for Down Syndrome, University of Colorado, Anschutz Medical Campus, Aurora, CO, USA.
Background: Increasing age is the greatest risk factor for age-associated cognitive decline (AACD) and, especially in females, for developing Alzheimer's disease (AD). Mechanisms underlying this connection are unknown, but neuronal loss and brain atrophy accompany aging and AD and likely contribute to cognitive deficits. There are currently no means to measure neuronal cell death during life and no means to prevent it.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Kentucky College of Medicine, Lexington, KY, USA.
Background: We have recently published that overexpressing a constitutively active form of the insulin receptor beta subunit (IR-β) in hippocampal neurons ameliorates spatial memory performance in the F344 rat model of aging (Frazier et al., 2020). Because astrocytes express IRs and are central to cellular energy and information transfer in the brain, here we focus on the knockdown of IR in astrocytes of the primary somatosensory cortex (S1) in the 5xFAD animal model.
View Article and Find Full Text PDFBackground: Synaptic degeneration is characteristic of neurodegenerative diseases. Amyloid-beta (Aβ) plaques and neurofibrillary tangles of hyperphosphorylated tau are known to induce the synapse pathologies directly or indirectly in Alzheimer's disease (AD). EphA4 is a member of the ephrin receptor subfamily which is predominantly expressed in the brain.
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