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High-throughput Fluorometric Measurement of Potential Soil Extracellular Enzyme Activities
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[Not Available].

Mohammad Torabi-Nami1, Mohammad Nasehi2, Mohammad-Reza Zarrindast3

  • 1Institute for Cognitive Science Studies, Tehran, Iran ; Department of Neuroscience, School of Advanced Medical Science and Technologies, Shiraz University of Medical Sciences, Shiraz, Iran.

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Summary
This summary is machine-generated.

Chronic partial sleep restriction causes cognitive decline and hippocampal pathology in rats, potentially via tumor necrosis factor-alpha (TNFα) pathways. Treatment with an anti-TNFα antibody reversed these effects, suggesting inflammation’s role in sleep deprivation-induced neurodegeneration.

Keywords:
BDNFcorticosteronedentate gyruselevated plus-mazeimmunohistochemistryinfliximabrat(s)sleep deprivation

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Area of Science:

  • Neuroscience
  • Sleep Research
  • Neuroinflammation

Background:

  • Sleep deprivation (SD) and chronic partial sleep restriction (CPSR) induce cognitive impairments, possibly due to neuroinflammation and accelerated neurodegeneration.
  • Tumor necrosis factor-alpha (TNFα) is a suspected mediator of sleep deprivation-induced neurodegeneration.

Purpose of the Study:

  • To investigate the effects of total sleep deprivation (TSD) and CPSR on memory, anxiety, and neuroinflammation in rats.
  • To assess the role of TNFα in sleep restriction-induced cognitive and pathological changes.

Main Methods:

  • Male Wistar rats were subjected to TSD or CPSR using a modified disk-over-water apparatus.
  • Behavioral tests (Elevated Plus-Maze), serum analysis (BDNF, corticosterone), and immunohistochemistry (amyloid-beta, hyper-phosphorylated tau) were performed.
  • Rats were treated with infliximab (IFX), a TNFα neutralizing antibody, to assess its therapeutic potential.

Main Results:

  • TSD and CPSR impaired memory, increased corticosterone, and decreased BDNF levels in rats not treated with IFX.
  • CPSR led to hyper-phosphorylated tau deposition and reduced neuronal density in the hippocampus.
  • IFX treatment prevented cognitive deficits, biochemical alterations, and hippocampal pathology induced by sleep restriction.

Conclusions:

  • CPSR, mimicking shift work, induces cognitive and biochemical changes, and hippocampal pathology, potentially mediated by TNFα.
  • Targeting TNFα with infliximab effectively reverses the negative impacts of sleep restriction on the brain.
  • These findings highlight the critical role of neuroinflammation in sleep deprivation-related cognitive decline and neurodegeneration.