4.5 Article

Propylparaben Reduces the Long-Term Consequences in Hippocampus Induced by Traumatic Brain Injury in Rats: Its Implications as Therapeutic Strategy to Prevent Neurodegenerative Diseases

Journal

JOURNAL OF ALZHEIMERS DISEASE
Volume 82, Issue -, Pages S215-S226

Publisher

IOS PRESS
DOI: 10.3233/JAD-200914

Keywords

Alzheimer's disease; brain trauma; hippocampus; neuroprotection; propylparaben

Categories

Funding

  1. National Council for Sciences and Technology of Mexico (CONACYT Scholarship) [615621 CSC]
  2. Research Coordination of IMSS research coordination [99097560]

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The study found that subchronic administration of PPB can reduce the long-term effects of TBI on the hippocampus in rats, including neuronal protection and reduced excitability. While MRI results showed lower hippocampal volume in the PPB group, other outcomes were better than in the group not treated with PPB.
Background: Severe traumatic brain injury (TBI), an important risk factor for Alzheimer's disease, induces long-term hippocampal damage and hyperexcitability. On the other hand, studies support that propylparaben (PPB) induces hippocampal neuroprotection in neurodegenerative diseases. Objective: Experiments were designed to evaluate the effects of subchronic treatment with PPB on TBI-induced changes in the hippocampus of rats. Methods: Severe TBI was induced using the lateral fluid percussion model. Subsequently, rats received subchronic administration with PPB (178 mg/kg, TBI+PPB) or vehicle (TBI+PEG) daily for 5 days. The following changes were examined during the experimental procedure: sensorimotor dysfunction, changes in hippocampal excitability, as well as neuronal damage and volume. Results: TBI+PEG group showed sensorimotor dysfunction (p <0.001), hyperexcitability (64.2%, p <0.001), and low neuronal preservation ipsi- and contralateral to the trauma. Magnetic resonance imaging (MRI) analysis revealed lower volume (17.2%; p <0.01) and great damage to the ipsilateral hippocampus. TBI+PPB group showed sensorimotor dysfunction that was partially reversed 30 days after trauma. This group showed hippocampal excitability and neuronal preservation similar to the control group. However, MRI analysis revealed lower hippocampal volume (p < 0.05) when compared with the control group. Conclusion: The present study confirms that post-TBI subchronic administration with PPB reduces the long-term consequences of trauma in the hippocampus. Implications of PPB as a neuroprotective strategy to prevent the development of Alzheimer's disease as consequence of TBI are discussed.

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