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Schiff Base Complex rescues mice against scopolamine-induced cognitive dysfunction.

Saima Noreen1, Ruqia Nazir1, Muslim Khan1

  • 1Department of Chemistry, Kohat University of Science and Technology, Kohat, Pakistan.

Drug and Chemical Toxicology
|January 2, 2026
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Summary
This summary is machine-generated.

This study shows a novel Schiff base complex, Copper(II) 4-(benzylideneamino)-3-hydroxynaphthalene-1-sulfonic acid, effectively protected against cognitive deficits and neuroinflammation in mice. The compound demonstrated significant neuroprotective effects, offering potential for Alzheimer's disease treatment.

Keywords:
GSHSchiff Base Complexcatalasep-Akt/Nrf-2scopolaminesynapses

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Alzheimer's disease (AD) is a prevalent neurodegenerative disorder marked by cognitive decline.
  • Oxidative stress and neuroinflammation are key contributors to AD pathogenesis.
  • Current treatments for AD are limited, necessitating the development of novel therapeutic agents.

Purpose of the Study:

  • To synthesize and evaluate the neuroprotective potential of a novel Schiff base complex, Copper(II) 4-(benzylideneamino)-3-hydroxynaphthalene-1-sulfonic acid [Cu(BAHN)2].
  • To investigate the complex's efficacy against scopolamine-induced (SCOP) cognitive and synaptic deficits in a mouse model.
  • To elucidate the underlying biochemical and molecular mechanisms of the complex's neuroprotective action.

Main Methods:

  • Adult male BALB/c mice were divided into control, SCOP-induced deficit, and treatment groups.
  • Cognitive function was assessed using behavioral tests: Morris Water Maze (MWM) and Y-maze.
  • Biochemical analyses included antioxidant enzyme activity assays, western blotting for synaptic proteins, and assessment of inflammatory markers.

Main Results:

  • The Schiff base complex significantly restored antioxidant enzyme activities (CAT, POD, SOD, GSH) and reduced lipid peroxidation (LPO) in SCOP-treated mice.
  • The complex ameliorated SCOP-induced decreases in pre- and post-synaptic proteins, correlating with improved cognitive performance.
  • Mechanistically, the compound activated the Akt/Nrf2 pathway while downregulating NF-kB and IL-1β, indicating reduced neuroinflammation.

Conclusions:

  • The synthesized Schiff base complex exhibits significant neuroprotective effects against SCOP-induced cognitive and synaptic deficits.
  • The complex mitigates oxidative stress and neuroinflammation, likely through the regulation of the p-Akt/Nrf2 signaling pathway.
  • These findings suggest the Schiff base complex holds therapeutic potential for dementia and related neurodegenerative disorders, warranting further investigation.