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<p>Alzheimer’s disease (AD) is a neurodegenerative disorder characterised by neurodegeneration and a decline in cognition and memory. D-galactose (D-gal) and aluminium chloride (AlCl<sub>3</sub>) have been used to induce cognitive deterioration in rat models that mimic the alterations observed in AD. This study assesses the neurotherapeutic effect of ∆<sup>9</sup>THC on cognitive abilities, brain morphology, neurogenesis activity, and neuropathological markers in Wistar rats induced by D-gal + AlCl<sub>3</sub>. For 10 weeks, 60 mg/kg of D-gal (i.p.) and 200&#xa0;mg/kg of AlCl<sub>3</sub> (oral) were administered to male albino Wistar rats daily. The rats were treated by giving increasing concentrations of ∆<sup>9</sup>THC (0.75, 1.5, and 3.0 mg/kg) for 28 days. The rats were assessed for behavioural tests: novel object recognition and modified elevated plus maze. The viable granule cells of the dentate gyrus were determined, whereas immunohistochemistry was conducted to evaluate neurogenesis activity. Amyloid precursor protein and p-tau Thr231 were evaluated through a molecular study. ∆<sup>9</sup>THC treatment accelerates the changes caused by D-gal and AlCl<sub>3</sub>, such as improving cognitive performances, preventing granular cell loss in the dentate gyrus, increasing neurogenesis cell markers (GFAP+, DCX+, calbindin+, NeuN immunoreactive area), and reduced amyloid precursor protein and p-tau Thr231 expressions, which imply that ∆<sup>9</sup>THC has promising therapeutic potential against AD.</p>

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Delta-9-tetrahydrocannabinol delineates D-galactose and aluminium chloride-induced cognitive dysfunction and neurodegeneration in the hippocampus of the Wistar rat model

  • 期刊论文

  • 发表日期：

    2026年6月16日

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  • Fatin Nadzirah Zakaria,
  • Mohamad Taufik Hidayat Baharuldin,
  • Che Norma Mat Taib,
  • Hasiah Ab Hamid,
  • Hafizah Abdul Hamid,
  • Samaila Musa Chiroma,
  • Mohamad Aris Mohd Moklas

摘要

Alzheimer’s disease (AD) is a neurodegenerative disorder characterised by neurodegeneration and a decline in cognition and memory. D-galactose (D-gal) and aluminium chloride (AlCl3) have been used to induce cognitive deterioration in rat models that mimic the alterations observed in AD. This study assesses the neurotherapeutic effect of ∆9THC on cognitive abilities, brain morphology, neurogenesis activity, and neuropathological markers in Wistar rats induced by D-gal + AlCl3. For 10 weeks, 60 mg/kg of D-gal (i.p.) and 200 mg/kg of AlCl3 (oral) were administered to male albino Wistar rats daily. The rats were treated by giving increasing concentrations of ∆9THC (0.75, 1.5, and 3.0 mg/kg) for 28 days. The rats were assessed for behavioural tests: novel object recognition and modified elevated plus maze. The viable granule cells of the dentate gyrus were determined, whereas immunohistochemistry was conducted to evaluate neurogenesis activity. Amyloid precursor protein and p-tau Thr231 were evaluated through a molecular study. ∆9THC treatment accelerates the changes caused by D-gal and AlCl3, such as improving cognitive performances, preventing granular cell loss in the dentate gyrus, increasing neurogenesis cell markers (GFAP+, DCX+, calbindin+, NeuN immunoreactive area), and reduced amyloid precursor protein and p-tau Thr231 expressions, which imply that ∆9THC has promising therapeutic potential against AD.