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

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.

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