Lansoprazole induces hippocampal cell apoptosis and impairs learning and memory functions via activation of tau phosphorylation and Aβ (1–42) pathway in adult rats

Studies revealed that long-term use of lansoprazole for ulcers, Zollinger–Ellison syndrome, and gastroesophageal reflux disease causes dementia in patients. The novel research was designed to check whether lansoprazole administration in rats may enhance oxidative stress, Aβ accumulation, and neurodegeneration.

In the current study, rats were given lansoprazole at 15 and 30 mg/kg p.o. doses for 28 days. The Morris water maze, elevated plus maze and radial arm maze, were performed to assess rats spatial, working and recognition memory deficits. On day 29th, the rats were sacrificed, and the brain (hippocampus) was used to test for biochemicals, neuroinflammatory markers, neurotransmitters, Aβ (1–42) levels, nuclear factor-kappa B (NF-κB) analysis, and blood–brain barrier (BBB) disruption.

Lansoprazole administrated altered recognition and spatial memory, depletion of antioxidant enzymes, neurotransmitter concentration, and elevated proinflammatory cytokine release in a dose-dependent manner. Lansoprazole also enhanced the accumulation of Aβ (1–42) and tau protein phosphorylation in the hippocampus. The histological and immunohistochemistry analysis showed that lansoprazole caused neuronal death and activated the NF-κB in the hippocampal neuronal cell.

A study finding indicates that lansoprazole produced a neurobiological alteration in rats and degeneration of the endogenous antioxidant defence system in a dose-dependent manner.