Neurodegenerative disease management · 2025
Neuroprotective effects of ivermectin on Alzheimer's model induced by streptozotocin in rats.
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Farajpour Neda, Soraya Hamid
Аннотация
BACKGROUND: Alzheimer's disease is a neurodegenerative condition characterized by memory deficits and cognitive decline. Ivermectin, an antiparasitic agent, has shown neuroprotective effects. The present study was conducted to determine the protective effects of ivermectin in a streptozocin-induced Alzheimer's model in rats.
METHODS: Alzheimer's model was induced by bilateral intracerebroventricular injection of streptozocin (3 mg/kg BW, 2 doses). Ivermectin was administered intraperitoneally at a dose of 2 mg/kg. On day 19, after behavioral memory and learning tests, the samples were collected for histological and enzymatic studies.
RESULTS: Ivermectin reduced the histopathological changes, including pyknotic and dead neurons and the accumulation of Aβ plaques. Ivermectin administration also reduced serum (p < 0.0001) and brain tissue (p < 0.01) acetylcholinesterase activity as well as improved learning (p < 0.05) and spatial memory (p < 0.0001).
CONCLUSIONS: Ivermectin demonstrates protective effects in the STZ-induced Alzheimer's model by reducing pathological changes and Aβ plaques, acetylcholinesterase activity, as well as improving memory and learning.
METHODS: Alzheimer's model was induced by bilateral intracerebroventricular injection of streptozocin (3 mg/kg BW, 2 doses). Ivermectin was administered intraperitoneally at a dose of 2 mg/kg. On day 19, after behavioral memory and learning tests, the samples were collected for histological and enzymatic studies.
RESULTS: Ivermectin reduced the histopathological changes, including pyknotic and dead neurons and the accumulation of Aβ plaques. Ivermectin administration also reduced serum (p < 0.0001) and brain tissue (p < 0.01) acetylcholinesterase activity as well as improved learning (p < 0.05) and spatial memory (p < 0.0001).
CONCLUSIONS: Ivermectin demonstrates protective effects in the STZ-induced Alzheimer's model by reducing pathological changes and Aβ plaques, acetylcholinesterase activity, as well as improving memory and learning.