Levetiracetam: A Promising Treatment for Alzheimer’s Disease

Published on August 25, 2022

Imagine a bustling city with a complicated transportation system. When there’s a network malfunction, traffic grinds to a halt and chaos ensues. In a similar way, the brains of Alzheimer’s disease (AD) patients experience neuronal network dysfunction, leading to cognitive decline. But fear not! Researchers have discovered a potential remedy in the form of levetiracetam (LEV), a drug typically used to treat seizures. In an animal model of AD, low doses of LEV improved memory and rescued neurons from dystrophy and cell death. The drug achieved this by reducing tau phosphorylation, inflammation, and impairments in the autophagy process. Additionally, high concentrations of LEV showed promise in reducing the production and deposition of amyloid beta-peptide, a hallmark of AD. However, caution is advised as high LEV concentrations induced neuronal apoptosis and impaired movement. These findings suggest that restoring proper network activity might be key to alleviating cognitive deficits in AD. Excited to learn more? Dive into the fascinating research to uncover the potential of LEV in treating Alzheimer’s disease!

BackgroundPatients with Alzheimer’s disease (AD) have a significantly higher risk of seizures than other individuals in an age-matched population, suggesting a close association between epilepsy and AD. We aimed to examine the effects of levetiracetam (LEV)—a drug for treating seizures—on learning and memory and the neuropathological features of AD.MethodsWe crossbred APP23 mice with microtubule-associated protein tau (MAPT) transgenic mice to generate APP23/MAPT mice. These mice were treated with different concentrations of LEV in the presence of kainic acid (KA) for 3 months.ResultsLow doses of LEV alleviated the effects of KA on memory defects in APP23/MAPT mice. Mechanistic investigations showed that low concentrations of LEV decreased tau phosphorylation by reducing the activities of cyclin-dependent kinase 5 and glycogen synthase kinase 3α/β, thus rescuing neurons from synaptic dystrophy and apoptosis. Low doses of LEV inhibited the effects of KA (i.e., inducing neuroinflammation and impairing the autophagy of amyloid β-peptide), thus improving cognitive decline. High concentrations of LEV decreased the production and deposition of amyloid β-peptide (Aβ) by reducing the expression of β-site APP-cleaving enzyme 1 and presenilin 1. However, high concentrations of LEV also induced neuronal apoptosis, decreased movement ability in mice, and did not alleviate cognitive decline in AD mice.ConclusionOur results support the hypothesis that aberrant network activity contributes to the synaptic and cognitive deficits in APP23/MAPT mice. A low concentration of LEV may help ameliorate abnormalities of AD; however, a high LEV concentration did not induce similar results.

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