Anas Saifi, Mohd Akbar Iqbal Siddiqui, Aisha Aziz
Vol. 19, Issue 1, Jan-Jun 2025
Abstract:
Alzheimer's disease (AD)—a progressive neurodegenerative condition—is defined by memory loss, cognitive decline, and behavioural disturbances. Existing treatments, despite wide-ranging research, remain symptomatic and relaxing, as no drugs are available to cure. Drug repurposing, the application of existing drugs to new therapeutic indications, is an extensive and powerful approach to accelerating drug finding [1]. Antiepileptics drugs (AEDs), used to control epilepsy, have been investigated for their promise in treating AD based on neuroprotective, anti-inflammatory, and anti-excitotoxic properties. AEDs can modulate neuronal hyperexcitability, oxidative stress, and neurotransmitter imbalance—hallmark pathological mechanisms that occur in epilepsy and AD. Research conducted before clinical studies (in the "preclinical" phase) has shown that some AEDs (antiepileptic drugs), for example, levetiracetam, valproic acid, carbamazepine, lamotrigine and phenytoin, can enhance cognition and reduce the accumulation of amyloid plaques. Levetiracetam and carbamazepine, in particular, demonstrated promising but limited outcomes in clinical practices, and data was inconclusive for valproic acid, lamotrigine, and phenytoin. The current review systematically delves into the role of AEDs in Alzheimer's disease therapy, summarizing their mechanisms of action, preclinical and clinical evidence, safety considerations, and hurdles to clinical translation. It also highlights the socioeconomic demand for better AD therapies and the benefits of repurposing established agents with known safety profiles. Although the initial observations are promising, larger and more robust clinical studies are necessary for confirmation and appropriate dosing regimens. AEDs could be used in combination therapy with existing AD therapy, potentially providing new treatments that target multiple pathways involved in disease progression. In conclusion, this review highlights the therapeutic potential of AEDs in alveolar spaces of Aβ toxicity in AD; this may benefit biological research and clinical research in AD.
DOI: http://doi.org/10.37648/ijrmst.v19i01.004
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