Pharmacologically induced models of dementia: Еxperimental approaches and applications
DOI:
https://doi.org/10.14748/91nkeb14Keywords:
dementia models, experimental models, Alzheimer's disease, dementiaAbstract
Introduction: Dementia is a progressive and multifactorial syndrome affecting higher cortical functions. Globally, more than 57 million people were living with dementia in 2021, and the number is projected to exceed 130 million by 2050. Alzheimer’s disease (AD) is the most prevalent form. The absence of curative therapies explains the need to explore new treatment strategies, including natural compounds with neuroprotective potential. Reliable experimental models are essential for reproducing the key mechanisms of dementia and evaluating novel treatments before clinical trials.
Aim: The purpose of this study is to provide a clear summary of the main pharmacologically induced models of dementia.
Materials and Methods: This review summarizes pharmacologically induced models of dementia based on a literature search in PubMed, Scopus, and Google Scholar covering the period 2010–2026. Inclusion criteria were English-language, peer-reviewed studies focused on pharmacologically induced experimental models of dementia and related therapeutic approaches. Exclusion criteria were irrelevant topics, unavailable full texts, non-English publications, and non–peer-reviewed or outdated sources. The selected studies were classified according to the type of pharmacological induction (e.g., cholinergic, glutamatergic, oxidative, and other neurotoxic models).
Results and Conclusion: Pharmacologically induced models are widely used due to their reproducibility and relative simplicity. These models reproduce specific aspects of the disease, including cholinergic dysfunction, oxidative stress, neurotoxicity, excitotoxicity, neuroinflammation, and accelerated brain aging. The present review summarizes the main pharmacologically induced models of dementia, including scopolamine, botulinum neurotoxin type B, streptozotocin, colchicine, kainic acid, quinolinic acid, Poly I:C, okadaic acid, amyloid-beta peptide, and D-galactose-induced models. Their mechanisms, experimental applications, advantages, and limitations are discussed.
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