A systematic review for the development of Alzheimer’s disease in in vitro models: a focus on different inducing agents

Autor: Manisha Prajapat, Gurjeet Kaur, Gajendra Choudhary, Paras Pahwa, Seema Bansal, Rupa Joshi, Gitika Batra, Abhishek Mishra, Rubal Singla, Harminder Kaur, Praisy K. Prabha, Ajay Prakash Patel, Bikash Medhi
Jazyk: angličtina
Rok vydání: 2023
Předmět:
Zdroj: Frontiers in Aging Neuroscience, Vol 15 (2023)
Druh dokumentu: article
ISSN: 1663-4365
98016288
DOI: 10.3389/fnagi.2023.1296919
Popis: Alzheimer’s disease (AD) is the most common progressive neurodegenerative disease and is associated with dementia. Presently, various chemical and environmental agents are used to induce in-vitro models of Alzheimer disease to investigate the efficacy of different therapeutic drugs. We screened literature from databases such as PubMed, ScienceDirect, and Google scholar, emphasizing the diverse targeting mechanisms of neuro degeneration explored in in-vitro models. The results revealed studies in which different types of chemicals and environmental agents were used for in-vitro development of Alzheimer-targeting mechanisms of neurodegeneration. Studies using chemically induced in-vitro AD models included in this systematic review will contribute to a deeper understanding of AD. However, none of these models can reproduce all the characteristics of disease progression seen in the majority of Alzheimer’s disease subtypes. Additional modifications would be required to replicate the complex conditions of human AD in an exact manner. In-vitro models of Alzheimer’s disease developed using chemicals and environmental agents are instrumental in providing insights into the disease’s pathophysiology; therefore, chemical-induced in-vitro AD models will continue to play vital role in future AD research. This systematic screening revealed the pivotal role of chemical-induced in-vitro AD models in advancing our understanding of AD pathophysiology and is therefore important to understand the potential of these chemicals in AD pathogenesis.
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