Release Date: 2024-05-28

Experimental Models of Alzheimer’s Disease

Alev Meltem Ercan (Author)

Release Date: 2024-05-28

This section discusses the importance of developing experimental models for Alzheimer’s Disease (AD) to understand its mechanisms, prevent its development, enable early diagnosis, and identify effective therapies. Key experimental models for AD are summarized, focusing on their features and usage. Traditional models have concentrated on the in vitro production of tau and amyloid-beta (Aβ) aggregates, [...]

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    Work TypeBook Chapter
    Published inAlzheimer’s Disease From Molecular Mechanisms to Clinical Practices
    First Page153
    Last Page174
    DOIhttps://doi.org/10.69860/nobel.9786053359166.7
    LanguageENG
    Page Count22
    Copyright HolderNobel Tıp Kitabevleri
    Licensehttps://nobelpub.com/publish-with-us/copyright-and-licensing

    This section discusses the importance of developing experimental models for Alzheimer’s Disease (AD) to understand its mechanisms, prevent its development, enable early diagnosis, and identify effective therapies. Key experimental models for AD are summarized, focusing on their features and usage. Traditional models have concentrated on the in vitro production of tau and amyloid-beta (Aβ) aggregates, given their central role in AD pathology. Advances in structural methods have facilitated the characterization of these aggregates at the atomic level, aiding the discovery of new pharmaceutical targets and the development of in silico models. In vivo and cellular models, particularly those overexpressing tau or Aβ markers, have been crucial. However, due to differences between human pathology and animal models and numerous clinical trial failures, newer models mimicking the human brain have been developed. Experimental AD models are essential for understanding the disease’s pathology and conducting preclinical studies on new treatments. These models should ideally mimic the progressive neurodegeneration and formation of amyloid plaques and neurofibrillary tangles seen in AD. Animal models, especially transgenic mice expressing human genes related to AD, are widely used. Alternative models, such as zebrafish, Drosophila melanogaster, and Caenorhabditis elegans, face limitations due to physiological differences with humans. Transgenic mouse models produce amyloid plaques and neurofibrillary tangles, reflecting diverse disease features. The development of cell culture methods has advanced experimental models using human-induced pluripotent stem cells or neural precursor cells, addressing inconsistencies from interspecies differences. These human cell-based models do not rely on post-mortem brain tissues, overcoming a significant obstacle in developing adult human cell-based experimental models.

    Alev Meltem Ercan (Author)
    Professor, Istanbul Cerrahpasa University
    https://orcid.org/0000-0002-4533-4907

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