A Comprehensive Review on Preclinical Alzheimer's Disease Models: Evaluating their Clinical Relevance

被引:0
|
作者
Kushwaha, Virendra [1 ]
Sahu, Kantrol Kumar [1 ]
机构
[1] GLA Univ, Inst Pharmaceut Res, Mathura 281406, UP, India
关键词
Alzheimer's disease; rodent model; primate model; animal model; biomarkers; neurodegeneration; amyloid beta; PHEOCHROMOCYTOMA PC12 CELLS; BLOOD-PRESSURE VARIABILITY; PLURIPOTENT STEM-CELLS; AMYLOID-BETA; A-BETA; MEMORY IMPAIRMENT; OXIDATIVE STRESS; TRANSGENIC MICE; COGNITIVE DYSFUNCTION; CELLULAR SENESCENCE;
D O I
10.2174/0113892010331845240802073645
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Alzheimer's disease (AD) is a neurological disorder that increases with age and must be treated immediately by worldwide healthcare systems. Internal neurofibrillary tau tangles and extracellular amyloid accumulation have been widely recognized as the primary causes of Alzheimer's disease. These degenerative age-related ailments are expected to proliferate exponentially as life expectancy rises. Experimental models of AD are essential for acquiring a deep knowledge of its pathogenesis and determining the viability of novel therapy options. Although there isn't a model that encompasses all the characteristics of real AD, these models are nonetheless highly helpful for the research of various modifications associated with it, even though they are only partially indicative of the disease circumstances being studied. Better knowledge of the advantages and disadvantages of each of the different models, as well as the use of more than one model to evaluate potential medications, would increase the effectiveness of therapy translation from preclinical research to patients. We outline the pathogenic characteristics and limitations of the main experimental models of AD in this review, including transgenic mice, transgenic rats, primates and non-primate models along with in-vitro cell culture models in humans. Additionally, it highlights the possible future of experimental modeling of AD and includes the co-morbid models.
引用
收藏
页码:186 / 207
页数:22
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