Use of Zebrafish Genetic Models to Study Etiology of the Amyloid-Beta
and Neurofibrillary Tangle Pathways in Alzheimer's Disease

Kiper, Keturah; Freeman, Jennifer L.

doi:10.2174/1570159x19666210524155944

Cited by 13 publications

(8 citation statements)

References 106 publications

(118 reference statements)

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“…The recent availability and feasibility of using genome editing technology provide an exciting opportunity for the development of genetic models of zebrafish neurodegenerative diseases. There are many methods to edit zebrafish genome, such as the nontargeted transgene method used to characterize gene location, CRISPR‐Cas technology used to determine whether the protein function of zebrafish is conserved and determine the protein‐coding region and so on (Kiper & Freeman, 2022; Newman et al., 2014). To more effectively analyze future AD transgenic and mutant zebrafish models, we need to conduct more in‐depth studies of zebrafish.…”

Section: Ad Animal Modelmentioning

confidence: 99%

Nutritional assessment models for Alzheimer's disease: Advances and perspectives

Wen

Zhang

et al. 2023

Food Frontiers

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Alzheimer's disease (AD) is a neurodegenerative disease of uncertain pathogenesis that develops in the elderly population and is characterized by loss of cognitive function, memory loss, and deterioration of everyday behavior. The development of biological models of AD is constrained by the complexity of the pathogenesis and multiple causes. Creating disease models can aid in understanding the pathophysiology of AD and developing effective therapeutic drugs. In this review, the animal and cellular models that are currently being utilized to research AD are outlined and described in detail according to modeling approaches. The main animal models are natural aging models, transgenic models, and drug‐induced models. The main cellular models are traditional 2D cells, human induced pluripotent stem 2D cells (neurons and glial cells), and 3D cells, as well as organoid models, and the benefits and drawbacks of their various biological models are assessed. They do have their limitations due to an incomplete reflection of AD pathology. Therefore, new models for AD research are needed in the future. The summary of existing models is intended to provide a basis for the subsequent development of new disease models and to provide a reference for the study of disease mechanisms, clinical research, and new drug development in AD.

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Section: Ad Animal Modelmentioning

confidence: 99%

Nutritional assessment models for Alzheimer's disease: Advances and perspectives

Wen

Zhang

et al. 2023

Food Frontiers

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“…SAD is correlated with the expression of the apolipoprotein E (ApoE) variant, ε4 ( Xia, 2010 ). In zebrafish, various homologous gene encoding such as PS1, PS2, APP, and ApoE have been identified ( Newman et al, 2014 ; Kiper and Freeman, 2021 ). Table 2 enlists the genes that have a prominent role in AD and their orthologs in zebrafish.…”

Section: Genes Implicated In Human and Zebrafish Alzheimer’s Diseasementioning

confidence: 99%

The Brilliance of the Zebrafish Model: Perception on Behavior and Alzheimer’s Disease

Shenoy

Banerjee

Upadhya

et al. 2022

Front. Behav. Neurosci.

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Alzheimer’s disease (AD) has become increasingly prevalent in the elderly population across the world. It’s pathophysiological markers such as overproduction along with the accumulation of amyloid beta (Aβ) plaques and neurofibrillary tangles (NFT) are posing a serious challenge to novel drug development processes. A model which simulates the human neurodegenerative mechanism will be beneficial for rapid screening of potential drug candidates. Due to the comparable neurological network with humans, zebrafish has emerged as a promising AD model. This model has been thoroughly validated through research in aspects of neuronal pathways analogous to the human brain. The cholinergic, glutamatergic, and GABAergic pathways, which play a role in the manifested behavior of the zebrafish, are well defined. There are several behavioral models in both adult zebrafish and larvae to establish various aspects of cognitive impairment including spatial memory, associative memory, anxiety, and other such features that are manifested in AD. The zebrafish model eliminates the shortcomings of previously recognized mammalian models, in terms of expense, extensive assessment durations, and the complexity of imaging the brain to test the efficacy of therapeutic interventions. This review highlights the various models that analyze the changes in the normal behavioral patterns of the zebrafish when exposed to AD inducing agents. The mechanistic pathway adopted by drugs and novel therapeutic strategies can be explored via these behavioral models and their efficacy to slow the progression of AD can be evaluated.

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“…Alzheimer's disease (AD) is a degenerative disease of the central nervous system (CNS) characterized by deposition of β-amyloid (Aβ) and hyperphosphorylation of tau protein (Kiper & Freeman, 2022). With the aging of the population, the incidence of AD is on the rise year by year.…”

Section: Introductionmentioning

confidence: 99%

Diabetes mellitus and Alzheimer's disease: Vacuolar adenosine triphosphatase as a potential link

Guo,

Li,

Liu

et al. 2024

Eur J of Neuroscience

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Globally, the incidence of diabetes mellitus (DM) and Alzheimer's disease (AD) is increasing year by year, causing a huge economic and social burden, and their pathogenesis and aetiology have been proven to have a certain correlation. In recent years, more and more studies have shown that vacuolar adenosine triphosphatases (v‐ATPases) in eukaryotes, which are biomolecules regulating lysosomal acidification and glycolipid metabolism, play a key role in DM and AD. This article describes the role of v‐ATPase in DM and AD, including its role in glycolysis, insulin secretion and insulin resistance (IR), as well as its relationship with lysosomal acidification, autophagy and β‐amyloid (Aβ). In DM, v‐ATPase is involved in the regulation of glucose metabolism and IR. v‐ATPase is closely related to glycolysis. On the one hand, v‐ATPase affects the rate of glycolysis by affecting the secretion of insulin and changing the activities of key glycolytic enzymes hexokinase (HK) and phosphofructokinase 1 (PFK‐1). On the other hand, glucose is the main regulator of this enzyme, and the assembly and activity of v‐ATPase depend on glucose, and glucose depletion will lead to its decomposition and inactivation. In addition, v‐ATPase can also regulate free fatty acids, thereby improving IR. In AD, v‐ATPase can not only improve the abnormal brain energy metabolism by affecting lysosomal acidification and autophagy but also change the deposition of Aβ by affecting the production and degradation of Aβ. Therefore, v‐ATPase may be the bridge between DM and AD.

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Use of Zebrafish Genetic Models to Study Etiology of the Amyloid-Beta and Neurofibrillary Tangle Pathways in Alzheimer's Disease

Cited by 13 publications

References 106 publications

Nutritional assessment models for Alzheimer's disease: Advances and perspectives

Nutritional assessment models for Alzheimer's disease: Advances and perspectives

The Brilliance of the Zebrafish Model: Perception on Behavior and Alzheimer’s Disease

Diabetes mellitus and Alzheimer's disease: Vacuolar adenosine triphosphatase as a potential link

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