Animal Models of Alzheimer's Disease

Bharadwaj, Prashant

doi:10.1002/9781119356752.ch10

Cited by 2 publications

(2 citation statements)

References 108 publications

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“…One major drawback is the translatability of AD drugs from animal models to human clinical trials [85]. Additionally, AD pathology in humans develops over decades, while in transgenic mice the disease develops in just a few months and only with familial AD mutations [85]. Another discrepancy between most AD mouse models and humans is the lack of neurofibrillary tangles—which is an important hallmark of AD.…”

Section: Activation Of Autophagy As a Therapeutic Target For Amylomentioning

confidence: 99%

“…Another discrepancy between most AD mouse models and humans is the lack of neurofibrillary tangles—which is an important hallmark of AD. Although tau protein hyperphosphorylation occurs in these mice, no neurofibrillary tangles develop and therefore these transgenic mice only model certain aspects of disease [85]. Additionally, effects of autophagy activation may vary significantly depending on the physiological state of the cell—especially during proteotoxic stress.…”

Section: Activation Of Autophagy As a Therapeutic Target For Amylomentioning

confidence: 99%

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Autophagy Modulation as a Treatment of Amyloid Diseases

et al. 2019

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Amyloids are fibrous proteins aggregated into toxic forms that are implicated in several chronic disorders. More than 30 diseases show deposition of fibrous amyloid proteins associated with cell loss and degeneration in the affected tissues. Evidence demonstrates that amyloid diseases result from protein aggregation or impaired amyloid clearance, but the connection between amyloid accumulation and tissue degeneration is not clear. Common examples of amyloid diseases are Alzheimer’s disease (AD), Parkinson’s disease (PD) and tauopathies, which are the most common forms of neurodegenerative diseases, as well as polyglutamine disorders and certain peripheral metabolic diseases. In these diseases, increased accumulation of toxic amyloid proteins is suspected to be one of the main causative factors in the disease pathogenesis. It is therefore important to more clearly understand how these toxic amyloid proteins accumulate as this will aide in the development of more effective preventive and therapeutic strategies. Protein homeostasis, or proteostasis, is maintained by multiple cellular pathways—including protein synthesis, quality control, and clearance—which are collectively responsible for preventing protein misfolding or aggregation. Modulating protein degradation is a very complex but attractive treatment strategy used to remove amyloid and improve cell survival. This review will focus on autophagy, an important clearance pathway of amyloid proteins, and strategies for using it as a potential therapeutic target for amyloid diseases. The physiological role of autophagy in cells, pathways for its modulation, its connection with apoptosis, cell models and caveats in developing autophagy as a treatment and as a biomarker is discussed.

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Section: Activation Of Autophagy As a Therapeutic Target For Amylomentioning

confidence: 99%

Section: Activation Of Autophagy As a Therapeutic Target For Amylomentioning

confidence: 99%

Autophagy Modulation as a Treatment of Amyloid Diseases

et al. 2019

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The Role of the Gut Microbiota and Microbial Metabolites in the Pathogenesis of Alzheimer’s Disease

Wang

2023

CNSNDDT

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Alzheimer’s disease is a neurodegenerative disease that causes memory loss, cognitive dysfunction and dementia. It is a multifactorial disease involving a wide range of pathological factors that have yet to be fully understood. As proposed by scientists and supported by a growing amount of evidence in recent years, the gut microbiota plays an important role in the pathogenesis of Alzheimer’s disease via a constant bidirectional communication through the brain-gut-microbiota axis which is a multifunctional network involving the nervous system and the peripheral circulatory system. This communication pathway facilitates the exchange of information and signals between the brain and the gut, such as microbe-derived metabolites and neurotransmitters, which allows gut microbes to influence the central nervous system. This review summarizes recent research findings on the pathological risk factors of Alzheimer’s disease, the brain-gut-microbiota axis, the role of gut microbe-derived products in neurological disorders, and clinical/preclinical studies investigating the role of the gut microbiota in Alzheimer’s disease. In addition, some suggestions for future research are proposed.

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Animal Models of Alzheimer's Disease

Cited by 2 publications

References 108 publications

Autophagy Modulation as a Treatment of Amyloid Diseases

Autophagy Modulation as a Treatment of Amyloid Diseases

The Role of the Gut Microbiota and Microbial Metabolites in the Pathogenesis of Alzheimer’s Disease

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