Insights from Drosophila melanogaster model of Alzheimer s disease

Tuệ, Nguyễn Trọng; Dat, Tran Quoc; Ly, Luong Linh; Anh, Vu Duc; Yoshida, Hideki

doi:10.2741/4798

Cited by 25 publications

(21 citation statements)

References 26 publications

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“…In dominant expression neuronal cells could rescue this phenotype significantly. In addition, APP also plays a significant role in Drosophila melanogaster, and the suppression of APPL gene causes an alteration of chemotactic behavior [32]. Interestingly, high levels of APPL are associated with the neuronal regeneration in the brain injury model of Drosophila increased mortality.…”

Section: Neuronal Roles Of Appmentioning

confidence: 99%

Promising Modulatory Effects of Autophagy on APP Processing as a Potential Treatment for Alzheimer's Disease

Rahman¹,

Rahman²,

Rahman³

et al. 2020

Preprint

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Autophagy refers to the degradation of cytoplasmic constituents by a lysosomal-mediated pathway, which plays a critical role in maintaining cellular homeostasis. Importantly, dysregulation of autophagy has been implicated in multiple neurodegenerative disorders. Previous studies reported that autophagy affects the processing of amyloid precursor protein (APP), thus stimulating β‐amyloid (Aβ) production in Alzheimer’s disease (AD) eventually. Although the mechanism of autophagy modulation on APP processing and its pathogenesis has not yet been fully elucidated at the molecular level, but modulation of autophagy has received considerable attention as a promising approach for the treatment of AD. In the early stage of AD, Aβ may prompt autophagy to facilitate its removal via mTOR‐independent as well as-dependent pathways. However, a recent study proposed that autophagy processes are not properly regulated as AD continues to progress, and consequently, the production of Aβ tends to accumulate rapidly. Meanwhile, a number of autophagy-related genes (Atg) as well as APP genes are also thought to influence the development of AD, which may serve as a bi‐directional link to autophagy and AD pathology. In this review, we summarized current observations related to autophagy regulation and APP processing, focusing on their dynamic modifications associated with the progression of AD. Recent findings together highlight the essential role of autophagy in the removal and clearance of APP and Aβ deposition in the pathological condition of AD.

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Section: Neuronal Roles Of Appmentioning

confidence: 99%

Promising Modulatory Effects of Autophagy on APP Processing as a Potential Treatment for Alzheimer's Disease

Rahman¹,

Rahman²,

Rahman³

et al. 2020

Preprint

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“…Alzheimer, ilerleyen hafıza kaybı ile sonuçlanan, korteks ve hipokampüste nöron kaybına neden olan bilincin ve davranışların etkilendiği nörodejeneratif bir hastalıktır. Hastalığın patogenezinde hücre dışı amiloid plak birikimi, sinaptik bozulmalar ve nöron ölümleri görülmektedir [58][59][60][61] . Amiloid beta plak birikimi Alzheimer hastalığının en temel nedenleri arasındadır.…”

Section: Alzheimer Hastalığıunclassified

Nörodejeneratif Hastalık Araştırmalarında Drosophila melanogaster Modeli

Hazir

Bora

Erdem‐Yurter

2020

Uludağ Üniversitesi Tıp Fakültesi Dergisi

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Drosophila melanogaster yaşam döngüsünün kısa olması, nükleotit dizisi bilinen küçük bir genoma sahip olması, insan hastalıklarına neden olan genlerin birçoğunun ortoloğunu bulundurması, temel hücresel olayların/sinyal yolaklarının korunmuş olması ve etik problem yaratmaması gibi önemli avantajları olan omurgasız bir canlıdır. Bu avantajlar sayesinde insan hastalıklarının modellenmesi mümkün olmuş ve patofizyolojilerin araştırılması, yeni genlerin ve genetik düzenleyicilerin tanımlanması, klinik çeşitlilik nedenlerinin açıklanabilmesi ve yeni tanı/tedavi geliştirme çalışmaları hız kazanmıştır. Bu derlemede Drosophila melanogaster'in model organizma olarak avantajları ve nörodejeneratif hastalıklarla ilişkili araştırmalarda kullanılmasına ilişkin bilgiler özetlenmiştir.

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“…As Drosophila melanogaster shares a similar yet simpler central nervous system in relation to mammals, its use in investigating neurodegenerative diseases has been incredibly valuable 22 – 25 . Plus, it has been suggested to be an interesting model for exploring gut-brain-axis interactions within these diseases 26 , 27 .…”

Section: Introductionmentioning

confidence: 99%

Kefir metabolites in a fly model for Alzheimer’s disease

Batista

Malta

Silva

et al. 2021

Sci Rep

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Alzheimer’s Disease (AD) is the most common cause of dementia among elderly individuals worldwide, leading to a strong motor-cognitive decline and consequent emotional distress and codependence. It is traditionally characterized by amyloidogenic pathway formation of senile plaques, and recent studies indicate that dysbiosis is also an important factor in AD’s pathology. To overcome dysbiosis, probiotics—as kefir—have shown to be a great therapeutic alternative for Alzheimer’s disease. In this present work, we explored kefir as a probiotic and a metabolite source as a modulator of microbiome and amyloidogenic pathway, using a Drosophila melanogaster model for AD (AD-like flies). Kefir microbiota composition was determined through 16S rRNA sequencing, and the metabolome of each fraction (hexane, dichloromethane, ethyl acetate, and n-butanol) was investigated. After treatment, flies had their survival, climbing ability, and vacuolar lesions accessed. Kefir and fraction treated flies improved their climbing ability survival rate and neurodegeneration index. In conclusion, we show that kefir in natura, as well as its fractions may be promising therapeutic source against AD, modulating amyloidogenic related pathways.

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Insights from Drosophila melanogaster model of Alzheimer s disease

Cited by 25 publications

References 26 publications

Promising Modulatory Effects of Autophagy on APP Processing as a Potential Treatment for Alzheimer's Disease

Promising Modulatory Effects of Autophagy on APP Processing as a Potential Treatment for Alzheimer's Disease

Nörodejeneratif Hastalık Araştırmalarında Drosophila melanogaster Modeli

Kefir metabolites in a fly model for Alzheimer’s disease

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