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Development of a Novel Treatment Strategy to Treat Parkinsonian Neurodegeneration by Targeting Both Lewy Body Aggregation and Dopaminergic Neuronal Degradation in a Drosophila melanogaster Model

Sama et al. | Sep 25, 2019

Development of a Novel Treatment Strategy to Treat Parkinsonian Neurodegeneration by Targeting Both Lewy Body Aggregation and Dopaminergic Neuronal Degradation in a <em>Drosophila melanogaster</em> Model

In this article the authors address the complex and life quality-diminishing neurodegenerative disease known as Parkinson's. Although genetic and/or environmental factors contribute to the etiology of the disease, the diagnostic symptoms are the same. By genetically modifying fruit flies to exhibit symptoms of Parkinson's disease, they investigate whether drugs that inhibit mitochondrial calcium uptake or activate the lysosomal degradation of proteins could improve the symptoms of Parkinson's these flies exhibit. The authors report the most promising outcome to be that when both types of drugs were used together. Their data provides encouraging evidence to support further investigation of the utility of such drugs in the treatment of human Parkinson's patients.

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The role of CYP46A1 and its metabolic product, 24S-hydroxycholesterol, in Neuro 2A cell death

Ni et al. | May 11, 2021

The role of CYP46A1 and its metabolic product, 24S-hydroxycholesterol, in Neuro 2A cell death

Cholesterol is a major component of neuronal cell membrane and myelin sheath. In this study, the authors either transfected Neuro 2A cells with CYP46A1 cDNA or treated the cells with 24SHC. Cells expressing CYP46A1 had significantly less viability compared to the negative control. Up to 55% reduction in cell viability was also observed in 24S-HC-treated cells. This work supports that CYP46A1 and 24S-HC could directly trigger cell death. The direct involvement of 24S-HC in cell death provides further evidence that 24S-HC can be a promising biomarker for diagnosing brain damage severity.

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The non-nutritive sweeteners acesulfame potassium and neotame slow the regeneration rate of planaria

Russo et al. | Nov 29, 2023

The non-nutritive sweeteners acesulfame potassium and neotame slow the regeneration rate of planaria
Image credit: Russo et al. 2023

The consumption of sugar substitute non-nutritive sweeteners (NNS) has dramatically increased in recent years. Despite being advertised as a healthy alternative, NNS have been linked to adverse effects on the body, such as neurodegenerative diseases (NDs). In NDs, neural stem cell function is impaired, which inhibits neuron regeneration. The purpose of this study was to determine if the NNS acesulfame potassium (Ace-K) and neotame affect planaria neuron regeneration rates. Since human neurons may regenerate, planaria, organisms with extensive regenerative capabilities due to stem cells called neoblasts, were used as the model organism. The heads of planaria exposed to either a control or non-toxic concentrations of NNS were amputated. The posterior regions of the planaria were observed every 24 hours to see the following regeneration stages: (1) wound healing, (2) blastema development, (3) growth, and (4) differentiation. The authors hypothesized that exposure to the NNS would slow planaria regeneration rates. The time it took for the planaria in the Ace-K group and the neotame group to reach the second, third, and fourth regeneration stage was significantly greater than that of the control. The results of this study indicated that exposure to the NNS significantly slowed regeneration rates in planaria. This suggests that the NNS may adversely impact neoblast proliferation rates in planaria, implying that it could impair neural stem cell proliferation in humans, which plays a role in NDs. This study may provide insight into the connection between NNS, human neuron regeneration, and NDs.

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Effect of Natural Compounds Curcumin and Nicotinamide on α-synuclein Accumulation in a C. elegans Model of Parkinson’s Disease

Mehrotra et al. | Jan 29, 2018

Effect of Natural Compounds Curcumin and Nicotinamide on α-synuclein Accumulation in a C. elegans Model of Parkinson’s Disease

Parkinson's disease is a neurodegenerative disorder that affects over 10 million people worldwide. It is caused by destruction of dopamine-producing neurons, which results in severe motor and movement symptoms. In this study, the authors investigated the anti-Parkinsonian effects of two natural compounds curcumin and nicotinamide using C. elegans as a model organism.

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Effects on Learning and Memory of a Mutation in Dα7: A D. melanogaster Homolog of Alzheimer's Related Gene for nAChR α7

Sanyal et al. | Oct 01, 2019

Effects on Learning and Memory of a Mutation in Dα7: A <em>D. melanogaster</em> Homolog of Alzheimer's Related Gene for nAChR α7

Alzheimer's disease (AD) involves the reduction of cholinergic activity due to a decrease in neuronal levels of nAChR α7. In this work, Sanyal and Cuellar-Ortiz explore the role of the nAChR α7 in learning and memory retention, using Drosophila melanogaster as a model organism. The performance of mutant flies (PΔEY6) was analyzed in locomotive and olfactory-memory retention tests in comparison to wild type (WT) flies and an Alzheimer's disease model Arc-42 (Aβ-42). Their results suggest that the lack of the D. melanogaster-nAChR causes learning, memory, and locomotion impairments, similar to those observed in Alzheimer's models Arc-42.

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The sweetened actualities of neural membrane proteins: A computational structural analysis

Chauhan et al. | Nov 03, 2022

The sweetened actualities of neural membrane proteins: A computational structural analysis

Here, seeking to better understand the roles of glycans in the receptors of active sites of neuronal cells, the authors used molecular dynamics simulations to to uncover the dynamic nature of N-glycans on membrane proteins. The authors suggest the study of theinteractions of these membrane poreins could provide future potential therapeutic targets to treat mental diseases.

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