Human amyloid beta and α-synuclein co-expression in neurons impair behavior and recapitulate features for Lewy body dementia in Caenorhabditis elegans

Huang, Xiande; Wang, Changliang; Chen, Liang; Zhang, Tianjiao; Leung, Ka Lai; Wong, Garry

doi:10.1016/j.bbadis.2021.166203

Cited by 16 publications

(18 citation statements)

References 93 publications

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“…Aβ42 significantly reduced the expression level of heme oxygenase-1 in various brain regions of rats [ 45 ]. Aβand α-synuclein are two key proteins found in lesions associated with age-related neurodegenerative disease including AD [ 46 ]. The localization of Aβ plaques, particularly in regions rich in cholinergic neurons, led to the discovery that Aβ binds to a7 nAChRs with high affinity [ 47 ].…”

Section: Ad Relation To the Cholinergic Systemmentioning

confidence: 99%

Role of Cholinergic Signaling in Alzheimer’s Disease

et al. 2022

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Acetylcholine, a neurotransmitter secreted by cholinergic neurons, is involved in signal transduction related to memory and learning ability. Alzheimer’s disease (AD), a progressive and commonly diagnosed neurodegenerative disease, is characterized by memory and cognitive decline and behavioral disorders. The pathogenesis of AD is complex and remains unclear, being affected by various factors. The cholinergic hypothesis is the earliest theory about the pathogenesis of AD. Cholinergic atrophy and cognitive decline are accelerated in age-related neurodegenerative diseases such as AD. In addition, abnormal central cholinergic changes can also induce abnormal phosphorylation of ttau protein, nerve cell inflammation, cell apoptosis, and other pathological phenomena, but the exact mechanism of action is still unclear. Due to the complex and unclear pathogenesis, effective methods to prevent and treat AD are unavailable, and research to explore novel therapeutic drugs is various and active in the world. This review summaries the role of cholinergic signaling and the correlation between the cholinergic signaling pathway with other risk factors in AD and provides the latest research about the efficient therapeutic drugs and treatment of AD.

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Section: Ad Relation To the Cholinergic Systemmentioning

confidence: 99%

Role of Cholinergic Signaling in Alzheimer’s Disease

et al. 2022

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“…Lipid molecules' functions are not limited to building membranous cellular components, supporting structure formation, and participanting in various actions of neurotransmissions in the CNS (Huang et al, 2021). Protein α‐Syn has associations with lipid contents and fatty acid modifications, and collectively they start vesicle formations via a definite mechanism.…”

Section: Resultsmentioning

confidence: 99%

Section: Reo Augmented Lipid Depositions In α-Syn Expressing C Elegansmentioning

confidence: 99%

Rose essential oil diminishes dopaminergic neuron degenerations and reduces α‐synuclein aggregation in Caenorhabditis elegans models of Parkinson's disease

Muhammad

Liu

Wang

et al. 2023

Phytotherapy Research

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Parkinson's disease (P.D.) is the second most progressive neurodegenerative disorder in the elderly. Degeneration of dopaminergic (DA) neurons and α-synuclein (α-Syn) accumulated toxicity is the major contributor to this disease. At present, the disease has no effective treatment. Many recent studies focus on identifying novel therapeutics that provide benefits to stop the disease progression in P.D. patients. Screening novel and effective drugs in P.D. animal models is time-and cost-consuming. Rose Essential Oil (REO) extracted from Rosa Rugosa species (R. Setate Â R. Rugosa). REO contains Citronellol, Geraniol, and Octadiene that possess anti-Aβ, anti-oxidative, and anti-depression-like properties, but no reports have defined the REO effect on P.D. yet. The present study examines the REO neuroprotective potential in transgenic Caenorhabditis elegans P.D. models. We observed that REO reduced α-Syn aggregations and diminished DA neuron degenerations induced by 6-OHDA, reduced food-sensing behavioural disabilities, and prolonged the lifespan of the nematode. Moreover, REO augmented the chymotrypsin-like proteasome and SOD-3 activities. Further, we observed the anti-oxidative role of REO by reducing internal cells ROS.Together, these findings supported REO as an anti-PD drug and may exert its effects by lowering oxidative stress via the anti-oxidative pathway.

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“…The thrashing assay was performed by placing the worm in a drop of M9 buffer and allowing it to recover for 30 s (Huang et al., 2021). The number of body bends was manually counted and recorded at 30 s intervals.…”

Section: Methodsmentioning

confidence: 99%

Impaired mitophagosome–lysosome fusion mediates olanzapine‐induced aging

Chen,

Wang,

Zheng

et al. 2023

Aging Cell

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The lifespan of schizophrenia patients is significantly shorter than the general population. Olanzapine is one of the most commonly used antipsychotic drugs (APDs) for treating patients with psychosis, including schizophrenia and bipolar disorder. Despite their effectiveness in treating positive and negative symptoms, prolonged exposure to APDs may lead to accelerated aging and cognitive decline, among other side effects. Here we report that dysfunctional mitophagy is a fundamental mechanism underlying accelerated aging induced by olanzapine, using in vitro and in vivo (Caenorhabditis elegans) models. We showed that the aberrant mitophagy caused by olanzapine was via blocking mitophagosome–lysosome fusion. Furthermore, olanzapine can induce mitochondrial damage and hyperfragmentation of the mitochondrial network. The mitophagosome–lysosome fusion in olanzapine‐induced aging models can be restored by a mitophagy inducer, urolithin A, which alleviates defective mitophagy, mitochondrial damage, and fragmentation of the mitochondrial network. Moreover, the mitophagy inducer ameliorated behavioral changes induced by olanzapine, including shortened lifespan, and impaired health span, learning, and memory. These data indicate that olanzapine impairs mitophagy, leading to the shortened lifespan, impaired health span, and cognitive deficits. Furthermore, this study suggests the potential application of mitophagy inducers as therapeutic strategies to reverse APD‐induced adverse effects associated with accelerated aging.

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Human amyloid beta and α-synuclein co-expression in neurons impair behavior and recapitulate features for Lewy body dementia in Caenorhabditis elegans

Cited by 16 publications

References 93 publications

Role of Cholinergic Signaling in Alzheimer’s Disease

Role of Cholinergic Signaling in Alzheimer’s Disease

Rose essential oil diminishes dopaminergic neuron degenerations and reduces α‐synuclein aggregation in Caenorhabditis elegans models of Parkinson's disease

Impaired mitophagosome–lysosome fusion mediates olanzapine‐induced aging

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