Human tau fibrillization and neurotoxicity in the presence of magnesium oxide nanoparticle fabricated through laser ablation method

Aliakbari, Fakhteh; Attar, Farideh; Movahedi, Monireh; Falahati, Mojtaba

doi:10.1016/j.saa.2022.121372

Cited by 3 publications

(2 citation statements)

References 39 publications

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“…It is believed that Aβ causes the hyperphosphorylation of tau, which, on the one hand, disrupts the normal function of the latter, and, on the other hand, leads to fibrillation and neurotoxicity [ 52 ]. Notably, tau phosphorylation is an ordinary event in cell physiology [ 53 , 54 ], and eight possible phosphorylation sites have been discovered on all six isoforms of tau [ 55 , 56 ].…”

Section: Aβ and Its Protein Interactorsmentioning

confidence: 99%

Protein Interactome of Amyloid-β as a Therapeutic Target

et al. 2023

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The amyloid concept of Alzheimer’s disease (AD) assumes the β-amyloid peptide (Aβ) as the main pathogenic factor, which injures neural and other brain cells, causing their malfunction and death. Although Aβ has been documented to exert its cytotoxic effect in a solitary manner, there is much evidence to claim that its toxicity can be modulated by other proteins. The list of such Aβ co-factors or interactors includes tau, APOE, transthyretin, and others. These molecules interact with the peptide and affect the ability of Aβ to form oligomers or aggregates, modulating its toxicity. Thus, the list of potential substances able to reduce the harmful effects of the peptide should include ones that can prevent the pathogenic interactions by specifically binding Aβ and/or its partners. In the present review, we discuss the data on Aβ-based complexes in AD pathogenesis and on the compounds directly targeting Aβ or the destructors of its complexes with other polypeptides.

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Section: Aβ and Its Protein Interactorsmentioning

confidence: 99%

Protein Interactome of Amyloid-β as a Therapeutic Target

et al. 2023

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“…Particularly relevant to this study is the fact that UFPM/NPs are very effective in their capacity to aggregate, conglomerate, and produce protein folding, destabilization, and fibrillation (5,61,63,65,67,69,70,(79)(80)(81)(82). John et al (81) referred to large nanostructures of ≥20 nm affecting the kinetic peptide aggregation, thus size and shape matter.…”

Section: Introductionmentioning

confidence: 99%

Sleep matters: Neurodegeneration spectrum heterogeneity, combustion and friction ultrafine particles, industrial nanoparticle pollution, and sleep disorders—Denial is not an option

Calderón‐Garcidueñas

Torres‐Jardón²,

Greenough³

et al. 2023

Front. Neurol.

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Sustained exposures to ubiquitous outdoor/indoor fine particulate matter (PM2.5), including combustion and friction ultrafine PM (UFPM) and industrial nanoparticles (NPs) starting in utero, are linked to early pediatric and young adulthood aberrant neural protein accumulation, including hyperphosphorylated tau (p-tau), beta-amyloid (Aβ1 − 42), α-synuclein (α syn) and TAR DNA-binding protein 43 (TDP-43), hallmarks of Alzheimer's (AD), Parkinson's disease (PD), frontotemporal lobar degeneration (FTLD), and amyotrophic lateral sclerosis (ALS). UFPM from anthropogenic and natural sources and NPs enter the brain through the nasal/olfactory pathway, lung, gastrointestinal (GI) tract, skin, and placental barriers. On a global scale, the most important sources of outdoor UFPM are motor traffic emissions. This study focuses on the neuropathology heterogeneity and overlap of AD, PD, FTLD, and ALS in older adults, their similarities with the neuropathology of young, highly exposed urbanites, and their strong link with sleep disorders. Critical information includes how this UFPM and NPs cross all biological barriers, interact with brain soluble proteins and key organelles, and result in the oxidative, endoplasmic reticulum, and mitochondrial stress, neuroinflammation, DNA damage, protein aggregation and misfolding, and faulty complex protein quality control. The brain toxicity of UFPM and NPs makes them powerful candidates for early development and progression of fatal common neurodegenerative diseases, all having sleep disturbances. A detailed residential history, proximity to high-traffic roads, occupational histories, exposures to high-emission sources (i.e., factories, burning pits, forest fires, and airports), indoor PM sources (tobacco, wood burning in winter, cooking fumes, and microplastics in house dust), and consumption of industrial NPs, along with neurocognitive and neuropsychiatric histories, are critical. Environmental pollution is a ubiquitous, early, and cumulative risk factor for neurodegeneration and sleep disorders. Prevention of deadly neurological diseases associated with air pollution should be a public health priority.

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Nanoparticles and neurodegeneration: Insights on multiple pathways of programmed cell death regulated by nanoparticles

Chen,

2024

Science of The Total Environment

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Human tau fibrillization and neurotoxicity in the presence of magnesium oxide nanoparticle fabricated through laser ablation method

Cited by 3 publications

References 39 publications

Protein Interactome of Amyloid-β as a Therapeutic Target

Protein Interactome of Amyloid-β as a Therapeutic Target

Sleep matters: Neurodegeneration spectrum heterogeneity, combustion and friction ultrafine particles, industrial nanoparticle pollution, and sleep disorders—Denial is not an option

Nanoparticles and neurodegeneration: Insights on multiple pathways of programmed cell death regulated by nanoparticles

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