Dynamic effect of beta-amyloid 42 on cell mechanics

Gao, Qi; Fang, Yuqiang; Zhang, Shiqing; Wong, Ho Sze Hersey; Chan, Yee Edward; Wong, Samantha Sze Man; Yung, Kin Lam; Lai, King Wai Chiu

doi:10.1016/j.jbiomech.2019.01.046

Cited by 17 publications

(28 citation statements)

References 48 publications

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“…Recent works have been studying the MEDI1814, a monoclonal antibody as a potential disease-modifying treatment for Alzheimer’s disease. This strategy is based on the ability of MEDI1814 to selectively target β-amyloid 42 [128], which is highly associated with Alzheimer’s disease [129]. As early trials have proved that MEDI1814 can reduce the levels of the β-amyloid 42, AstraZeneca and Lily are co-developing it as part of the BACE alliance.…”

Section: Nanomedicine In Central Nervous System Disordersmentioning

confidence: 99%

Neuronanomedicine: An Up-to-Date Overview

et al. 2019

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The field of neuronanomedicine has recently emerged as the bridge between neurological sciences and nanotechnology. The possibilities of this novel perspective are promising for the diagnosis and treatment strategies of severe central nervous system disorders. Therefore, the development of nano-vehicles capable of permeating the blood–brain barrier (BBB) and reaching the brain parenchyma may lead to breakthrough therapies that could improve life expectancy and quality of the patients diagnosed with brain disorders. The aim of this review is to summarize the recently developed organic, inorganic, and biological nanocarriers that could be used for the delivery of imaging and therapeutic agents to the brain, as well as the latest studies on the use of nanomaterials in brain cancer, neurodegenerative diseases, and stroke. Additionally, the main challenges and limitations associated with the use of these nanocarriers are briefly presented.

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Section: Nanomedicine In Central Nervous System Disordersmentioning

confidence: 99%

Neuronanomedicine: An Up-to-Date Overview

et al. 2019

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“…This effect was reported to be more robust in the case of oligomers and fibrils, but was still present in the case of the peptides. Aβ-42 was also reported to decrease Young's modulus in neural cells [27]. Furthermore, it was reported that Aβ oligomers are inducing neural elasticity changes [28].…”

Section: Effect Of Aβ Peptides On Bending Rigidity Coefficientmentioning

confidence: 95%

Effect of Amyloid-β Monomers on Lipid Membrane Mechanical Parameters–Potential Implications for Mechanically Driven Neurodegeneration in Alzheimer’s Disease

Drabik

Chodaczek

Kraszewski

2020

IJMS

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Alzheimer’s disease (AD) is a neurodegenerative disease that results in memory loss and the impairment of cognitive skills. Several mechanisms of AD’s pathogenesis were proposed, such as the progressive accumulation of amyloid-β (Aβ) and τ pathology. Nevertheless, the exact neurodegenerative mechanism of the Aβ remains complex and not fully understood. This paper proposes an alternative hypothesis of the mechanism based on maintaining the neuron membrane’s mechanical balance. The incorporation of Aβ decreases the lipid membrane’s elastic properties, which eventually leads to the impairment of membrane clustering, disruption of mechanical wave propagation, and change in gamma oscillations. The first two disrupt the neuron’s ability to function correctly while the last one decreases sensory encoding and perception enabling. To begin discussing this mechanical-balance hypothesis, we measured the effect of two selected peptides, Aβ-40 and Aβ-42, as well as their fluorescently labeled modification, on membrane mechanical properties. The decrease of bending rigidity, consistent for all investigated peptides, was observed using molecular dynamic studies and experimental flicker-noise techniques. Additionally, wave propagation was investigated with molecular dynamic studies in membranes with and without incorporated neurodegenerative peptides. A change in membrane behavior was observed in the membrane system with incorporated Aβ.

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“…Thus, just as alterations in axonal transport can lead to amyloid pathology, there is also extensive evidence that Aβ itself can cause microtubulebased transport defects (Pigino et al, 2009;Zhao et al, 2010;Calkins and Reddy, 2011;Tang et al, 2012;Cruz et al, 2018;Zhang et al, 2018). In this line, and considering the role of microtubules in axonal transport, several studies have focused on the effects of Aβ on the integrity of the microtubule network (Fifre et al, 2006;Gevorkian et al, 2008;Silva et al, 2011;Mota et al, 2012;Pianu et al, 2014;Wang et al, 2018;Gao et al, 2019). For instance, Sadleir et al (2016) hypothesized that presynaptic dystrophies were triggered by Aβ-mediated microtubule disruption.…”

Section: Axonal Transport Disruption Associated With Aβmentioning

confidence: 99%

Axonal Degeneration in AD: The Contribution of Aβ and Tau

Salvadores

Gerónimo‐Olvera

Court

2020

Front. Aging Neurosci.

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Alzheimer's disease (AD) represents the most common age-related neurodegenerative disorder, affecting around 35 million people worldwide. Despite enormous efforts dedicated to AD research over decades, there is still no cure for the disease. Misfolding and accumulation of Aβ and tau proteins in the brain constitute a defining signature of AD neuropathology, and mounting evidence has documented a link between aggregation of these proteins and neuronal dysfunction. In this context, progressive axonal degeneration has been associated with early stages of AD and linked to Aβ and tau accumulation. As the axonal degeneration mechanism has been starting to be unveiled, it constitutes a promising target for neuroprotection in AD. A comprehensive understanding of the mechanism of axonal destruction in neurodegenerative conditions is therefore critical for the development of new therapies aimed to prevent axonal loss before irreversible neuronal death occurs in AD. Here, we review current evidence of the involvement of Aβ and tau pathologies in the activation of signaling cascades that can promote axonal demise.

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Dynamic effect of beta-amyloid 42 on cell mechanics

Cited by 17 publications

References 48 publications

Neuronanomedicine: An Up-to-Date Overview

Neuronanomedicine: An Up-to-Date Overview

Effect of Amyloid-β Monomers on Lipid Membrane Mechanical Parameters–Potential Implications for Mechanically Driven Neurodegeneration in Alzheimer’s Disease

Axonal Degeneration in AD: The Contribution of Aβ and Tau

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