Impact of phospholipid bilayer saturation on amyloid-β protein aggregation intermediate growth: A quartz crystal microbalance analysis

Kotarek, Joseph A.; Moss, Melissa A.

doi:10.1016/j.ab.2009.12.016

Cited by 24 publications

(13 citation statements)

References 72 publications

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“…However, DHA can also affect the progress of some cells through the cell cycle [101]. The notion that saturation levels of the fatty acid residues (FARs) of phospholipids in membranes play a role in modulating the rate of oligomerization agrees with measurements from model systems that indicate that saturated fatty acid residues lower the energetic barrier to aggregation [102].…”

Section: Misfolded Proteins and The Lipid Profile Of The Membranesupporting

confidence: 62%

Detection of mis-folded protein aggregates from a clinical perspective

et al. 2016

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Neurodegenerative Protein Misfolding Diseases (PMDs), such as Alzheimer's (AD), Parkinson's (PD) and prion diseases, are generally difficult to diagnose before irreversible damage to the central nervous system damage has occurred. Detection of the misfolded proteins that ultimately lead to these conditions offers a means for providing early detection and diagnosis of this class of disease. In this review, we discuss recent developments surrounding protein misfolding diseases with emphasis on the cytotoxic oligomers implicated in their aetiology. We also discuss the relationship of misfolded proteins with biological membranes. Finally, we discuss how far techniques for providing early diagnoses for PMDs have advanced and describe promising clinical approaches. We conclude that antibodies with specificity towards oligomeric species of AD and PD and lectins with specificity for particular glycosylation, show promise. However, it is not clear which approach may yield a reliable clinical test first. Relevance for patients: Individuals suffering from protein misfolding diseases will likely benefit form earlier, less-or even non-invasive diagnosis techniques. The current state and possible future directions for these are subject of this review.

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Section: Misfolded Proteins and The Lipid Profile Of The Membranesupporting

confidence: 62%

Detection of mis-folded protein aggregates from a clinical perspective

et al. 2016

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“…As we know, aggregation of Ab enhances its interaction ability with lipid membrane [23]. Ab aggregation-intermediates are more toxic to cell membrane than fibrils themselves [24].…”

Section: Cantilever-based Liposome Biosensormentioning

confidence: 99%

β-Amyloid Biomarker Detection for Alzheimer’s Disease

Grajales

Shuang

et al. 2017

J. Anal. Test.

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Alzheimer's disease (AD) is a neurodegenerative disease. It is a type of dementia and it mainly deals with thinking, memory and behavioral aspects. It is a progressive disease, which in course of time damages most sections of the brain. Beta amyloid peptides (Ab) have been recognized as potential biomarkers to monitor AD. The Ab protein is made up of 39-42 amino acids, which are the main components of the plaques found in the AD brain. This beta amyloid is toxic to the neurons and causes degeneration. In order to measure these biomarkers, nanobiosensing techniques are used. Timely monitoring of Ab levels helps in the detection of the irreversible disease called AD. These techniques fall in two categories, viz., in vitro and in vivo. Several techniques like electrochemical techniques, cantilever-based liposome biosensor, ELISA, PET scan, microdialysis, etc., are discussed further in the article. These techniques can prove to be effective methods for quantifying amyloid deposition within specific brain regions.

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“…Membranes support the better growth of amyloid fibrils [63]. Also the presence of lipid rafts may provide a singular environment to regulate fibril formation and aggregation [64].…”

Section: Inflammation and Membrane Damagementioning

confidence: 99%

“…(1) Saturated phospholipids and gel phase membranes support the growth of amyloid intermediates better [63, 68]. …”

Section: Inflammation and Membrane Damagementioning

confidence: 99%

Is membrane homeostasis the missing link between inflammation and neurodegenerative diseases?

Groot

Torrent

2015

Cell. Mol. Life Sci.

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Systemic inflammation and infections are associated with neurodegenerative diseases. Unfortunately, the molecular bases of this link are still largely undiscovered. We, therefore, review how inflammatory processes can imbalance membrane homeostasis and theorize how this may have an effect on the aggregation behavior of the proteins implicated in such diseases. Specifically, we describe the processes that generate such imbalances at the molecular level, and try to understand how they affect protein folding and localization. Overall, current knowledge suggests that microglia pro-inflammatory mediators can generate membrane damage, which may have an impact in terms of triggering or accelerating disease manifestation.

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Impact of phospholipid bilayer saturation on amyloid-β protein aggregation intermediate growth: A quartz crystal microbalance analysis

Cited by 24 publications

References 72 publications

Detection of mis-folded protein aggregates from a clinical perspective

Detection of mis-folded protein aggregates from a clinical perspective

β-Amyloid Biomarker Detection for Alzheimer’s Disease

Is membrane homeostasis the missing link between inflammation and neurodegenerative diseases?

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