Polyamines and its analogue modulates amyloid fibrillation in lysozyme: A comparative investigation

This study, thus, potentiates, the development of a polyamine analogue that can perform as an effective inhibitor targeted towards aggregation of amyloidogenic proteins.Graphical abstract
Source: Biochimica et Biophysica Acta (BBA) General Subjects - Category: Biochemistry Source Type: research

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Abstract Misfolded and natively disordered globular proteins tend to aggregate together in an interwoven fashion to form fibrous, proteinaceous deposits referred to as amyloid fibrils. Formation and deposition of such insoluble fibrils are the characteristic features of a broad group of diseases, known as amyloidosis. Some of these proteins are known to cause several degenerative disorders in humans, such as Amyloid-Beta (Aβ) in Alzheimer's disease (AD), human Islet Amyloid Polypeptide (hIAPP, amylin) in type 2 diabetes, α-synuclein (α-syn) in Parkinson's disease (PD) and so on. The fact that thes...
Source: Archives of Biochemistry and Biophysics - Category: Biochemistry Authors: Tags: Arch Biochem Biophys Source Type: research
CONCLUSION: C3 and C7 are novel 4-methylthiocoumarin derivatives that can be used as a lead for alleviation and symptoms associated with protein aggregation disorders. PMID: 32933456 [PubMed - as supplied by publisher]
Source: Current Pharmaceutical Biotechnology - Category: Biotechnology Authors: Tags: Curr Pharm Biotechnol Source Type: research
We report a new class of natural-product-inspired covalent inhibitors of telomerase that target the catalytic active site. Age-Related Epigenetic Changes that Suppress Mitochondrial Function https://www.fightaging.org/archives/2020/03/age-related-epigenetic-changes-that-suppress-mitochondrial-function/ Today's open access research reports on two specific epigenetic changes observed in old individuals that act to reduce mitochondrial function. This joins an existing list of genes for which expression changes are known to impact mitochondrial function with age. A herd of hundreds of mitochondria are found ...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
Abstract Accumulation of amyloid fibrils in organism accompanies many serious diseases, such as Alzheimer's and Parkinson's diseases, diabetes, prion diseases, etc. It is generally accepted that amyloids are highly resistant to degradation, which complicates their elimination in vivo and is one of the reasons for their pathogenicity. However, using a wide range of physicochemical approaches and specially elaborated method for the tested samples preparation by equilibrium microdialysis technique, it is proved that the stability of amyloids is greatly exaggerated. It turned out that amyloid fibrils formed from at le...
Source: International Journal of Biological Macromolecules - Category: Biochemistry Authors: Tags: Int J Biol Macromol Source Type: research
Publication date: Available online 13 December 2019Source: Journal of Pharmaceutical AnalysisAuthor(s): Jiaojiao Hu, Huiyong Sun, Haiping Hao, Qiuling ZhengAbstractAmyloid fibrils are found in systemic amyloidosis diseases such as Alzheimer's disease, Parkinson's disease, and type II diabetes. Currently, these diseases are diagnosed by observation of fibrils or plaques, which is an ineffective method for early diagnosis and treatment of disease. The goal of this study was to develop a simple and quick method to predict the possibility and speed of fibril formation before its occurrence. Oligomers generated from seven repre...
Source: Journal of Pharmaceutical Analysis - Category: Drugs & Pharmacology Source Type: research
In conclusion, T2D impairs vascular function by dysregulated autophagy. Therefore, autophagy could be a potential target for overcoming diabetic microvascular complications. To What Degree Does Loss of Skeletal Muscle with Age Contribute to Immunosenescence? https://www.fightaging.org/archives/2019/11/to-what-degree-does-loss-of-skeletal-muscle-with-age-contribute-to-immunosenescence/ Sarcopenia, the progressive loss of muscle mass and strength, is characteristic of aging. A perhaps surprisingly large fraction of the losses can be averted by strength training, but there are nonetheless inexorable process...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
In conclusion, we show here that sEVs are responsible for mediating paracrine senescence and speculate that they could be involved in inducing bystander senescence during therapy-induced senescence or aging. In fact, when compared to soluble factors, sEVs have different biophysical and biochemical properties as they have a longer lifespan than do soluble factors and they are more resistant to protease degradation. The idea that blocking sEV secretion could be a potential therapeutic approach to alleviate senescence "spreading" during chemotherapy-induced senescence or in aging tissues presents itself as a very at...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
In conclusion, there is solid evidence that obesity deregulates cellular mechanisms related to nutrient sensing. Altered Intercellular Communication It is accepted that aging impacts the organism at the cellular level, but also decreases the capacity of cells of an organism to interact. During aging, there is a decreased communication at the neuronal, neuroendocrine, and endocrine levels. Two of the most compelling examples of impaired communication are inflammaging and immunosenescence. The inflammaging phenotype results in elevated cytokines. These cytokines can accelerate and propagate the aging process. T...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
Many neurodegenerative conditions are associated with the accumulation of forms of metabolic waste in the central nervous system, protein aggregates that form solid deposits between or within cells. Tauopathies such as frontotemporal dementia are associated with tau aggregates, synucleinopathies such as Parkinson's disease with α-synuclein, and amyloidoses with varying forms of amyloid, such as the amyloid-β found in elevated amounts in Alzheimer's disease patients. Alzheimer's itself is an amyloidosis that also becomes a tauopathy in its later stages. These protein aggregates and their surrounding halos of harm...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs
Abstract Protein and peptides are converted from their soluble forms into highly ordered fibrillar aggregates under various conditions inside the cell. Such transitions confer diverse neurodegenerative diseases including Alzheimer's disease, Huntington's disease Prion's disease, Parkinson's disease, polyQ and share abnormal folding of potentially cytotoxic protein species linked with degeneration and death of precise neuronal populations. Presently, major advances are made to understand and get detailed insight into the structural basis and mechanism of amyloid formation, cytotoxicity and therapeutic approaches to...
Source: International Journal of Biological Macromolecules - Category: Biochemistry Authors: Tags: Int J Biol Macromol Source Type: research
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