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Amyloid beta

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https://www.readbyqxmd.com/read/28079198/oligomerization-of-fvflm-peptides-and-their-ability-to-inhibit-beta-amyloid-peptides-aggregation-consideration-as-a-possible-model
#1
M Kouza, A Banerji, A Kolinski, I A Buhimschi, A Kloczkowski
Preeclampsia, a pregnancy-specific disorder, shares typical pathophysiological features with protein misfolding disorders including Alzheimer's disease. Characteristic for preeclampsia is the involvement of multiple proteins of which fragments of SERPINA1 and β-amyloid co-aggregate in urine and placenta of preeclamptic women. To explore the biophysical basis of this interaction, we investigated the multidimensional efficacy of the FVFLM sequence in SERPINA1, as a model inhibitory agent of β-amyloid aggregation...
January 12, 2017: Physical Chemistry Chemical Physics: PCCP
https://www.readbyqxmd.com/read/28078911/c5a-increases-the-injury-to-primary-neurons-elicited-by-fibrillar-amyloid-beta
#2
Michael X Hernandez, Pouya Namiranian, Eric Nguyen, Maria I Fonseca, Andrea J Tenner
C5aR1, the proinflammatory receptor for C5a, is expressed in the central nervous system on microglia, endothelial cells, and neurons. Previous work demonstrated that the C5aR1 antagonist, PMX205, decreased amyloid pathology and suppressed cognitive deficits in two Alzheimer's Disease (AD) mouse models. However, the cellular mechanisms of this protection have not been definitively demonstrated. Here, primary cultured mouse neurons treated with exogenous C5a show reproducible loss of MAP-2 staining in a dose-dependent manner within 24 hr of treatment, indicative of injury to neurons...
February 2017: ASN Neuro
https://www.readbyqxmd.com/read/28074940/alpha7-nicotinic-acetylcholine-receptor-is-required-for-amyloid-pathology-in-brain-endothelial-cells-induced-by-glycoprotein-120-methamphetamine-and-nicotine
#3
Liqun Liu, Jingyi Yu, Li Li, Bao Zhang, Lingjuan Liu, Chun-Hua Wu, Ambrose Jong, Ding-An Mao, Sheng-He Huang
One of the most challenging issues in HIV-associated neurocognitive disorders (HAND) caused by HIV-1 virotoxins and drug abuse is the lack of understanding the underlying mechanisms that are commonly associated with disorders of the blood-brain barrier (BBB), which mainly consists of brain microvascular endothelial cells (BMEC). Here, we hypothesized that Glycoprotein 120 (gp120), methamphetamine (METH) and nicotine (NT) can enhance amyloid-beta (Aβ) accumulation in BMEC through Alpha7 nicotinic acetylcholine receptor (α7 nAChR)...
January 11, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28072821/maysin-and-its-flavonoid-derivative-from-centipedegrass-attenuates-amyloid-plaques-by-inducting-humoral-immune-response-with-th2-skewed-cytokine-response-in-the-tg-appswe-ps1de9-alzheimer-s-mouse-model
#4
Yuno Song, Hong-Duck Kim, Min-Kwon Lee, Il-Hwa Hong, Chung-Kil Won, Hyoung-Woo Bai, Seung Sik Lee, SungBeom Lee, Byung Yeoup Chung, Jae-Hyeon Cho
Alzheimer's disease (AD) is a slow, progressive neurodegenerative disease and the most common type of dementia in the elderly. The etiology of AD and its underlying mechanism are still not clear. In a previous study, we found that an ethyl acetate extract of Centipedegrass (CG) (i.e., EA-CG) contained 4 types of Maysin derivatives, including Luteolin, Isoorientin, Rhamnosylisoorientin, and Derhamnosylmaysin, and showed protective effects against Amyloid beta (Aβ) by inhibiting oligomeric Aβ in cellular and in vitro models...
2017: PloS One
https://www.readbyqxmd.com/read/28069541/a-bispecific-tribody-pet-radioligand-for-visualization-of-amyloid-beta-protofibrils-a-new-concept-for-neuroimaging
#5
Stina Syvänen, Xiaotian T Fang, Greta Hultqvist, Silvio R Meier, Lars Lannfelt, Dag Sehlin
Antibodies are highly specific for their target molecules, but their poor brain penetrance has restricted their use as PET ligands for imaging of targets within the CNS. The aim of this study was to develop an antibody-based radioligand, using the Tribody(TM) format, for PET imaging of soluble amyloid-beta (Aβ) protofibrils, which are suggested to cause neurodegeneration in Alzheimer's disease. Antibodies, even when expressed in smaller engineered formats, are large molecules that do not enter the brain in sufficient amounts for imaging purposes...
January 6, 2017: NeuroImage
https://www.readbyqxmd.com/read/28067349/the-synergistic-effect-between-klvff-and-self-assembly-chaperones-on-both-disaggregation-of-beta-amyloid-fibrils-and-reducing-consequent-toxicity
#6
Aoting Qu, Fan Huang, Ang Li, Huiru Yang, Hao Zhou, Jiafu Long, Linqi Shi
By combining KLVFF peptide and self-assembly chaperone we fabricate a new system to achieve the synchronization between Aβ fibril disaggregation and reducing toxicity of Aβ fragments (monomers or oligomers) that consequently formed. When the KLVFF peptides disaggregate fibrils into fragments, the hydrophobic domains of self-assembly chaperones promptly bind them at the same time. This binding blocks the re-aggregation of the fragments and their interaction with cells, and hence reduces the toxicity of these dangerous fragments...
January 9, 2017: Chemical Communications: Chem Comm
https://www.readbyqxmd.com/read/28067167/6-benzothiazolyl-ureas-thioureas-and-guanidines-are-potent-inhibitors-of-abad-17%C3%AE-hsd10-and-potential-drugs-for-alzheimer-s-disease-treatment-design-synthesis-and-in-vitro-evaluation
#7
Ondrej Benek, Lukas Hroch, Laura Aitken, Rafael Dolezal, Patrick Guest, Marketa Benkova, Ondrej Soukup, Karel Musil, Kamil Kuca, Terry K Smith, Frank Gunn-Moore, Kamil Musilek
BACKGROUND: The mitochondrial enzyme amyloid beta-binding alcohol dehydrogenase (ABAD) also known as 17β-hydroxysteroid dehydrogenase type 10 (17β-HSD10) has been connected with the pathogenesis of Alzheimer's disease (AD). ABAD/ 17β-HSD10 is a binding site for the amyloid-beta peptide (Aβ) inside the mitochondrial matrix where it exacerbates Aβ toxicity. Interaction between these two proteins triggers a series of events leading to mitochondrial dysfunction as seen in AD. METHODS: As ABAD's enzymatic activity is required for mediating Aβ toxicity, its inhibition presents a promising strategy for AD treatment...
January 9, 2017: Medicinal Chemistry
https://www.readbyqxmd.com/read/28066098/novel-strategies-for-alzheimer-s-disease-treatment-an-overview-of-anti-amyloid-beta-monoclonal-antibodies
#8
Katarzyna Rygiel
Alzheimer's disease (AD) is a multifactorial, progressive neurodegenerative disorder with a poor prognosis, and thus, novel therapies for AD are certainly needed in a growing population of elderly patients or asymptomatic individuals, who are at risk for AD, worldwide. It has been established that some AD biomarkers such as amyloid-beta load in the brain, precede the onset of the disease, by approximately 20 years. Therefore, the therapy to prevent or effectively treat AD has to be initiated before the emergence of symptoms...
November 2016: Indian Journal of Pharmacology
https://www.readbyqxmd.com/read/28064323/-heat-shock-protein-hsp70-reduces-the-secretion-of-tnf%C3%AE-by-neuroblastoma-cells-and-human-monocytes-induced-with-beta-amyloid-peptides
#9
M M Yurinskaya, V A Mit'kevich, M B Evgen'ev, A A Makarov, M G Vinokurov
The progress of neurodegeneration in Alzheimer's disease is closely associated with inflammatory processes in the brain tissues induced by beta-amyloid peptides (Aβ). In this paper, we showed that Aβ(1-42) and isoAβ(1-42) in human neuroblastoma cells SK-N-SH and promonocyte THP-1 activated the production of tumor necrosis factor (TNFα). Notably, isoAβ(1-42) had the strongest effect on the increase in the level of TNFα. The addition of recombinant heat-shock protein HSP70 reduces TNFα production induced by Aβ, which leads to a decrease in neuronal cell damage at the organism level...
November 2016: Molekuliarnaia Biologiia
https://www.readbyqxmd.com/read/28064322/-zinc-induced-interactions-of-the-metal-binding-domain-of-beta-amyloid-with-nucleic-acids-and-glycosaminoglycans
#10
S A Khmeleva, S A Kozin, Y Y Kiseleva, V A Mitkevich, A A Makarov, S P Radko
Zinc ions form complexes with β-amyloid peptides and play an important role in Alzheimer's disease pathogenesis. It has been demonstrated by turbidimetry and correlation spectroscopy that synthetic peptide Aβ16 representing the metal-binding domain of β-amyloid is able to interact with nucleic acids, chondroitin polysulfate, and dextran sulfates in the presence of zinc ions. The amino acid D7H substitution enhanced the peptide binding to polyanions, whereas the H6R and H6A-H13A substitutions abolished this interaction...
November 2016: Molekuliarnaia Biologiia
https://www.readbyqxmd.com/read/28063983/loss-of-laforin-or-malin-results-in-increased-drp1-level-and-concomitant-mitochondrial-fragmentation-in-lafora-disease-mouse-models
#11
Mamta Upadhyay, Saloni Agarwal, Pratibha Bhadauriya, Subramaniam Ganesh
Lafora disease (LD) is an autosomal recessive form of a fatal disorder characterized by the myoclonus epilepsy, ataxia, psychosis, dementia, and dysarthria. A hallmark of LD is the presence of abnormal glycogen inclusions called Lafora bodies in the affected tissues including the neurons. LD can be caused by defects either in the laforin phosphatase coded by the EPM2A gene or in the malin E3 ubiquitin ligase coded by the NHLRC1 gene. The mouse models of LD, created by the targeted disruption of the LD genes, display several neurodegenerative changes...
January 4, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28061031/inhibition-and-degradation-of-amyloid-beta-a%C3%AE-40-fibrillation-by-designed-small-pep-tide-a-combined-spectroscopy-microscopy-and-cell-toxicity-study
#12
Anirban Ghosh, Nibedita Pradhan, Swapna Bera, Aritreyee Datta, Janarthanan Krishnamoorthy, Nikhil R Jana, Anirban Bhunia
A designed non-toxic, non-hemolytic 11-residue peptide, NF11 (NAVRWSLMRPF) not only inhibits the aggregation of Amyloid beta (Aβ40) protein but also disaggregates the pre-formed oligomers and mature Aβ fibrils thereby reducing associated-toxicity. NMR experiments provide evidence of NF11's ability to inhibit fibril formation, primarily through interaction with the N-terminus region as well as the central hydrophobic cluster of Aβ40. NF11 has micro molar binding affinity towards both monomeric and aggregated species for efficient clearance of toxic aggregates...
January 6, 2017: ACS Chemical Neuroscience
https://www.readbyqxmd.com/read/28060279/quantitative-3d-in-silico-modeling-q3dism-of-cerebral-amyloid-beta-phagocytosis-in-rodent-models-of-alzheimer-s-disease
#13
Marie-Victoire Guillot-Sestier, Tara M Weitz, Terrence Town
Neuroinflammation is now recognized as a major etiological factor in neurodegenerative disease. Mononuclear phagocytes are innate immune cells responsible for phagocytosis and clearance of debris and detritus. These cells include CNS-resident macrophages known as microglia, and mononuclear phagocytes infiltrating from the periphery. Light microscopy has generally been used to visualize phagocytosis in rodent or human brain specimens. However, qualitative methods have not provided definitive evidence of in vivo phagocytosis...
December 26, 2016: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/28059487/%C3%AE-tocopheryl-phosphate-induces-vegf-expression-via-cd36-pi3k%C3%AE-in-thp-1-monocytes
#14
Jean-Marc Zingg, Angelo Azzi, Mohsen Meydani
The CD36 scavenger receptor binds several ligands and mediates ligand uptake and ligand-dependent signal transduction and gene expression, events that may involve CD36 internalization. Here we show that CD36 internalization in THP-1 monocytes is triggered by α-tocopherol (αT) and more strongly by α-tocopheryl phosphate (αTP) and EPC-K1, a phosphate diester of αTP and L-ascorbic acid. αTP-triggered CD36 internalization is prevented by the specific covalent inhibitor of selective lipid transport by CD36, sulfo-N-succinimidyl oleate (SSO)...
January 6, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/28056358/administrations-of-human-adult-ischemia-tolerant-mesenchymal-stem-cells-and-factors-reduce-amyloid-beta-pathology-in-a-mouse-model-of-alzheimer-s-disease
#15
Taoufiq Harach, Fabien Jammes, Charles Muller, Nicolas Duthilleul, Victoria Cheatham, Valentin Zufferey, David Cheatham, Yelizaveta A Lukasheva, Theo Lasser, Tristan Bolmont
The impact of human adult ischemia-tolerant mesenchymal stem cells (hMSCs) and factors (stem cell factors) on cerebral amyloid beta (Aβ) pathology was investigated in a mouse model of Alzheimer's disease (AD). To this end, hMSCs were administered intravenously to APPPS1 transgenic mice that normally develop cerebral Aβ. Quantitative reverse transcriptase polymerase chain reaction biodistribution revealed that intravenously delivered hMSCs were readily detected in APPPS1 brains 1 hour following administration, and dropped to negligible levels after 1 week...
November 24, 2016: Neurobiology of Aging
https://www.readbyqxmd.com/read/28054501/modulation-in-the-conformational-and-stability-attributes-of-the-alzheimer-s-disease-associated-amyloid-beta-mutants-and-their-favorable-stabilization-by-curcumin-molecular-dynamics-simulation-analysis
#16
Manika Awasthi, Swati Singh, Veda P Pandey, Upendra N Dwivedi
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive accumulation of amyloid-beta (Aβ) peptides in brain. In the present study, two familial Aβ42 mutations, namely A2V (harmful) and A2T (protective) have been analyzed and compared with the wild-type (WT) by performing all-atom molecular dynamics (MD) simulations in the absence and presence of curcumin, a well known inhibitor of Aβ plaque formation. Mutant A2V was found to exhibit highest stability followed by WT and mutant A2T in the absence of curcumin...
January 5, 2017: Journal of Biomolecular Structure & Dynamics
https://www.readbyqxmd.com/read/28054176/oleanane-triterpenoids-from-akebiae-caulis-exhibit-inhibitory-effects-on-a%C3%AE-42-induced-fibrillogenesis
#17
Md Anisuzzaman Chowdhury, Hae Ju Ko, Hwan Lee, Md Aminul Haque, Il-Seon Park, Dong-Sung Lee, Eun-Rhan Woo
Previous phytochemical investigations of Akebiae Caulis resulted in the isolation of triterpenes, triterpene glycosides, phenylethanoid glycosides and megastigmane glycoside. Amyloid beta (Aβ), the main component of the senile plaques detected in Alzheimer's disease, induces cell death. However, only a limited number of studies have addressed the biological and pharmacological effects of Akebiae Caulis. In particular, the inhibitory activity of Akebiae Caulis against Aβ42 fibrillogenesis remains unclear. Herein, a new triterpene glycoside, akequintoside F (1), along with nine known compounds pulsatilla saponin A (2), collinsonidin (3), akebonic acid (4), hederagenin (5), 1-(3',4'-dihydroxycinnamoyl) cyclopentane-2,3-diol (6), asperosaponin C (7), leontoside A (8), quinatic acid (9), and quinatoside A (10) were isolated from Akebiae Caulis using repeated column chromatography with silica gel, LiChroprep RP-18, and MCI gel...
January 4, 2017: Archives of Pharmacal Research
https://www.readbyqxmd.com/read/28051272/tgf-%C3%AE-1-factor-in-the-cerebrovascular-diseases-of-alzheimer-s-disease
#18
X Zhang, W-J Huang, W-W Chen
Transforming growth factor betas (TGF-βs) belong to three isoforms (TGF-β1, TGF-β2 and TGF-β3) members of a large pleiotropic superfamily of around 100 distinct proteins participating in the regulation of key events of development and disease, and tissue repair. In the central nervous system (CNS), all the three isoforms are produced by both glial and neuronal cells and are involved in essential tissue functions such as cell-cycle control, regulation of early development and differentiation, neuronal survival and astrocytes differentiation...
December 2016: European Review for Medical and Pharmacological Sciences
https://www.readbyqxmd.com/read/28049728/familial-alzheimer-s-disease-mutations-within-the-amyloid-precursor-protein-alter-the-aggregation-and-conformation-of-the-amyloid-beta-peptide
#19
Asa Hatami, Sanaz Monjazeb, Saskia Milton, Charles G Glabe
Most cases of Alzheimer's disease (AD) are sporadic, while a small percentage of AD cases, called familial AD (FAD), are associated with mutations in presinilins 1 and 2 and the amyloid precursor protein (APP). APP mutations falling within the Aβ sequence lead to a wide range of disease phenotypes. There is increasing evidence that distinct amyloid structures distinguished by amyloid conformation-dependent monoclonal antibodies have varying roles in pathology. It is possible that the phenotypic diversity of FAD associated with mutations within the Aβ sequence is due to differences in the conformations adopted by mutant Aβ peptides...
January 3, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28049401/alzheimer-s-disease-and-natural-products-future-regimens-emerging-from-nature
#20
Md Asiful Islam, Shahad Saif Khandker, Fahmida Alam, Md Ibrahim Khalil, Mohammad Amjad Kamal, Siew Hua Gan
Alzheimer's disease (AD), which largely affects the elderly, has become a global burden. Patients with AD have both short- and long-term memory impairments. The neuronal loss in AD occurs due to abnormally folded amyloid beta proteins and aggregation of hyperphosphorylated tau proteins in the brain. Eventually, amyloid plaques and neurofibrillary tangles are formed, which subsequently disintegrate the neuronal transport system. There are several factors which are involved in AD pathogenesis, including oxidative stress, inflammation and the presence of metal ions...
January 3, 2017: Current Topics in Medicinal Chemistry
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