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https://www.readbyqxmd.com/read/28453927/tir-domain-containing-adapter-inducing-interferon-%C3%AE-trif-forms-filamentous-structures-whose-pro-apoptotic-signalling-is-terminated-by-autophagy
#1
I E Gentle, K T McHenry, A Weber, A Metz, O Kretz, D Porter, G Häcker
The formation of amyloid-like protein structures has recently emerged as a feature in signal transduction, particularly in innate immunity. These structures appear to depend on defined domains for their formation but likely also require dedicated ways to terminate signalling. We here define the innate immunity protein/Toll-like receptor adaptor TRIF as a novel platform of fibril formation and probe signal initiation through TRIF as well as its termination in toll-like receptor 3 (TLR3)-stimulated melanoma cells...
April 28, 2017: FEBS Journal
https://www.readbyqxmd.com/read/28453493/s-adenosylmethionine-attenuates-oxidative-stress-and-neuroinflammation-induced-by-amyloid-%C3%AE-through-modulation-of-glutathione-metabolism
#2
Qian Li, Jing Cui, Chen Fang, Min Liu, Guowen Min, Liang Li
Oxidative stress and neuroinflammation are mainly involved in the pathogenic mechanisms of Alzheimer's disease (AD). Amyloid-β (Aβ), the main component of senile plaques, is a kind of strong inducer of oxidative stress. Glutathione is an endogenous antioxidant protecting cells from oxidative injury. S-adenosylmethionine (SAM) produced in the methionine cycle is the primary methyl donor and the precursor of glutathione. In this study, the Aβ intrahippocampal injection rat model and cultured SH-SY5Y cells were used to explore the neuroprotective effect of SAM...
April 28, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28453492/quantification-of-butyrylcholinesterase-activity-as-a-sensitive-and-specific-biomarker-of-alzheimer-s-disease
#3
Ian R Macdonald, Selena P Maxwell, G Andrew Reid, Meghan K Cash, Drew R DeBay, Sultan Darvesh
Amyloid-β (Aβ) plaques are a neuropathological hallmark of Alzheimer's disease (AD); however, a significant number of cognitively normal older adults can also have Aβ plaques. Thus, distinguishing AD from cognitively normal individuals with Aβ plaques (NwAβ) based on Aβ plaque detection is challenging. It has been observed that butyrylcholinesterase (BChE) accumulates in plaques preferentially in AD. Thus, detecting BChE-associated plaques has the potential as an improved AD biomarker. We present Aβ, thioflavin-S, and BChE quantification of 26 postmortem brain tissues; AD (n = 8), NwAβ (n = 6), cognitively normal without plaques (n = 8), and other common dementias including corticobasal degeneration, frontotemporal dementia with tau, dementia with Lewy bodies, and vascular dementia...
April 28, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28453491/neurofibrillary-tangles-of-a%C3%AE-x-40-in-alzheimer-s-disease-brains
#4
Ana-María Lacosta, Daniel Insua, Hassnae Badi, Pedro Pesini, Manuel Sarasa
The two pathognomonic lesions in the brain of AD patients are senile plaques and intraneuronal neurofibrillary tangles (NFT). Previous studies have demonstrated that amyloid-β (Aβ) is a component of both senile plaques and NFTs, and have showed that intracellular accumulation of Aβ is toxic for cells and precedes the appearance of extracellular amyloid deposits. Here we report that there are numerous intraneuronal NFT and extraneuronal NFT immunoreactive for Aβx-40 in which there is no co-localization with tau staining suggesting the existence of two different neurodegenerating populations associated with the intracellular accumulation of either tau protein or Aβx-40 in AD...
April 28, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28453490/plasma-amyloid-%C3%AE-and-alzheimer-s-disease-related-changes-in-late-life-depression
#5
Chiemi Yamazaki, Toshio Tamaoki, Akihiko Nunomura, Kenichi Tamai, Kazuyuki Yasuda, Nobutaka Motohashi
To elucidate an involvement of amyloid dysmetabolism in the pathophysiology of depression, we investigated associations of plasma amyloid-β (Aβ) levels with Alzheimer's disease-related changes in neuroimaging and cognitive dysfunction in patients with late-life depression. Higher plasma Aβ40, but not Aβ42 nor Aβ40/Aβ42 ratio, was associated with higher degree of parahippocampal atrophy and lower verbal fluency performance. Indeed, high plasma Aβ40 predicted poor cognitive prognosis of depressed patients with mild cognitive impairment...
April 25, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28453488/assessment-of-novel-curcumin-derivatives-as-potent-inhibitors-of-inflammation-and-amyloid-%C3%AE-aggregation-in-alzheimer-s-disease
#6
Johant Lakey-Beitia, Yisett González, Deborah Doens, David E Stephens, Ricardo Santamaría, Enrique Murillo, Marcelino Gutiérrez, Patricia L Fernández, K S Rao, Oleg V Larionov, Armando A Durant-Archibold
Alzheimer's disease (AD) is the most common neurodegenerative disorder affecting the elderly population worldwide. Brain inflammation plays a key role in the progression of AD. Deposition of senile plaques in the brain stimulates an inflammatory response with the overexpression of pro-inflammatory mediators, such as the neuroinflammatory cytokine. interleukin-6. Curcumin has been revealed to be a potential agent for treating AD following different neuroprotective mechanisms, such as inhibition of aggregation and decrease in brain inflammation...
April 25, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28453487/neuropsychiatric-symptoms-and-alzheimer-s-disease-biomarkers-predict-driving-decline-brief-report
#7
Ganesh M Babulal, Sarah H Stout, Denise Head, David M Holtzman, Anne M Fagan, John C Morris, Catherine M Roe
We examined whether neuropsychiatric symptoms (NPS) interact with cerebrospinal fluid (CSF) biomarkers (amyloid-β42 [Aβ42], tau, phosphorylated tau181 [ptau181], tau/Aβ42, and ptau181/Aβ42) of Alzheimer's disease pathology to predict driving decline among cognitively-normal older adults (N = 116) aged ≥65. Cox proportional hazards models examined time to receiving a rating of marginal or fail on the driving test. Age, education, and gender were adjusted in the models. Participants with more abnormal CSF (Aβ42, tau/Aβ42, ptau181/Aβ42) and NPS were faster to receive a marginal/fail on the road test compared to those without NPS...
April 28, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28453484/can-better-management-of-periodontal-disease-delay-the-onset-and-progression-of-alzheimer-s-disease
#8
Alice Harding, Sarita Robinson, St John Crean, Sim K Singhrao
A risk factor relationship exists between periodontal disease and Alzheimer's disease (AD) via tooth loss, and improved memory following dental intervention. This links the microbial contribution from indigenous oral periodontal pathogens to the manifestation of chronic conditions, such as AD. Here, we use Porphyromonas gingivalis infection to illustrate its effect on mental health. P. gingivalis infection, in its primary sub-gingival niche, can cause polymicrobial synergy and dysbiosis. Dysbiosis describes the residency of select commensals from the oral cavity following co-aggregation around the dominant keystone pathogen, such as P...
April 25, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28453483/remyelination-a-potential-therapeutic-strategy-for-alzheimer-s-disease
#9
Junjun Sun, Hong Zhou, Feng Bai, Zhijun Zhang, Qingguo Ren
Myelin is a lipid-rich multilamellar membrane that wraps around long segments of neuronal axons and it increases the conduction of action potentials, transports the necessary trophic support to the neuronal axons, and reduces the energy consumed by the neuronal axons. Together with axons, myelin is a prerequisite for the higher functions of the central nervous system and complex forms of network integration. Myelin impairments have been suggested to lead to neuronal dysfunction and cognitive decline. Accumulating evidence, including brain imaging and postmortem and genetic association studies, has implicated myelin impairments in Alzheimer's disease (AD)...
April 28, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28453480/a-multifunctional-biocompatible-drug-candidate-is-highly-effective-in-delaying-pathological-signs-of-alzheimer-s-disease-in-5xfad-mice
#10
Hadar Segal-Gavish, Ortal Danino, Yael Barhum, Tali Ben-Zur, Ella Shai, David Varon, Daniel Offen, Bilha Fischer
BACKGROUND: Metal-ion-chelation was suggested to prevent zinc and copper ions-induced amyloid-β (Aβ) aggregation and oxidative stress, both implicated in the pathophysiology of Alzheimer's disease (AD). In a quest for biocompatible metal-ion chelators potentially useful for AD therapy, we previously tested a series of nucleoside 5'-phosphorothioate derivatives as agents for decomposition of Cu(I)/Cu(II)/Zn(II)-Aβ-aggregates, and as inhibitors of OH radicals formation in Cu(I) or Fe(II) /H2O2 solution...
April 28, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28453479/cognitive-domain-dispersion-association-with-alzheimer-s-disease-pathology
#11
Michael Malek-Ahmadi, Sophie Lu, YanYan Chan, Sylvia E Perez, Kewei Chen, Elliott J Mufson
Within neuropsychology, the term dispersion refers to the degree of variation in performance between different cognitive domains for an individual. Previous studies have demonstrated that cognitively normal individuals displaying higher dispersion are at an increased risk for progressing to mild cognitive impairment (MCI) and Alzheimer's disease (AD). Therefore, we determined 1) whether increased dispersion in older adults was associated with amyloid plaques and neurofibrillary tangles (NFTs) and 2) whether increased cognitive dispersion accurately differentiated MCI and AD from non-cognitively impaired (NCI) individuals...
April 28, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28453476/reduced-cerebral-blood-flow-in-mild-cognitive-impairment-assessed-using-phase-contrast-mri
#12
Reyes García de Eulate, Irene Goñi, Alvaro Galiano, Marta Vidorreta, Miriam Recio, Mario Riverol, José L Zubieta, María A Fernández-Seara
There is increasing evidence of a vascular contribution to Alzheimer's disease (AD). In some cases, prior work suggests that chronic brain hypoperfusion could play a prime pathogenic role contributing to the accumulation of amyloid-β,while other studies favor the hypothesis that vascular dysfunction and amyloid pathology are independent, although synergistic, mechanisms contributing to cognitive impairment. Vascular dysfunction can be evaluated by assessing cerebral blood flow impairment. Phase contrast velocity mapping by MRI offers a non-invasive means of quantifying the total inflow of blood to the brain...
April 25, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28448956/concentration-dependent-switch-in-the-kinetic-pathway-of-lysozyme-fibrillation-spectroscopic-and-microscopic-analysis
#13
E Kiran Kumar, Deepak Kumar Prasad, N Prakash Prabhu
Formation of amyloid fibrils is found to be a general tendency of many proteins. Investigating the kinetic mechanisms and structural features of the intermediates and the final fibrillar state is essential to understand their role in amyloid diseases. Lysozyme, a notable model protein for amyloidogenic studies, readily formed fibrils in vitro at neutral pH in the presence of urea. It, however, showed two different kinetic pathways under varying urea concentrations when probed with thioflavin T (ThT) fluorescence...
April 17, 2017: Spectrochimica Acta. Part A, Molecular and Biomolecular Spectroscopy
https://www.readbyqxmd.com/read/28448946/oral-administration-of-methysticin-improves-cognitive-deficits-in-a-mouse-model-of-alzheimer-s-disease
#14
Athanassios Fragoulis, Stephanie Siegl, Markus Fendt, Sandra Jansen, Ulf Soppa, Lars-Ove Brandenburg, Thomas Pufe, Joachim Weis, Christoph Jan Wruck
INTRODUCTION: There is increasing evidence for the involvement of chronic inflammation and oxidative stress in the pathogenesis of Alzheimer's disease (AD). Nuclear factor erythroid 2-related factor 2 (Nrf2) is an anti-inflammatory transcription factor that regulates the oxidative stress defense. Our previous experiments demonstrated that kavalactones protect neuronal cells against Amyloid β (Aβ)-induced oxidative stress in vitro by Nrf2 pathway activation. Here, we tested an in vivo kavalactone treatment in a mouse model of AD...
April 19, 2017: Redox Biology
https://www.readbyqxmd.com/read/28448032/a-tailored-hplc-purification-protocol-that-yields-high-purity-amyloid-beta-42-and-amyloid-beta-40-peptides-capable-of-oligomer-formation
#15
Christopher J A Warner, Subrata Dutta, Alejandro R Foley, Jevgenij A Raskatov
Amyloidogenic peptides such as the Alzheimer's disease-implicated Amyloid beta (Aβ), can present a significant challenge when trying to obtain high purity material. Here we present a tailored HPLC purification protocol to produce high-purity amyloid beta 42 (Aβ42) and amyloid beta 40 (Aβ40) peptides. We have found that the combination of commercially available hydrophobic poly(styrene/divinylbenzene) stationary phase, polymer laboratory reverse phase - styrenedivinylbenzene (PLRP-S) under high pH conditions, enables the attainment of high purity (>95%) Aβ42 in a single chromatographic run...
March 27, 2017: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/28447730/pioglitazone-ameliorates-a%C3%AE-42-deposition-in-rats-with-diet-induced-insulin-resistance-associated-with-akt-gsk3%C3%AE-activation
#16
Sisi Yang, Zhe Chen, Ming Cao, Renjie Li, Zhigang Wang, Muxun Zhang
Pioglitazone may have potential benefits as an alternative therapeutic treatment for patients with Alzheimer's disease (AD), particularly in individuals that also have comorbid diabetes; however, the mechanisms of action remain unclear. The present study aimed to explore the effects of pioglitazone on amyloid β, isoform 42 (Aβ42) deposition in rats with diet‑induced insulin resistance (IR). Diet‑induced IR model rats were established in the presence or absence of pioglitazone. Plasma glucose and insulin levels, and cerebrospinal fluid insulin levels were measured; in addition, hippocampal tissues were collected for immunohistochemical analysis of Aβ42 expression...
March 16, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28446944/protective-effects-of-proline-rich-peptide-in-a-rat-model-of-alzheimer-disease-an-electrophysiological-study
#17
Naser Khalaji, John Sarkissian, Vergine Chavushyan, Vaghinak Sarkisian
INTRODUCTION: Alzheimer disease (AD) is the most common form of dementia in the elderly that slowly destroys memory and cognitive functions. The disease has no cure and leads to significant structural and functional brain abnormalities. To facilitate the treatment of this disease, we aimed to investigate proline-rich peptide (PRP-1) action of hypothalamus on hippocampal (HP) neurons and dynamics of their recovery, after intracerebroventricular (ICV) injection of amyloid-β (Aβ). METHODS: Experiments were carried out on 24 adult, male Albino rats (average weight: 230±30 g)...
January 2017: Basic and Clinical Neuroscience
https://www.readbyqxmd.com/read/28446186/fingolimod-attenuates-experimental-autoimmune-neuritis-and-contributes-to-schwann-cell-mediated-axonal-protection
#18
Björn Ambrosius, Kalliopi Pitarokoili, Lisa Schrewe, Xiomara Pedreiturria, Jeremias Motte, Ralf Gold
BACKGROUND: Fingolimod, a sphingosine-1-phosphate receptor modulator with well-described immunomodulatory properties involving peripheral immune cell trafficking, was the first oral agent approved for the treatment of relapsing remitting multiple sclerosis. Analogous immunomodulatory treatment options for chronic peripheral autoimmune neuropathies are lacking. METHODS: We tested fingolimod in the animal model of experimental autoimmune neuritis in Lewis rat. Six to eight-week-old female rats were immunized with P2 peptide and from this day on treated with fingolimod...
April 26, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28445753/pyroglutamate-modified-amyloid-%C3%AE-3-42-shows-%C3%AE-helical-intermediates-before-amyloid-formation
#19
Christina Dammers, Kerstin Reiss, Lothar Gremer, Justin Lecher, Tamar Ziehm, Matthias Stoldt, Melanie Schwarten, Dieter Willbold
Pyroglutamate-modified amyloid-β (pEAβ) has been described as a relevant Aβ species in Alzheimer's-disease-affected brains, with pEAβ (3-42) as a dominant isoform. Aβ (1-40) and Aβ (1-42) have been well characterized under various solution conditions, including aqueous solutions containing trifluoroethanol (TFE). To characterize structural properties of pEAβ (3-42) possibly underlying its drastically increased aggregation propensity compared to Aβ (1-42), we started our studies in various TFE-water mixtures and found striking differences between the two Aβ species...
April 25, 2017: Biophysical Journal
https://www.readbyqxmd.com/read/28445751/curcumin-dictates-divergent-fates-for-the-central-salt-bridges-in-amyloid-%C3%AE-40-and-amyloid-%C3%AE-42
#20
Bappaditya Chandra, Venus Singh Mithu, Debanjan Bhowmik, Anand Kant Das, Bankanidhi Sahoo, Sudipta Maiti, Perunthiruthy K Madhu
There are three specific regions in the Amyloid beta (Aβ) peptide sequence where variations cause enhanced toxicity in Alzheimer's disease: the N-terminus, the central salt bridge, and the C-terminus. Here, we investigate if there is a close conformational connection between these three regions, which may suggest a concerted mechanism of toxicity. We measure the effects of Zn(2+) and curcumin on Aβ40, and compare these with their previously reported effects on Aβ42. Aβ42 and Aβ40 differ only near the C-terminus, where curcumin interacts, while Zn(2+) interacts near the N-terminus...
April 25, 2017: Biophysical Journal
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