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Amyloid-β

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https://www.readbyqxmd.com/read/28453493/s-adenosylmethionine-attenuates-oxidative-stress-and-neuroinflammation-induced-by-amyloid-%C3%AE-through-modulation-of-glutathione-metabolism
#1
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
#2
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
#3
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
#4
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
#5
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/28453484/can-better-management-of-periodontal-disease-delay-the-onset-and-progression-of-alzheimer-s-disease
#6
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
#7
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
#8
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/28453476/reduced-cerebral-blood-flow-in-mild-cognitive-impairment-assessed-using-phase-contrast-mri
#9
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/28448946/oral-administration-of-methysticin-improves-cognitive-deficits-in-a-mouse-model-of-alzheimer-s-disease
#10
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/28447730/pioglitazone-ameliorates-a%C3%AE-42-deposition-in-rats-with-diet-induced-insulin-resistance-associated-with-akt-gsk3%C3%AE-activation
#11
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
#12
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/28445753/pyroglutamate-modified-amyloid-%C3%AE-3-42-shows-%C3%AE-helical-intermediates-before-amyloid-formation
#13
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/28442216/trem2-microglia-and-neurodegenerative-diseases
#14
REVIEW
Felix L Yeh, David V Hansen, Morgan Sheng
Alzheimer's disease (AD) is the most common form of dementia and the 6th leading cause of death in the US. The neuropathological hallmarks of the disease are extracellular amyloid-β (Aβ) plaques and intraneuronal hyperphosphorylated tau aggregates. Genetic variants of TREM2 (triggering receptor expressed on myeloid cells 2), a cell-surface receptor expressed selectively in myeloid cells, greatly increase the risk of AD, implicating microglia and the innate immune system as pivotal factors in AD pathogenesis...
April 22, 2017: Trends in Molecular Medicine
https://www.readbyqxmd.com/read/28441965/evaluation-of-a-dna-a%C3%AE-42-vaccine-in-adult-rhesus-monkeys-macaca-mulatta-antibody-kinetics-and-immune-profile-after-intradermal-immunization-with-full-length-dna-a%C3%AE-42-trimer
#15
Doris Lambracht-Washington, Min Fu, Pat Frost, Roger N Rosenberg
BACKGROUND: Aggregated amyloid-β peptide 1-42 (Aβ42), derived from the cellular amyloid precursor protein, is one of the pathological hallmarks of Alzheimer's disease (AD). Although active immunization against Aβ42 peptide was successful in AD mouse models and led to removal of plaques and improved memory, a similar clinical trial in humans (Aβ42 peptide immunization with QS-21 adjuvant) was stopped in phase II, when 6% of the treated patients developed encephalitis. Currently ongoing passive immunizations with the injection of preformed monoclonal antibodies against different epitopes within the Aβ1-42 peptide, which do not lead to activation of the immune system, have shown some effects in slowing AD pathology...
April 26, 2017: Alzheimer's Research & Therapy
https://www.readbyqxmd.com/read/28441961/the-influence-of-insulin-resistance-on-cerebrospinal-fluid-and-plasma-biomarkers-of-alzheimer-s-pathology
#16
REVIEW
Sarah Westwood, Benjamine Liu, Alison L Baird, Sneha Anand, Alejo J Nevado-Holgado, Danielle Newby, Maria Pikkarainen, Merja Hallikainen, Johanna Kuusisto, Johannes R Streffer, Gerald Novak, Kaj Blennow, Ulf Andreasson, Henrik Zetterberg, Ulf Smith, Markku Laakso, Hilkka Soininen, Simon Lovestone
BACKGROUND: Insulin resistance (IR) has previously been associated with an increased risk of developing Alzheimer's disease (AD), although the relationship between IR and AD is not yet clear. Here, we examined the influence of IR on AD using plasma and cerebrospinal fluid (CSF) biomarkers related to IR and AD in cognitively healthy men. We also aimed to characterise the shared protein signatures between IR and AD. METHODS: Fifty-eight cognitively healthy men, 28 IR and 30 non-IR (age and APOE ε4 matched), were drawn from the Metabolic Syndrome in Men study in Kuopio, Finland...
April 26, 2017: Alzheimer's Research & Therapy
https://www.readbyqxmd.com/read/28441758/acteoside-and-isoacteoside-protect-amyloid-%C3%AE-peptide-induced-cytotoxicity-cognitive-deficit-and-neurochemical-disturbances-in-vitro-and-in-vivo
#17
Young-Ji Shiao, Muh-Hwan Su, Hang-Ching Lin, Chi-Rei Wu
Acteoside and isoacteoside, two phenylethanoid glycosides, coexist in some plants. This study investigates the memory-improving and cytoprotective effects of acteoside and isoacteoside in amyloid β peptide 1-42 (Aβ 1-42)-infused rats and Aβ 1-42-treated SH-SY5Y cells. It further elucidates the role of amyloid cascade and central neuronal function in these effects. Acteoside and isoacteoside ameliorated cognitive deficits, decreased amyloid deposition, and reversed central cholinergic dysfunction that were caused by Aβ 1-42 in rats...
April 24, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28439555/structural-and-biochemical-differences-between-the-notch-and-the-amyloid-precursor-protein-transmembrane-domains
#18
Catherine L Deatherage, Zhenwei Lu, Brett M Kroncke, Sirui Ma, Jarrod A Smith, Markus W Voehler, Robert L McFeeters, Charles R Sanders
γ-Secretase cleavage of the Notch receptor transmembrane domain is a critical signaling event for various cellular processes. Efforts to develop inhibitors of γ-secretase cleavage of the amyloid-β precursor C99 protein as potential Alzheimer's disease therapeutics have been confounded by toxicity resulting from the inhibition of normal cleavage of Notch. We present biochemical and structural data for the combined transmembrane and juxtamembrane Notch domains (Notch-TMD) that illuminate Notch signaling and that can be compared and contrasted with the corresponding traits of C99...
April 2017: Science Advances
https://www.readbyqxmd.com/read/28438208/amelioration-of-amyloid-%C3%AE-induced-deficits-by-dcr3-in-an-alzheimer-s-disease-model
#19
Yi-Ling Liu, Wei-Ting Chen, Yu-Yi Lin, Po-Hung Lu, Shie-Liang Hsieh, Irene Han-Juo Cheng
BACKGROUND: Microglia mediate amyloid-beta peptide (Aβ)-induced neuroinflammation, which is one of the key events in the pathogenesis of Alzheimer's disease (AD). Decoy receptor 3 (DcR3)/TNFRSF6B is a pleiotropic immunomodulator that promotes macrophage differentiation toward the M2 anti-inflammatory phenotype. Based on its role as an immunosupressor, we examined whether DcR3 could alleviate neuroinflammation and AD-like deficits in the central nervous system. METHOD: We crossed human APP transgenic mice (line J20) with human DcR3 transgenic mice to generate wild-type, APP, DcR3, and APP/DcR3 mice for pathological analysis...
April 24, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28436304/the-pten-inhibitor-bpv-pic-promotes-neuroprotection-against-amyloid-%C3%AE-peptide-25-35-induced-oxidative-stress-and-neurotoxicity
#20
Xiao-Ying Liu, Li-Jing Zhang, Zhou Chen, Li-Bin Liu
OBJECTIVES: The aim of this study was to elucidate the mechanism underlying the neuroprotective effects of the phosphatase and tensin homolog (PTEN) inhibitor, bisperoxovanadium-pic [bpV(pic)]. METHODS: We determined the effects of bpV(pic) on amyloid-β-peptide-(25-35)-induced neurotoxicity, particularly intracellular reactive oxygen species (ROS) production and mitochondria-mediated apoptotic signaling, in a human neuroblastoma (SH-SY5Y) cell model. RESULTS: We found that exposure of SH-SY5Y cells to amyloid β peptides (Aβ25-35) resulted in a significant reduction in cell viability accompanied by increased lactate dehydrogenase (LDH) release, elevated levels of intracellular ROS, and decreased superoxide dismutase (SOD) activities, all of which were reversed by co-treatment with bpV(pic)...
April 23, 2017: Neurological Research
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