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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/28453488/assessment-of-novel-curcumin-derivatives-as-potent-inhibitors-of-inflammation-and-amyloid-%C3%AE-aggregation-in-alzheimer-s-disease
#4
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/28453483/remyelination-a-potential-therapeutic-strategy-for-alzheimer-s-disease
#5
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/28453479/cognitive-domain-dispersion-association-with-alzheimer-s-disease-pathology
#6
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/28442216/trem2-microglia-and-neurodegenerative-diseases
#7
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
#8
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/28441426/identification-of-genes-associated-with-dissociation-of-cognitive-performance-and-neuropathological-burden-multistep-analysis-of-genetic-epigenetic-and-transcriptional-data
#9
Charles C White, Hyun-Sik Yang, Lei Yu, Lori B Chibnik, Robert J Dawe, Jingyun Yang, Hans-Ulrich Klein, Daniel Felsky, Alfredo Ramos-Miguel, Konstantinos Arfanakis, William G Honer, Reisa A Sperling, Julie A Schneider, David A Bennett, Philip L De Jager
INTRODUCTION: The molecular underpinnings of the dissociation of cognitive performance and neuropathological burden are poorly understood, and there are currently no known genetic or epigenetic determinants of the dissociation. METHODS AND FINDINGS: "Residual cognition" was quantified by regressing out the effects of cerebral pathologies and demographic characteristics on global cognitive performance proximate to death. To identify genes influencing residual cognition, we leveraged neuropathological, genetic, epigenetic, and transcriptional data available for deceased participants of the Religious Orders Study (n = 492) and the Rush Memory and Aging Project (n = 487)...
April 2017: PLoS Medicine
https://www.readbyqxmd.com/read/28438208/amelioration-of-amyloid-%C3%AE-induced-deficits-by-dcr3-in-an-alzheimer-s-disease-model
#10
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/28432017/dual-functional-nanoparticles-for-precise-drug-delivery-to-alzheimer-s-disease-lesions-targeting-mechanisms-pharmacodynamics-and-safety
#11
Xiaoyao Zheng, Chi Zhang, Qian Guo, Xu Wan, Xiayan Shao, Qingfeng Liu, Qizhi Zhang
Alzheimer's disease (AD) is the most common form of dementia and is characterized by the cerebral accumulation of extracellular amyloid plaques. In a previous study, this histopathological hallmark was used as a target on a dual-functional nanoparticle (TQNP) to deliver biotechnological drugs, such as the H102 peptide, a β-sheet breaker, to AD lesions precisely. This delivery system could reduce the amyloid-β (Aβ) burden in the brains of AD model mice, as well as ameliorated the memory impairment of the mice...
April 18, 2017: International Journal of Pharmaceutics
https://www.readbyqxmd.com/read/28429406/haplodeficiency-of-cathepsin-d-does-not-affect-cerebral-amyloidosis-and-autophagy-in-app-ps1-transgenic-mice
#12
Shaowu Cheng, Willayat Y Wani, David A Hottman, Angela Jeong, Dongfeng Cao, Kyle J LeBlanc, Paul Saftig, Jianhua Zhang, Ling Li
Autophagy and lysosomal function are important for protein homeostasis and their dysfunction have been associated with Alzheimer's disease (AD). Increased immunoreactivities of an important lysosomal protease, cathepsin D (Cat D), are evident in amyloid plaques and neurons in patients with AD. The current study tests the hypothesis that deleting one allele of the cathepsin D gene (Ctsd) impacts cerebral β-amyloidosis in APPsw/PS1dE9 (APP/PS1) double transgenic mice. Despite a significant 38% decrease of Cat D level in APP/PS1/Ctsd+/- compared to APP/PS1/Ctsd+/+ mice, no changes in steady state levels and deposition of Aβ were found in the brain...
April 21, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28424166/applying-fluid-biomarkers-to-alzheimer-s-disease
#13
Henrik Zetterberg
Alzheimer's disease (AD) is a common neurodegenerative disease that starts with a clinically silent phase of a decade or more during which brain pathologies accumulate predominantly in the medial temporal lobe but also elsewhere in the brain. Network dysfunction and clinical symptoms typically appear when senile plaque (amyloid β) and neurofibrillary tangle (tau) pathologies meet in the brain parenchyma, producing synapse and neuronal loss. For plaque and tangle pathologies, reliable fluid biomarkers have been developed...
April 19, 2017: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/28422821/how-the-cognitive-reserve-interacts-with-%C3%AE-amyloid-deposition-in-mitigating-fdg-metabolism-an-observational-study
#14
Elena Carapelle, Laura Serra, Sergio Modoni, Michele Falcone, Carlo Caltagirone, Marco Bozzali, Luigi Maria Specchio, Carlo Avolio
This observational study had the aim to assess the interaction between cognitive reserve (CR) and cerebrospinal fluid β-amyloid1-42 (Aβ1-42) in modulating brain [18F]fluorodeoxyglucose positron emission tomography (FDG-PET) metabolism in patients with moderate Alzheimer disease (AD).Twenty-seven patients with probable AD and 25 neurological normal subjects (NNS) entered the study. All participants had an FDG-PET scan, and AD patients also received a lumbar puncture to measure Aβ1-42, 181p-tau, and Tau concentrations...
April 2017: Medicine (Baltimore)
https://www.readbyqxmd.com/read/28419929/-r-and-s-18-f-labeled-2-arylbenzofurans-with-improved-pharmacokinetics-as-%C3%AE-amyloid-imaging-probes
#15
Jia Song, Xiaoyang Zhang, Yunling Zhao, Hui Yang, Jinming Zhang, Xiaojun Zhang, Jiapei Dai, Mengchao Cui
A new class of optical isomers of 2-arylbenzofuran derivatives were synthesized and evaluated as potential β-amyloid plaques imaging agents. Both lipophilicity and signal-to-noise ratio were significantly improved by adding a chiral hydroxyl group to 1-fluoro-3-(oxidanyl)propan-2-ol side chain. These derivatives displayed moderate to high binding affinity towards Aβ1-42 aggregates. Four tracers possessing potent binding affinity (Ki < 30 nM) were chosen for further investigation. In in vitro autoradiography studies, the four selected probes showed effective binding to Aβ plaques in Tg mouse and AD human brain tissue after labeled by (18)F...
April 3, 2017: European Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/28417668/exploring-molecular-structural-requirement-for-ache-inhibition-through-multi-chemometric-and-dynamics-simulation-analyses
#16
Tabassum Hossain, Achintya Saha, Arup Mukherjee
The acetylcholinesterase enzyme (AChE) plays an important role in central and peripheral nervous systems. Acetylcholine (ACh) acts through the regulation of AChE activity, which can play a key role in accelerating senile amyloid β-peptide (Aβ) plaque deposition. Therefore, inhibition of the AChE enzyme can be used as a key principle to prevent ACh depletion. The present study has been emphasized to explore both ligand- and structure-based 3D QSAR, HQSAR, pharmacophore, molecular docking and simulation studies on a set of structurally diverse inhibitors to optimize prime structural features responsible for selective binding to AChE, and vis-à-vis inhibiting enzyme activity...
April 18, 2017: Journal of Biomolecular Structure & Dynamics
https://www.readbyqxmd.com/read/28417423/evaluation-of-the-expression-of-amyloid-precursor-protein-and-the-ratio-of-secreted-amyloid-beta-42-to-amyloid-beta-40-in-sh-sy5y-cells-stably-transfected-with-wild-type-single-mutant-and-double-mutant-forms-of-the-app-gene-for-the-study-of-alzheimer-s-disease
#17
Aslina Pahrudin Arrozi, Siti Nur Syazwani Shukri, Wan Zurinah Wan Ngah, Yasmin Anum Mohd Yusof, Mohd Hanafi Ahmad Damanhuri, Suzana Makpol
Neuroblastoma cell lines such as SH-SY5Y are the most frequently utilized models in neurodegenerative research, and their use has advanced the understanding of the pathology of neurodegeneration over the past few decades. In Alzheimer's disease (AD), several pathogenic mutations have been described, all of which cause elevated levels of pathological hallmarks such as amyloid-beta (Aβ). Although the genetics of Alzheimer's disease is well known, familial AD only accounts for a small number of cases in the population, with the rest being sporadic AD, which contains no known mutations...
April 17, 2017: Applied Biochemistry and Biotechnology
https://www.readbyqxmd.com/read/28416568/pharmacological-and-toxicological-properties-of-the-potent-oral-%C3%AE-secretase-modulator-bpn-15606
#18
Steven L Wagner, Kevin D Rynearson, Steven K Duddy, Can Zhang, Phuong D Nguyen, Ann Becker, Uyen Vo, Deborah Masliah, Louise Monte, Justin B Klee, Corinne M Echmalian, Weiming Xia, Luisa Quinti, Graham Johnson, Jiunn H Lin, Doo Y Kim, William C Mobley, Robert A Rissman, Rudolph E Tanzi
Alzheimer's disease is characterized neuropathologically by an abundance of 1) neuritic plaques, which are primarily composed of a fibrillar 42 amino acid amyloid β peptide, as well as 2) neurofibrillary tangles composed of aggregates of hyperphosporylated tau. Elevations in the concentrations of the Aβ42 peptide in the brain, as a result of either increased production or decreased clearance are postulated to initiate and drive the AD pathological process. We initially introduced a novel class of bridged aromatics referred to as γ-secretase modulators that inhibited the production of the Aβ42 peptide and to a lesser degree the Aβ40 peptide while concomitantly increasing the production of the carboxyl-truncated Aβ38 and Aβ37 peptides...
April 17, 2017: Journal of Pharmacology and Experimental Therapeutics
https://www.readbyqxmd.com/read/28416393/tdp-43-expression-influences-amyloid%C3%AE-plaque-deposition-and-tau-aggregation
#19
Stephani A Davis, Kok Ann Gan, James A Dowell, Nigel J Cairns, Michael A Gitcho
Although the main focus in Alzheimer's disease (AD) has been an investigation of mechanisms causing Aβ plaque deposition and tau tangle formation, recent studies have shown that phosphorylated TDP-43 pathology is present in up to 50% of sporadic cases. Furthermore, elevated phosphorylated TDP-43 has been associated with more severe AD pathology. Therefore, we hypothesized that TDP-43 may regulate amyloid-beta precursor protein (APP) trafficking and tau phosphorylation/aggregation. In order to examine the role of TDP-43 in AD, we developed a transgenic mouse that overexpresses hippocampal and cortical neuronal TDP-43 in a mouse expressing familial mutations (K595N and M596L) in APP and presenilin 1 (PSEN1ΔE9)...
April 20, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28414234/impact-of-mutations-at-c-terminus-on-structures-and-dynamics-of-a%C3%AE-40-and-a%C3%AE-42-molecular-simulation-study
#20
Nguyen Hoang Linh, Thu Thi Minh Tran, Ly Anh Tu, Chin-Kun Hu, Mai Suan Li
Alzheimer's disease is presumably caused by formation of intracellular plaques of amyloid beta (Aβ) peptides inside neurons. The most abundant Aβ forms are Aβ40 and Aβ42 composing, respectively, of 40 and 42 residues. Recent experiments showed that triple Gly33Val-Val36Pro-Gly38Val (VPV) mutation makes Aβ42 become super-Aβ42 with elevated aggregation rates and toxicity. Upon VPV mutation oligomerization pathways of Aβ40 become similar to those of Aβ42 wild type. It was hypothesized that the super behavior of Aβ42 occurs due to enhanced content of the β-turn and β-hairpin, centered at residues 36-37 , while the similarity of oligomerization pathways of Aβ40-VPV and Aβ42-WT comes from increased β-turn population...
April 17, 2017: Journal of Physical Chemistry. B
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