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Amyloid plaque

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https://www.readbyqxmd.com/read/28222512/aqp4-association-with-amyloid-deposition-and-astrocyte-pathology-in-the-tg-arcswe-mouse-model-of-alzheimer-s-disease
#1
Jing Yang, Rui Zhang, Changhe Shi, Chengyuan Mao, Zhihua Yang, Zhenhe Suo, Reidun Torp, Yuming Xu
Amyloid-β deposition in senile plaques is one of the main pathological changes in Alzheimer's disease (AD). We previously reported that aquaporin-4 (AQP4) is redistributed within the astrocytes in cerebral amyloid angiopathy in the tg-ArcSwe mouse model of AD, suggesting that AQP4 may participate in amyloid-β deposition. However, the role of AQP4 in plaque formation is not currently clear. The objective of the current study was to explore the AQP4 distribution within plaques in the tg-ArcSwe mice in more depth by the combined application of immunofluorescence cytochemistry and immunogold electron microscopy...
February 10, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28222511/evaluation-of-a-dna-a%C3%AE-42-vaccine-in-aged-nzw-rabbits-antibody-kinetics-and-immune-profile-after-intradermal-immunization-with-full-length-dna-a%C3%AE-42-trimer
#2
Doris Lambracht-Washington, Min Fu, Mary Wight-Carter, Matthew Riegel, Roger N Rosenberg
A pathological hallmark of Alzheimer's disease (AD) are amyloid plaques in the brain consisting of aggregated amyloid-β 42 peptide (Aβ42) derived from cellular amyloid-β protein precursor (AβPP). Based on successful experiments in mouse AD models, active immunization with Aβ42 peptide and passive immunizations with anti-Aβ42 antibodies were started in clinical trials. Active Aβ42 peptide immunization in humans had led to an inflammatory autoimmune response, and the trial was stopped. Passive immunizations had shown some effects in slowing AD pathology...
February 7, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28222506/synaptic-compensation-as-a-probable-cause-of-prolonged-mild-cognitive-impairment-in-alzheimer-s-disease-implications-from-a-transgenic-mouse-model-of-the-disease
#3
Narjes Baazaoui, Michael Flory, Khalid Iqbal
Alzheimer's disease (AD) is a slow, progressive neurodegenerative disease in which cognitive decline takes place over a period of several years with a very variable period of mild cognitive impairment (MCI) and, in some cases, relatively long period before progression to dementia. The cognitive deficit during MCI is probably due to neuronal loss, an intermediate level of amyloid-β (Aβ) plaques and neurofibrillary tangles (NFT) and synaptosis, which is interrupted with a transient compensatory increase. We found impairment in reference memory accompanied by a decrease in the expression of synaptophysin, β-III tubulin, and MAP2 and a trend for GluR1, at 12 weeks of age in 3xTg-AD mice (hAPPSwe, P301L tau, PS1 [M146V] knock-in), a widely used transgenic model of AD...
February 7, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28218748/hiv-tat-protein-and-amyloid-%C3%AE-peptide-form-multifibrillar-structures-that-cause-neurotoxicity
#4
Alina Hategan, Mario A Bianchet, Joseph Steiner, Elena Karnaukhova, Eliezer Masliah, Adam Fields, Myoung-Hwa Lee, Alex M Dickens, Norman Haughey, Emilios K Dimitriadis, Avindra Nath
Deposition of amyloid-β plaques is increased in the brains of HIV-infected individuals, and the HIV transactivator of transcription (Tat) protein affects amyloidogenesis through several indirect mechanisms. Here, we investigated direct interactions between Tat and amyloid-β peptide. Our in vitro studies showed that in the presence of Tat, uniform amyloid fibrils become double twisted fibrils and further form populations of thick unstructured filaments and aggregates. Specifically, Tat binding to the exterior surfaces of the Aβ fibrils increases β-sheet formation and lateral aggregation into thick multifibrillar structures, thus producing fibers with increased rigidity and mechanical resistance...
February 20, 2017: Nature Structural & Molecular Biology
https://www.readbyqxmd.com/read/28217771/detection-inhibition-and-disintegration-of-amyloid-fibrils-the-role-of-optical-probes-and-macrocyclic-receptors
#5
Achikanath C Bhasikuttan, Jyotirmayee Mohanty
Amyloid fibrils are formed by the aberrant aggregation of proteins into highly ordered β-sheet structures and are believed to be the root cause of several neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, Prion diseases, etc. and have been the subject of extensive biochemical, biophysical and clinical studies. Developing methods for the early detection of fibril formation using optical spectroscopic techniques and inhibition/disintegration of amyloid fibrils/plaques by introducing small molecules have been a major challenge to establish a clinically facile therapeutic intervention to combat these neurodegenerative diseases...
February 20, 2017: Chemical Communications: Chem Comm
https://www.readbyqxmd.com/read/28217760/sleep-in-alzheimer-s-disease-beyond-amyloid
#6
Jerrah Holth, Tirth Patel, David M Holtzman
Sleep disorders are prevalent in Alzheimer's disease (AD) and a major cause of institutionalization. Like AD pathology, sleep abnormalities can appear years before cognitive decline and may be predictive of dementia. A bidirectional relationship between sleep and amyloid β (Aβ) has been well established with disturbed sleep and increased wakefulness leading to increased Aβ production and decreased Aβ clearance; whereas Aβ deposition is associated with increased wakefulness and sleep disturbances. Aβ fluctuates with the sleep wake cycle and is higher during wakefulness and lower during sleep...
January 2017: Neurobiology of Sleep and Circadian Rhythms
https://www.readbyqxmd.com/read/28211008/injected-amyloid-beta-in-the-olfactory-bulb-transfers-to-other-brain-regions-via-neural-connections-in-mice
#7
Baixuan He, Minying Zheng, Qiang Liu, Zhe Shi, Simei Long, Xilin Lu, Zhong Pei, Ti-Fei Yuan, Huanxing Su, Xiaoli Yao
Alzheimer's disease (AD) is characterized by progressive neuronal degeneration and pathological accumulation of amyloid plaques in the brain. It has been proposed that the prion-like spreading of amyloid beta (Aβ) protein could contribute to the progression of the disease. Olfactory bulb (OB) is one of the earliest brain regions affected in AD and olfaction is easily impaired prior to cognitive symptoms. However, it remains unclear whether Aβ accumulation in the OB would spread along olfactory projections to other connected brain regions and trigger further neurodegeneration...
February 16, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28208831/resveratrol-and-grape-extract-loaded-solid-lipid-nanoparticles-for-the-treatment-of-alzheimer-s-disease
#8
Joana A Loureiro, Stephanie Andrade, Ana Duarte, Ana Rute Neves, Joana Fontes Queiroz, Cláudia Nunes, Emmanuel Sevin, Laurence Fenart, Fabien Gosselet, Manuel A N Coelho, Maria Carmo Pereira
The aggregation of amyloid-β peptide (Aβ) has been linked to the formation of neuritic plaques, which are pathological hallmarks of Alzheimer's disease (AD). Various natural compounds have been suggested as therapeutics for AD. Among these compounds, resveratrol has aroused great interest due to its neuroprotective characteristics. Here, we provide evidence that grape skin and grape seed extracts increase the inhibition effect on Aβ aggregation. However, after intravenous injection, resveratrol is rapidly metabolized into both glucuronic acid and sulfate conjugations of the phenolic groups in the liver and intestinal epithelial cells (within less than 2 h), which are then eliminated...
February 13, 2017: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
https://www.readbyqxmd.com/read/28206782/process-dissociation-analyses-of-memory-changes-in-healthy-aging-preclinical-and-very-mild-alzheimer-disease-evidence-for-isolated-recollection-deficits
#9
Peter R Millar, David A Balota, Geoffrey B Maddox, Janet M Duchek, Andrew J Aschenbrenner, Anne M Fagan, Tammie L S Benzinger, John C Morris
OBJECTIVE: Recollection and familiarity are independent processes that contribute to memory performance. Recollection is dependent on attentional control, which has been shown to be disrupted in early stage Alzheimer's disease (AD), whereas familiarity is independent of attention. The present longitudinal study examines the sensitivity of recollection estimates based on Jacoby's (1991) process dissociation procedure to AD-related biomarkers in a large sample of well-characterized cognitively normal middle-aged and older adults (N = 519) and the extent to which recollection discriminates these individuals from individuals with very mild symptomatic AD (N = 64)...
February 16, 2017: Neuropsychology
https://www.readbyqxmd.com/read/28205585/neuronally-directed-effects-of-rxr-activation-in-a-mouse-model-of-alzheimer-s-disease
#10
M M Mariani, T Malm, R Lamb, T R Jay, L Neilson, B Casali, L Medarametla, G E Landreth
Alzheimer's disease (AD) is characterized by extensive neuron loss that accompanies profound impairments in memory and cognition. We examined the neuronally directed effects of the retinoid X receptor agonist bexarotene in an aggressive model of AD. We report that a two week treatment of 3.5 month old 5XFAD mice with bexarotene resulted in the clearance of intraneuronal amyloid deposits. Importantly, neuronal loss was attenuated by 44% in the subiculum in mice 4 months of age and 18% in layer V of the cortex in mice 8 months of age...
February 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28203202/plasma-exosomes-spread-and-cluster-around-%C3%AE-amyloid-plaques-in-an-animal-model-of-alzheimer-s-disease
#11
Tingting Zheng, Jiali Pu, Yanxing Chen, Yanfang Mao, Zhangyu Guo, Hongyu Pan, Ling Zhang, Heng Zhang, Binggui Sun, Baorong Zhang
Exosomes, a type of extracellular vesicle, have been shown to be involved in many disorders, including Alzheimer's disease (AD). Exosomes may contribute to the spread of misfolded proteins such as amyloid-β (Aβ) and α-synuclein. However, the specific diffusion process of exosomes and their final destination in brain are still unclear. In the present study, we isolated exosomes from peripheral plasma and injected them into the hippocampus of an AD mouse model, and investigated exosome diffusion. We found that injected exosomes can spread from the dentate gyrus (DG) to other regions of hippocampus and to the cortex...
2017: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/28197669/clearance-of-cerebral-a%C3%AE-in-alzheimer-s-disease-reassessing-the-role-of-microglia-and-monocytes
#12
REVIEW
Leah Zuroff, David Daley, Keith L Black, Maya Koronyo-Hamaoui
Deficiency in cerebral amyloid β-protein (Aβ) clearance is implicated in the pathogenesis of the common late-onset forms of Alzheimer's disease (AD). Accumulation of misfolded Aβ in the brain is believed to be a net result of imbalance between its production and removal. This in turn may trigger neuroinflammation, progressive synaptic loss, and ultimately cognitive decline. Clearance of cerebral Aβ is a complex process mediated by various systems and cell types, including vascular transport across the blood-brain barrier, glymphatic drainage, and engulfment and degradation by resident microglia and infiltrating innate immune cells...
February 14, 2017: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/28191738/the-role-of-neuroinflammation-and-amyloid-in-cognitive-impairment-in-an-app-ps1-transgenic-mouse-model-of-alzheimer-s-disease
#13
Shenghua Zhu, Junhui Wang, Yanbo Zhang, Jue He, Jiming Kong, Jun-Feng Wang, Xin-Min Li
AIMS: Both amyloid deposition and neuroinflammation appear in the early course of Alzheimer's disease (AD). However, the progression of neuroinflammation and its relationship with amyloid deposition and behavioral changes have not been fully elucidated. A better understanding the role of neuroinflammation in AD might extend our current knowledge to therapeutic intervention possibilities. METHODS: This study systematically characterized changes in behavioral abnormalities in APP/PS1 transgenic mice...
February 12, 2017: CNS Neuroscience & Therapeutics
https://www.readbyqxmd.com/read/28188218/focal-solute-trapping-and-global-glymphatic-pathway-impairment-in-a-murine-model-of-multiple-microinfarcts
#14
Minghuan Wang, Fengfei Ding, SaiYue Deng, Xuequn Guo, Wei Wang, Jeffrey J Iliff, Maiken Nedergaard
Microinfarcts occur commonly in the aging brain as a consequence of diffuse embolic events and are associated with the development of vascular dementia and Alzheimer's disease. Yet the manner in which disperse microscopic lesions reduce global cognitive function and increase the risk for Alzheimer's disease is unclear. The glymphatic system, which is a brain-wide perivascular network that supports the recirculation of CSF through the brain parenchyma, facilitates the clearance of interstitial solutes including amyloid beta and tau...
February 10, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28186506/epigenetic-regulation-of-hdac1-sumoylation-as-an-endogenous-neuroprotection-against-a%C3%AE-toxicity-in-a-mouse-model-of-alzheimer-s-disease
#15
Chih Chieh Tao, Wei Lun Hsu, Yun Li Ma, Sin Jhong Cheng, Eminy Hy Lee
Amyloid-β (Aβ) produces neurotoxicity in the brain and causes neuronal death, but the endogenous defense mechanism that is activated on Aβ insult is less well known. Here we found that acute Aβ increases the expression of PIAS1 and Mcl-1 via activation of MAPK/ERK, and Aβ induction of PIAS1 enhances HDAC1 SUMOylation in rat hippocampus. Knockdown of PIAS1 decreases endogenous HDAC1 SUMOylation and blocks Aβ induction of Mcl-1. Sumoylated HDAC1 reduces it association with CREB, increases CREB binding to the Mcl-1 promoter and mediates Aβ induction of Mcl-1 expression...
February 10, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28185264/amyloidogenicity-and-toxicity-of-the-reverse-and-scrambled-variants-of-amyloid-%C3%AE-1-42
#16
Devkee M Vadukul, Oyinkansola Gbajumo, Karen E Marshall, Louise C Serpell
β-amyloid 1-42 (Aβ1-42) is a self-assembling peptide that goes through many conformational and morphological changes before forming the fibrils that are deposited in extracellular plaques characteristic of Alzheimer's disease. The link between Aβ1-42 structure and toxicity is of major interest, in particular, the neurotoxic potential of oligomeric species. Many studies utilise reversed (Aβ42-1) and scrambled (AβS) forms of amyloid-β as control peptides. Here, using circular dichroism, Thioflavin T fluorescence and transmission electron microscopy, we reveal that both control peptides self-assemble to fibres within 24 hours...
February 10, 2017: FEBS Letters
https://www.readbyqxmd.com/read/28184302/the-role-of-exosomes-in-the-pathogenesis-of-alzheimer-disease
#17
REVIEW
Tingting Xiao, Weiwei Zhang, Bin Jiao, Chu-Zheng Pan, Xixi Liu, Lu Shen
Exosomes are small vesicles secreted by most cell types including neurons that function in intercellular communication through transfer of their cargo or encapsulate and eliminate unnecessary cellular components and therefore have a broad impact on nerve development, activation and regeneration. In addition, exosomes have been observed to be involved in spreading pathological misfolded proteins, thereby leading to the onset and propagation of disease. Alzheimer disease (AD) is the most common form of dementia and characterized by two types of lesions: amyloid plaques and neurofibrillary tangles...
2017: Translational Neurodegeneration
https://www.readbyqxmd.com/read/28181118/brain-uptake-and-safety-of-flutemetamol-f-18-injection-in-japanese-subjects-with-probable-alzheimer-s-disease-subjects-with-amnestic-mild-cognitive-impairment-and-healthy-volunteers
#18
Takami Miki, Hiroyuki Shimada, Jae-Seung Kim, Yasuji Yamamoto, Masakazu Sugino, Hisatomo Kowa, Kerstin Heurling, Michelle Zanette, Paul F Sherwin, Michio Senda
OBJECTIVE: This Phase 2 study assessed the performance of positron emission tomography (PET) brain images made with Flutemetamol F 18 Injection in detecting β-amyloid neuritic plaques in Japanese subjects. METHODS: Seventy subjects (25 with probable Alzheimer's disease (pAD), 20 with amnestic mild cognitive impairment (aMCI), and 25 cognitively normal healthy volunteers[HVs]) underwent PET brain imaging after intravenous Flutemetamol F 18 Injection (185 MBq). Images were interpreted as normal or abnormal for neuritic plaque density by each of five non-Japanese and five Japanese readers who were blinded to clinical data...
February 8, 2017: Annals of Nuclear Medicine
https://www.readbyqxmd.com/read/28180219/super-resolution-imaging-of-alpha-synuclein-polymorphisms-and-their-potential-role-in-neurodegeneration
#19
REVIEW
Eileen Nugent, Clemens F Kaminski, Gabriele S Kaminski Schierle
The conversion of soluble, functional proteins into amyloid fibrils has been linked to the development of neurodegenerative disorders, including Parkinson's and Alzheimer's disease. In the brains of patients with these disorders, the increasing presence of amyloid-containing plaques corresponds to neuronal cell death and the worsening of symptoms. However, protein amyloids are not merely confined to dying cells. Rather, some show a propensity to be transmitted to, and enter adjacent cells and induce the polymerization of the native monomer population...
February 9, 2017: Integrative Biology: Quantitative Biosciences From Nano to Macro
https://www.readbyqxmd.com/read/28176625/protective-effects-of-huang-lian-jie-du-tang-on-a%C3%AE-25-35-induced-memory-deficits-and-oxidative-stress-in-male-rats
#20
Wenbin Wu, Shuling Xie, Bin Li, Kun Yang, Xuehui Liu, Baiyang Li
BACKGROUND: Alzheimer's disease is a neurodegenerative disorder characterized by progressive cognitive deterioration and is the most common cause of dementia. Extracellular β-amyloid deposit in senile plaques is the most characteristic pathological hallmark. β-amyloid (Aβ) accumulation is associated with neurodegeneration and involved in memory impairment associated with Alzheimer's disease. It can also induce intracellular reactive oxygen species (ROS) production, which results in neurodegeneration and immune response...
February 6, 2017: Current Alzheimer Research
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