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https://www.readbyqxmd.com/read/29141366/-in-vitro-early-detection-of-amyloid-plaques-in-alzheimer-s-disease-by-pittsburgh-compound-b-modified-magnetic-nanoparticles
#1
J Q Zeng, J Q Wu, M H Li, P J Wang
Objective: To construct magnetic nanoparticles targeting β-amyloid (Aβ) plaques, the pathological biomarker of Alzheimer's disease (AD) and to study their binding capability in vitro. Methods: Superparamagnetic nanoparticles Mn(0.6)Zn(0.4)Fe(2)O(4) (MZF) were coated with amphiphilic star-block copolymeric micelles and modified with Aβ-specific probe Pittsburgh compound B (PiB) to construct a novel magnetic nanoparticle MZF-PiB, which specifically targeted amyloid plaques. Transmission electron microscope was used to study the morphological features of MZF-PiB...
November 7, 2017: Zhonghua Yi Xue za Zhi [Chinese medical journal]
https://www.readbyqxmd.com/read/29140083/a-critical-role-of-ser26-hydrogen-bonding-in-a%C3%AE-42-assembly-and-toxicity
#2
Robin Roychaudhuri, Tien-Phat V Huynh, Taylor R Whitaker, Elisabeth Hodara, Margaret M Condron, David B Teplow
Amyloid β-protein (Aβ) assembly is a seminal process in Alzheimer's disease. Elucidating the mechanistic features of this process is thought to be vital for the design and targeting of therapeutic agents. Com-putational studies of the most pathologic form of Aβ, the 42-residue Aβ42 peptide, have suggested that hydrogen bonding involving Ser 26 may be particularly important in organizing a monomer folding nucleus and in subse-quent peptide assembly. To study this question, we ex-perimentally determined structure-activity relationships among Aβ42 peptides in which Ser 26 was replaced with Gly, Ala, α-aminobutryic acid (Abu), or Cys...
November 15, 2017: Biochemistry
https://www.readbyqxmd.com/read/29138799/lychee-seed-extract-protects-against-neuronal-injury-and-improves-cognitive-function-in-rats-with-type-ii-diabetes-mellitus-with-cognitive-impairment
#3
Yong Tang, Chonglin Yu, Jianming Wu, Haixia Chen, Yuan Zeng, Xiuling Wang, Le Yang, Qibing Mei, Shousong Cao, Dalian Qin
Lychee seed is a traditional Chinese medicine and has many beneficial effects such as modulation of blood sugar and lipids, antioxidation, antivirus and antitumor. Studies have indicated that type II diabetes mellitus (T2DM) and Alzheimer's disease (AD) share common biological mechanisms including insulin resistance, impaired glucose metabolism, β‑amyloid (Aβ) formation, oxidative stress and presence of advanced glycation end products (AGEs). The present study investigated the effects of lychee seed extract (LSE) on neuroprotection, cognitive function improvement and possible underlying mechanisms in a rat model of T2DM with cognitive impairment...
November 9, 2017: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/29138762/identifying-cu-ii-amyloid-peptide-binding-intermediates-in-the-early-stages-of-aggregation-by-resonance-raman-spectroscopy-a-simulation-study
#4
Hao Ren, Yu Zhang, Sibei Guo, Na Lin, Li Deng, Tongtao Yue, Fang Huang
The aggregation of amyloid beta (Aβ) peptides plays a crucial role in the pathology and etiology of Alzheimer's disease. Experimental evidence shows that copper ion is an aggregation-prone species with the ability to coordinately bind to Aβ and further induce the formation of neurotoxic Aβ oligomers. However, the detailed structures of Cu(ii)-Aβ complexes have not been illustrated, and the kinetics and dynamics of the Cu(ii) binding are not well understood. Two Cu(ii)-Aβ complexes have been proposed to exist under physiological conditions, and another two might exist at higher pH values...
November 15, 2017: Physical Chemistry Chemical Physics: PCCP
https://www.readbyqxmd.com/read/29138055/merkel-cells-sense-cooling-with-trpm8-channels
#5
Valentine Bouvier, Yann Roudaut, Nancy Osorio, Jean-Marc Aimonetti, Edith Ribot-Ciscar, Virginie Penalba, Thierry Merrot, Nicolas Lebonvallet, Christelle Le Gall-Ianotto, Laurent Misery, Patrick Delmas, Marcel Crest
In the skin, Merkel cells (MCs) connect with keratinocytes and Aβ nerve fibers to form a touch receptor which functions as a slow adapting mechanoreceptor (SA1 receptor). In human and mouse MCs, we observed an increased concentration of intracellular Ca(2+) ions in response to cold temperature and transient receptor potential melastatine 8 (TRPM8) ion channel agonists. A reduction in the response to cooling and TRPM8 agonists occurred following addition of TRPM8 antagonists, as well as in TRPM8 knockout mice...
November 11, 2017: Journal of Investigative Dermatology
https://www.readbyqxmd.com/read/29137651/abnormal-dendritic-calcium-activity-and-synaptic-depotentiation-occur-early-in-a-mouse-model-of-alzheimer-s-disease
#6
Yang Bai, Miao Li, Yanmei Zhou, Lei Ma, Qian Qiao, Wanling Hu, Wei Li, Zachary Patrick Wills, Wen-Biao Gan
BACKGROUND: Alzheimer's disease (AD) is characterized by amyloid deposition, tangle formation as well as synapse loss. Synaptic abnormalities occur early in the pathogenesis of AD. Identifying early synaptic abnormalities and their underlying mechanisms is likely important for the prevention and treatment of AD. METHODS: We performed in vivo two-photon calcium imaging to examine the activities of somas, dendrites and dendritic spines of layer 2/3 pyramidal neurons in the primary motor cortex in the APPswe/PS1dE9 mouse model of AD and age-matched wild type control mice...
November 14, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29137322/the-c-jun-n-terminal-kinase-plays-a-key-role-in-ocular-degenerative-changes-in-a-mouse-model-of-alzheimer-disease-suggesting-a-correlation-between-ocular-and-brain-pathologies
#7
Lucia Buccarello, Alessandra Sclip, Matteo Sacchi, Anna Maria Castaldo, Ilaria Bertani, Andrea ReCecconi, Silvia Maestroni, Gianpaolo Zerbini, Paolo Nucci, Tiziana Borsello
Recently a range of ocular manifestations such as retinal and lens amyloid-beta accumulation and retinal nerve fiber layer loss have been proposed as potential biomarkers in Alzheimer disease (AD). The TgCRND8 mouse model of AD exhibits age-dependent amyloid β (Aβ) oligomers accumulation and cognitive defects, amyloid plaques and hyperphosphorylated Tau deposition and inflammation. We proved the correlation between ocular pathologies and AD, observing increased levels of p-APP and p-Tau, accumulation of Aβ oligomers in the retina, eye, and optic nerve...
October 10, 2017: Oncotarget
https://www.readbyqxmd.com/read/29137240/mutational-re-modeling-of-di-aspartyl-intramembrane-proteases-uncoupling-physiologically-relevant-activities-from-those-associated-with-alzheimer-s-disease
#8
Anastasia P Grigorenko, Youri K Moliaka, Olga V Plotnikova, Alexander Smirnov, Vera A Nikishina, Andrey Y Goltsov, Fedor Gusev, Tatiana V Andreeva, Omar Nelson, Ilya Bezprozvanny, Evgeny I Rogaev
The intramembrane proteolytic activities of presenilins (PSEN1/PS1 and PSEN2/PS2) underlie production of β-amyloid, the key process in Alzheimer's disease (AD). Dysregulation of presenilin-mediated signaling is linked to cancers. Inhibition of the γ-cleavage activities of PSENs that produce Aβ, but not the ε-like cleavage activity that release physiologically essential transcription activators, is a potential approach for the development of rational therapies for AD. In order to identify whether different activities of PSEN1 can be dissociated, we designed multiple mutations in the evolutionary conserved sites of PSEN1...
October 10, 2017: Oncotarget
https://www.readbyqxmd.com/read/29136781/andrographolide-sulfonate-improves-alzheimer-associated-phenotypes-and-mitochondrial-dysfunction-in-app-ps1-transgenic-mice
#9
Ji Geng, Wen Liu, Yuyun Xiong, Hongqun Ding, Chunhong Jiang, Xiaoling Yang, Xiang Li, Ahmed Elgehama, Yang Sun, Qiang Xu, Wenjie Guo, Jing Gao
Alzheimer's disease is a neurodegenerative disorder with Amyloid-β plaques onset, synaptic damage, and cognitive decline. Aβ deposits cause pathological events including oxidative stress, mitochondrial dysfunction, and neuron death. In this study, APPswe/PSENΔ9 double transgenic mice model was used to imitate Alzheimer's disease and the effect and possible mechanism of Andrographolide sulfonate were examined. Andrographolide sulfonate was given to the mice for 7 months before the onset of Aβ plaque. Spatial memory test showed that Andrographolide sulfonate treatment prevented cognitive decline...
November 8, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29136779/juglanin-ameliorates-lps-induced-neuroinflammation-in-animal-models-of-parkinson-s-disease-and-cell-culture-via-inactivating-tlr4-nf-%C3%AE%C2%BAb-pathway
#10
Fang-Xue Zhang, Ren-Shi Xu
Parkinson's disease (PD) is a common neuro-degenerative disorder, and novel therapeutic targets are required for the treatment of PD. Juglanin is a natural compound extracted from the crude Polygonum aviculare, exhibiting anti-inflammatory, anti-oxidant and anti-cancer activities. In our study, PD in mice was induced by systemic LPS treatment as evidenced by enhanced α-synuclein and reduced tyrosine hydroxylase (TH), which were reversed by juglanin treatment. Moreover, juglanin administration attenuated LPS-caused behavioral and memory impairments and reduced LPS-induced enhancement of neuro-degenerative markers, including amyloid β (Aβ) and p-Tau...
November 7, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29136123/amyloid-network-topology-characterizes-the-progression-of-alzheimer-s-disease-during-the-predementia-stages
#11
Joana B Pereira, Tor Olof Strandberg, Sebastian Palmqvist, Giovanni Volpe, Danielle van Westen, Eric Westman, Oskar Hansson
There is increasing evidence showing that the accumulation of the amyloid-β (Aβ) peptide into extracellular plaques is a central event in Alzheimer's disease (AD). These abnormalities can be detected as lowered levels of Aβ42 in the cerebrospinal fluid (CSF) and are followed by increased amyloid burden on positron emission tomography (PET) several years before the onset of dementia. The aim of this study was to assess amyloid network topology in nondemented individuals with early stage Aβ accumulation, defined as abnormal CSF Aβ42 levels and normal Florbetapir PET (CSF+/PET-), and more advanced Aβ accumulation, defined as both abnormal CSF Aβ42 and Florbetapir PET (CSF+/PET+)...
November 9, 2017: Cerebral Cortex
https://www.readbyqxmd.com/read/29135331/imaging-microglial-activation-and-amyloid-burden-in-amnestic-mild-cognitive-impairment
#12
Dunja Knezevic, Nicolaas Paul Lg Verhoeff, Sina Hafizi, Antonio P Strafella, Ariel Graff-Guerrero, Tarek Rajji, Bruce G Pollock, Sylvain Houle, Pablo M Rusjan, Romina Mizrahi
Amnestic mild cognitive impairment (aMCI) is defined as a transitional state between normal aging and Alzheimer's disease (AD). Given the replicated finding of increased microglial activation in AD, we sought to investigate whether microglial activation is also elevated in aMCI and whether it is related to amyloid beta (Aβ) burden in-vivo . Eleven aMCI participants and 14 healthy volunteers completed positron emission tomography (PET) scans with [(18)F]-FEPPA and [(11)C]-PIB. Given the known sensitivity in affinity of second-generation TSPO radioligands, participants were genotyped for the TSPO polymorphism and only high-affinity binders were included...
January 1, 2017: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/29134771/detection-of-%C3%AE-amyloid-by-sialic-acid-coated-bovine-serum-albumin-magnetic-nanoparticles-in-a-mouse-model-of-alzheimer-s-disease
#13
Seyedmehdi Hossaini Nasr, Hovig Kouyoumdjian, Christiane Mallett, Sherif Ramadan, David C Zhu, Erik M Shapiro, Xuefei Huang
The accumulation and formation of β-amyloid (Aβ) plaques in the brain are distinctive pathological hallmarks of Alzheimer's disease (AD). Designing nanoparticle (NP) contrast agents capable of binding with Aβ highly selectively can potentially facilitate early detection of AD. However, a significant obstacle is the blood brain barrier (BBB), which can preclude the entrance of NPs into the brain for Aβ binding. In this work, bovine serum albumin (BSA) coated NPs are decorated with sialic acid (NP-BSAx -Sia) to overcome the challenges in Aβ imaging in vivo...
November 14, 2017: Small
https://www.readbyqxmd.com/read/29134514/expression-of-bc1-impairs-spatial-learning-and-memory-in-alzheimer-s-disease-via-app-translation
#14
Tongmei Zhang, Pei Pang, Zemin Fang, Yu Guo, Hao Li, Xinyan Li, Tian Tian, Xin Yang, Wenting Chen, Shu Shu, Na Tang, Jianhua Wu, Houze Zhu, Lei Pei, Dan Liu, Qing Tian, Jian Wang, Lin Wang, Ling-Qiang Zhu, Youming Lu
Aggregation of amyloid-β (Aβ) peptides, which are the cleavage products of amyloid precursor protein (APP), is a major pathological hallmark in the brain of Alzheimer's disease (AD). Now, we know little about the roles of APP translation in the disease progression of AD. Here, we show that BC1, a long noncoding RNA (lncRNA), is expressed in the brain of AD mice. BC1 induces APP mRNA translation via association with a fragile X syndrome protein (FMRP). Inhibition of BC1 or BC1-FMRP association in AD mice blocks aggregation of Aβ in the brain and protects against the spatial learning and memory deficits...
November 13, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/29134321/co-occurrence-of-mixed-proteinopathies-in-late-stage-huntington-s-disease
#15
Isabelle St-Amour, Andréanne Turgeon, Claudia Goupil, Emmanuel Planel, Sébastien S Hébert
Accumulating evidence highlights the potential role of mixed proteinopathies (i.e., abnormal protein aggregation) in the development of clinical manifestations of neurodegenerative diseases (NDD). Huntington's disease (HD) is an inherited NDD caused by autosomal-dominant expanded CAG trinucleotide repeat mutation in the gene coding for Huntingtin (Htt). Previous studies have suggested the coexistence of phosphorylated-Tau, α-synuclein (α-Syn) and TAR DNA-binding protein 43 (TDP-43) inclusions in HD. However, definite evidence that HD pathology in humans can be accompanied by other proteinopathies is still lacking...
November 13, 2017: Acta Neuropathologica
https://www.readbyqxmd.com/read/29134111/periodontitis-induced-by-bacterial-infection-exacerbates-features-of-alzheimer-s-disease-in-transgenic-mice
#16
Naoyuki Ishida, Yuichi Ishihara, Kazuto Ishida, Hiroyuki Tada, Yoshiko Funaki-Kato, Makoto Hagiwara, Taslima Ferdous, Mohammad Abdullah, Akio Mitani, Makoto Michikawa, Kenji Matsushita
Periodontitis is a localized infectious disease caused by periodontopathic bacteria, such as Porphyromonas gingivalis. Recently, it has been suggested that bacterial infections may contribute to the onset and the progression of Alzheimer's disease (AD). However, we do not have any evidence about a causative relationship between periodontitis and AD. In this study, we investigated by using a transgenic mouse model of AD whether periodontitis evoked by P. gingivalis modulates the pathological features of AD. Cognitive function was significantly impaired in periodontitis-induced APP-Tg mice, compared to that in control APP-Tg mice...
2017: NPJ Aging and Mechanisms of Disease
https://www.readbyqxmd.com/read/29133432/locus-coeruleus-ablation-exacerbates-cognitive-deficits-neuropathology-and-lethality-in-p301s-tau-transgenic-mice
#17
Termpanit Chalermpalanupap, Jason P Schroeder, Jacki M Rorabaugh, L Cameron Liles, James J Lah, Allan I Levey, David Weinshenker
The brainstem locus coeruleus (LC) supplies norepinephrine (NE) to the forebrain and degenerates in Alzheimer's disease (AD). Loss of LC neurons is correlated with increased severity of other AD hallmarks including β-amyloid (Aβ) plaques, tau neurofibrillary tangles and cognitive deficits, suggesting that it contributes to the disease progression. Lesions of the LC in amyloid-based transgenic mouse models of AD exacerbate Aβ pathology, neuroinflammation, and cognitive deficits, but it is unknown how the loss of LC neurons affects tau-mediated pathology or behavioral abnormalities...
November 13, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29132916/insulin-degrading-enzyme-in-the-fight-against-alzheimer-s-disease
#18
REVIEW
Igor V Kurochkin, Enrico Guarnera, Igor N Berezovsky
After decades of research and clinical trials there is still no cure for Alzheimer's disease (AD). While impaired clearance of amyloid beta (Aβ) peptides is considered as one of the major causes of AD, it was recently complemented by a potential role of other toxic amyloidogenic species. Insulin-degrading enzyme (IDE) is the proteolytic culprit of various β-forming peptides, both extracellular and intracellular. On the basis of demonstrated allosteric activation of IDE against Aβ, it is possible to propose a new strategy for the targeted IDE-based cleansing of different toxic aggregation-prone peptides...
November 10, 2017: Trends in Pharmacological Sciences
https://www.readbyqxmd.com/read/29131706/alzheimer-s-disease-current-status-and-future-directions
#19
Deepshikha Bhardwaj, Connie Mitra, Chandrakala Aluganti Narasimhulu, Aladdin Riad, Mitsushita Doomra, Sampath Parthasarathy
Alzheimer's disease (AD) is an age-related neurodegenerative disorder of the brain. The presence of amyloid-beta (Aβ) plaques, neurofibrillary tangles (NFTs), loss of neurons, synapses, and altered sensory perceptions, including memory loss, delineate AD. However, the cause of AD is not clearly known. Several genetic and nongenetic factors have been implicated in the disease. Of the genes, the ɛ4 allele of apolipoprotein E is the largest known genetic risk factor of AD. This review article focuses on the various genetic and other predisposing factors that account for AD, pathophysiology of the disease, and the mechanisms by which Aβ plaques and NFTs are formed and could affect AD brain...
November 13, 2017: Journal of Medicinal Food
https://www.readbyqxmd.com/read/29131485/in-vitro-effects-of-serotonin-melatonin-and-other-related-indole-compounds-on-amyloid-%C3%AE-kinetics-and-neuroprotection
#20
Ruth Hornedo Ortega, Grégory Da Costa, Ana Belén Cerezo, Ana Mª Troncoso, Tristan Richard, Mª Carmen García Parrilla
SCOPE: Amyloid-β peptide (Aβ) is the main component of senile plaques in Alzheimer's disease (AD). The inhibition of Aβ assembly, the destabilisation of Aβ aggregates and the decrease of its cytotoxicity for the prevention of neuronal death are considered neuroprotective effects. In this work, the protective effects against Aβ aggregation and cytotoxicity of eight indolic compounds: tryptophan (Tryp), tryptamine (Trpa), serotonin (Ser), tryptophol (Phol), N-acetylserotonin (Nser), 3-indoleacetic acid (3IA), tryptophan ethyl ester (Tee) and melatonin (Mel) was evaluated...
November 12, 2017: Molecular Nutrition & Food Research
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