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https://www.readbyqxmd.com/read/27932977/human-neural-stem-cell-transplantation-rescues-cognitive-defects-in-app-ps1-model-of-alzheimer-s-disease-by-enhancing-neuronal-connectivity-and-metabolic-activity
#1
Xueyuan Li, Hua Zhu, Xicai Sun, Fuxing Zuo, Jianfeng Lei, Zhanjing Wang, Xinjie Bao, Renzhi Wang
Alzheimer's disease (AD), the most frequent type of dementia, is featured by Aβ pathology, neural degeneration and cognitive decline. To date, there is no cure for this disease. Neural stem cell (NSC) transplantation provides new promise for treating AD. Many studies report that intra-hippocampal transplantation of murine NSCs improved cognition in rodents with AD by alleviating neurodegeneration via neuronal complement or replacement. However, few reports examined the potential of human NSC transplantation for AD...
2016: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/27930341/analysis-of-138-pathogenic-mutations-in-presenilin-1-on-the-in-vitro-production-of-a%C3%AE-42-and-a%C3%AE-40-peptides-by-%C3%AE-secretase
#2
Linfeng Sun, Rui Zhou, Guanghui Yang, Yigong Shi
A hallmark of Alzheimer's disease (AD) is the aggregation of β-amyloid peptides (Aβ) into amyloid plaques in patient brain. Cleavage of amyloid precursor protein (APP) by the intramembrane protease γ-secretase produces Aβ of varying lengths, of which longer peptides such as Aβ42 are thought to be more harmful. Increased ratios of longer Aβs over shorter ones, exemplified by the ratio of Aβ42 over Aβ40, may lead to formation of amyloid plaques and consequent development of AD. In this study, we analyzed 138 reported mutations in human presenilin-1 (PS1) by individually reconstituting the mutant PS1 proteins into anterior-pharynx-defective protein 1 (APH-1)aL-containing γ-secretases and examining their abilities to produce Aβ42 and Aβ40 in vitro...
December 5, 2016: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/27928512/extracellular-vesicle-associated-a%C3%AE-mediates-trans-neuronal-bioenergetic-and-ca-2-handling-deficits-in-alzheimer-s-disease-models
#3
Erez Eitan, Emmette R Hutchison, Krisztina Marosi, James Comotto, Maja Mustapic, Saket M Nigam, Caitlin Suire, Chinmoyee Maharana, Gregory A Jicha, Dong Liu, Vasiliki Machairaki, Kenneth W Witwer, Dimitrios Kapogiannis, Mark P Mattson
Alzheimer's Disease (AD) is an age-related neurodegenerative disorder in which aggregation-prone neurotoxic amyloid β-peptide (Aβ) accumulates in the brain. Extracellular vesicles (EVs) are small 50-150 nanometer membrane vesicles that have recently been implicated in the prion-like spread of self-aggregating proteins. Here we report that EVs isolated from AD patient CSF and plasma, from the plasma of two AD mouse models, and from the medium of neural cells expressing familial AD presenilin 1 mutations, destabilize neuronal Ca(2+) homeostasis, impair mitochondrial function, and sensitize neurons to excitotoxicity...
2016: NPJ Aging and Mechanisms of Disease
https://www.readbyqxmd.com/read/27911305/nitrosylation-of-vesicular-transporters-in-brain-of-amyloid-precursor-protein-presenilin-1-double-transgenic-mice
#4
Ying Wang, Zhu Zhou, Hua Tan, Shenghua Zhu, Yiran Wang, Yingxia Sun, Xin-Min Li, Jun-Feng Wang
Nitric oxide can attack thiol groups of cysteine residues in proteins and induce protein cysteine S-nitrosylation. Cholinergic and glutamatergic systems are dysregulated in Alzheimer's disease. Vesicular acetylcholine transporter (VAChT) and vesicular glutamate transporter 1 (VGLUT1) are important in packaging acetylcholine and glutamate into vesicles, which is an important step for neurotransmission. Previously we found that VAChT and VGLUT1 can be nitrosylated and that S-nitrosylation of these transporters inhibits vesicular uptake of acetylcholine and glutamate...
November 26, 2016: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/27908425/copper-accumulation-in-rodent-brain-astrocytes-a-species-difference
#5
Brendan Sullivan, Gregory Robison, Yulia Pushkar, John K Young, Kebreten F Manaye
Changes in Cu homeostasis have been implicated in multiple neurodegenerative diseases. Factors controlling and regulating the distribution of Cu in the brain remain largely unknown. We have previously reported that a sub-set of astrocytes in the subventricular zone (SVZ) contain Cu-rich aggregates. Here we expand previous studies with detailed X-ray fluorescent imaging (XRF) analysis of the additional brain areas of hippocampus (HP) and rostral migratory stream (RMS). We also use conventional DAB (3,3'-diaminobenzidine) staining which accesses both peroxidase and pseudo-peroxidase activities...
January 2017: Journal of Trace Elements in Medicine and Biology
https://www.readbyqxmd.com/read/27904493/beta-2-adrenergic-receptor-activation-enhances-neurogenesis-in-alzheimer-s-disease-mice
#6
Gao-Shang Chai, Yang-Yang Wang, Amina Yasheng, Peng Zhao
Impaired hippocampal neurogenesis is one of the early pathological features of Alzheimer's disease. Enhancing adult hippocampal neurogenesis has been pursued as a potential therapeutic strategy for Alzheimer's disease. Recent studies have demonstrated that environmental novelty activates β2-adrenergic signaling and prevents the memory impairment induced by amyloid-β oligomers. Here, we hypothesized that β2-adrenoceptor activation would enhance neurogenesis and ameliorate memory deficits in Alzheimer's disease...
October 2016: Neural Regeneration Research
https://www.readbyqxmd.com/read/27889678/early-hippocampal-hyperexcitability-in-ps2app-mice-role-of-mutant-ps2-and-app
#7
Roberto Fontana, Mario Agostini, Emanuele Murana, Mufti Mahmud, Elena Scremin, Maria Rubega, Giovanni Sparacino, Stefano Vassanelli, Cristina Fasolato
Alterations of brain network activity are observable in Alzheimer's disease (AD) together with the occurrence of mild cognitive impairment, before overt pathology. However, in humans as well in AD mouse models, identification of early biomarkers of network dysfunction is still at its beginning. We performed in vivo recordings of local field potential activity in the dentate gyrus of PS2APP mice expressing the human amyloid precursor protein (APP) Swedish mutation and the presenilin-2 (PS2) N141I. From a frequency-domain analysis, we uncovered network hyper-synchronicity as early as 3 months, when intracellular accumulation of amyloid beta was also observable...
November 5, 2016: Neurobiology of Aging
https://www.readbyqxmd.com/read/27881772/store-operated-calcium-channel-complex-in-postsynaptic-spines-a-new-therapeutic-target-for-alzheimer-s-disease-treatment
#8
Hua Zhang, Suya Sun, Lili Wu, Ekaterina Pchitskaya, Olga Zakharova, Klementina Fon Tacer, Ilya Bezprozvanny
: Mushroom dendritic spine structures are essential for memory storage and the loss of mushroom spines may explain memory defects in aging and Alzheimer's disease (AD). The stability of mushroom spines depends on stromal interaction molecule 2 (STIM2)-mediated neuronal-store-operated Ca(2+) influx (nSOC) pathway, which is compromised in AD mouse models, in aging neurons, and in sporadic AD patients. Here, we demonstrate that the Transient Receptor Potential Canonical 6 (TRPC6) and Orai2 channels form a STIM2-regulated nSOC Ca(2+) channel complex in hippocampal mushroom spines...
November 23, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27875990/inverse-relationship-between-alzheimer-s-disease-and-cancer-and-other-factors-contributing-to-alzheimer-s-disease-a-systematic-review
#9
Ovais Shafi
BACKGROUND: The AD etiology is yet not properly known. Interactions among environmental factors, multiple susceptibility genes and aging, contribute to AD. This study investigates the factors that play role in causing AD and how changes in cellular pathways contribute to AD. METHODS: PUBMED database, MEDLINE database and Google Scholar were searched with no date restrictions for published articles involving cellular pathways with roles in cancers, cell survival, growth, proliferation, development, aging, and also contributing to Alzheimer's disease...
November 22, 2016: BMC Neurology
https://www.readbyqxmd.com/read/27836335/a-novel-presenilin-1-mutation-f388l-identified-in-a-chinese-family-with-early-onset-alzheimer-s-disease
#10
Yihong Zhan, Honghua Zheng, Chen Wang, Zhouyi Rong, Naian Xiao, Qilin Ma, Yun-Wu Zhang
A subset of Alzheimer's disease (AD) occurrence shows autosomal dominant, familial inheritance patterns. Such familial AD (FAD) are caused by mutations in APP, PSEN1, and PSEN2 genes, which encode amyloid-β (Aβ) precursor protein, presenilin 1 (PS1), and presenilin 2 (PS2), respectively. Here, we report a novel PSEN1 mutation (c.1164C > G, p.F388L, mutation nomenclature according to National Center for Biotechnology Information Reference Sequence: NM_000021.3) occurring in a Chinese family with early-onset AD and cosegregating with affected family members...
October 15, 2016: Neurobiology of Aging
https://www.readbyqxmd.com/read/27835671/an-anti-parkinson-s-disease-drug-via-targeting-adenosine-a2a-receptor-enhances-amyloid-%C3%AE-generation-and-%C3%AE-secretase-activity
#11
Jing Lu, Jin Cui, Xiaohang Li, Xin Wang, Yue Zhou, Wenjuan Yang, Ming Chen, Jian Zhao, Gang Pei
γ-secretase mediates the intramembranous proteolysis of amyloid precursor protein (APP) and determines the generation of Aβ which is associated with Alzheimer's disease (AD). Here we identified that an anti-Parkinson's disease drug, Istradefylline, could enhance Aβ generation in various cell lines and primary neuronal cells of APP/PS1 mouse. Moreover, the increased generation of Aβ42 was detected in the cortex of APP/PS1 mouse after chronic treatment with Istradefylline. Istradefylline promoted the activity of γ-secretase which could lead to increased Aβ production...
2016: PloS One
https://www.readbyqxmd.com/read/27833535/early-cortical-changes-in-gamma-oscillations-in-alzheimer-s-disease
#12
Alexandra S Klein, José R Donoso, Richard Kempter, Dietmar Schmitz, Prateep Beed
The entorhinal cortices in the temporal lobe of the brain are key structures relaying memory related information between the neocortex and the hippocampus. The medial entorhinal cortex (MEC) routes spatial information, whereas the lateral entorhinal cortex (LEC) routes predominantly olfactory information to the hippocampus. Gamma oscillations are known to coordinate information transfer between brain regions by precisely timing population activity of neuronal ensembles. Here, we studied the organization of in vitro gamma oscillations in the MEC and LEC of the transgenic (tg) amyloid precursor protein (APP)-presenilin 1 (PS1) mouse model of Alzheimer's Disease (AD) at 4-5 months of age...
2016: Frontiers in Systems Neuroscience
https://www.readbyqxmd.com/read/27818272/tetraspanin-3-a-central-endocytic-membrane-component-regulating-the-expression-of-adam10-presenilin-and-the-amyloid-precursor-protein
#13
Lisa Seipold, Markus Damme, Johannes Prox, Björn Rabe, Petr Kasparek, Radislav Sedlacek, Hermann Altmeppen, Michael Willem, Barry Boland, Markus Glatzel, Paul Saftig
Despite existing knowledge about the role of the A Disintegrin and Metalloproteinase 10 (ADAM10) as the α-secretase involved in the non-amyloidogenic processing of the amyloid precursor protein (APP) and Notch signalling we have only limited information about its regulation. In this study, we have identified ADAM10 interactors using a split ubiquitin yeast two hybrid approach. Tetraspanin 3 (Tspan3), which is highly expressed in the murine brain and elevated in brains of Alzheimer´s disease (AD) patients, was identified and confirmed to bind ADAM10 by co-immunoprecipitation experiments in mammalian cells in complex with APP and the γ-secretase protease presenilin...
January 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27816212/novel-presenilin-1-mutation-p-f386i-in-a-chinese-family-with-early-onset-alzheimer-s-disease
#14
Yat-Fung Shea, Angel On-Kei Chan, Leung-Wing Chu, Shui-Ching Lee, Chun-Yin Law, Chung-Him See, Kit-Ling Yiu, Patrick Ka-Chun Chiu
Autosomal dominant familial Alzheimer's disease accounts for 0.5% of all Alzheimer's disease. A familial Alzheimer's disease Chinese family, with 7 affected family members, underwent PSEN1 screening in 3 affected family members. A heterozygous novel missense mutation in the PSEN1 gene c.1156T>A, altering phenylalanine to isoleucine at codon 386, was identified. Because the change occurred in conserved domains of this gene and cosegregated with affected family members, this change may have a mutagenic and probably pathogenic effect...
October 15, 2016: Neurobiology of Aging
https://www.readbyqxmd.com/read/27810638/presenilin-1-mutations-influence-processing-and-trafficking-of-the-apoe-receptor-apoer2
#15
Wei Wang, Andrea M Moerman-Herzog, Arthur Slaton, Steven W Barger
Presenilin (PS)-1 is an intramembrane protease serving as the catalytic component of γ-secretase. Mutations in the PS1 gene are the most common cause of familial Alzheimer's disease (FAD). The low-density lipoprotein (LDL)-receptor family member apoER2 is a γ-secretase substrate that has been associated with AD in several ways, including acting as a receptor for apolipoprotein E (ApoE). ApoER2 is processed by γ-secretase into a C-terminal fragment (γ-CTF) that appears to regulate gene expression. FAD PS1 mutations were tested for effects on apoER2...
October 11, 2016: Neurobiology of Aging
https://www.readbyqxmd.com/read/27809235/protective-effect-of-genistein-against-neuronal-degeneration-in-apoe-mice-fed-a-high-fat-diet
#16
Yoon-Jin Park, Je Won Ko, Sookyoung Jeon, Young Hye Kwon
Altered cholesterol metabolism is believed to play a causal role in major pathophysiological changes in neurodegeneration. Several studies have demonstrated that the absence of apolipoprotein E (ApoE), a predominant apolipoprotein in the brain, leads to an increased susceptibility to neurodegeneration. Previously, we observed that genistein, a soy isoflavone, significantly alleviated apoptosis and tau hyperphosphorylation in SH-SY5Y cells. Therefore, we investigated the neuroprotective effects of dietary genistein supplementation (0...
October 31, 2016: Nutrients
https://www.readbyqxmd.com/read/27804997/a-presenilin-notch1-pathway-regulated-by-mir-375-mir-30a-and-mir-34a-mediates-glucotoxicity-induced-pancreatic-beta-cell-apoptosis
#17
Yating Li, Tao Zhang, Yuncai Zhou, Yi Sun, Yue Cao, Xiaoai Chang, Yunxia Zhu, Xiao Han
The presenilin-mediated Notch1 cleavage pathway plays a critical role in controlling pancreatic beta cell fate and survival. The aim of the present study was to investigate the role of Notch1 activation in glucotoxicity-induced beta cell impairment and the contributions of miR-375, miR-30a, and miR-34a to this pathway. We found that the protein levels of presenilins (PSEN1 and PSEN2), and NOTCH1 were decreased in INS-1 cells after treatment with increased concentrations of glucose, whereas no significant alteration of mRNA level of Notch1 was observed...
November 2, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27797115/inhibitory-effect-of-presenilin-inhibitor-ly411575-on-maturation-of-hepatitis-c-virus-core-protein-production-of-the-viral-particle-and-expression-of-host-proteins-involved-in-pathogenicity
#18
Teruhime Otoguro, Tomohisa Tanaka, Hirotake Kasai, Atsuya Yamashita, Kohji Moriishi
Hepatitis C virus (HCV) core protein is responsible for the formation of infectious viral particles and induction of pathogenicity. The C-terminal transmembrane region of the immature core protein is cleaved by signal peptide peptidase (SPP) for maturation of the core protein. SPP belongs to the family of presenilin-like aspartic proteases. Some presenilin inhibitors are expected to suppress HCV infection and production; however, this anti-HCV effect has not been investigated in detail. In this study, presenilin inhibitors were screened to identify anti-HCV compounds...
November 2016: Microbiology and Immunology
https://www.readbyqxmd.com/read/27795708/broad-spectrum-anticancer-activity-of-myo-inositol-and-inositol-hexakisphosphate
#19
REVIEW
Mariano Bizzarri, Simona Dinicola, Arturo Bevilacqua, Alessandra Cucina
Inositols (myo-inositol and inositol hexakisphosphate) exert a wide range of critical activities in both physiological and pathological settings. Deregulated inositol metabolism has been recorded in a number of diseases, including cancer, where inositol modulates different critical pathways. Inositols inhibit pRB phosphorylation, fostering the pRB/E2F complexes formation and blocking progression along the cell cycle. Inositols reduce PI3K levels, thus counteracting the activation of the PKC/RAS/ERK pathway downstream of PI3K activation...
2016: International Journal of Endocrinology
https://www.readbyqxmd.com/read/27793474/clinical-imaging-pathological-and-biochemical-characterization-of-a-novel-presenilin-1-mutation-n135y-causing-alzheimer-s-disease
#20
Marissa Natelson Love, David G Clark, J Nicholas Cochran, Kyle A Den Beste, David S Geldmacher, Tammie L Benzinger, Brian A Gordon, John C Morris, Randall J Bateman, Erik D Roberson
We present 2 cases of early-onset Alzheimer's disease due to a novel N135Y mutation in PSEN1. The proband presented with memory and other cognitive symptoms at age 32. Detailed clinical characterization revealed initial deficits in memory with associated dysarthria, progressing to involve executive dysfunction, spastic gait, and episodic confusion with polyspike discharges on long-term electroencephalography. Amyloid- and FDG-PET scans showed typical results of Alzheimer's disease. By history, the proband's father had developed cognitive symptoms at age 42 and died at age 48...
October 3, 2016: Neurobiology of Aging
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