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Mouse modell for alzheimers disease

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https://www.readbyqxmd.com/read/29141186/hyperbaric-oxygen-therapy-ameliorates-pathophysiology-of-3xtg-ad-mouse-model-by-attenuating-neuroinflammation
#1
Ronit Shapira, Beka Solomon, Shai Efrati, Dan Frenkel, Uri Ashery
There is a real need for new interventions for Alzheimer's disease (AD). Hyperbaric oxygen therapy (HBOT), the medical administration of 100% oxygen at conditions greater than 1 atmosphere absolute, has been used successfully to treat several neurological conditions, but its effects on AD pathology have never been thoroughly examined. Therefore, we exposed old triple-transgenic (3xTg) and non-transgenic mice to HBOT followed by behavioral, histological, and biochemical analyses. HBOT attenuated neuroinflammatory processes by reducing astrogliosis, microgliosis, and the secretion of proinflammatory cytokines (IL-1β and TNFα) and increasing expression of scavenger receptor A, arginase1, and antiinflammatory cytokines (IL-4 and IL-10)...
October 20, 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/29137651/abnormal-dendritic-calcium-activity-and-synaptic-depotentiation-occur-early-in-a-mouse-model-of-alzheimer-s-disease
#2
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
#3
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/29134771/detection-of-%C3%AE-amyloid-by-sialic-acid-coated-bovine-serum-albumin-magnetic-nanoparticles-in-a-mouse-model-of-alzheimer-s-disease
#4
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/29134678/systemic-immune-checkpoint-blockade-with-anti-pd1-antibodies-does-not-alter-cerebral-amyloid-%C3%AE-burden-in-several-amyloid-transgenic-mouse-models
#5
Martine Latta-Mahieu, Bradford Elmer, Alexis Bretteville, Yaming Wang, Mati Lopez-Grancha, Philippe Goniot, Nicolas Moindrot, Paul Ferrari, Véronique Blanc, Nathalie Schussler, Emmanuel Brault, Valérie Roudières, Véronique Blanchard, Zhi-Yong Yang, Pascal Barneoud, Philippe Bertrand, Bart Roucourt, Sofie Carmans, Astrid Bottelbergs, Liesbeth Mertens, Cindy Wintmolders, Peter Larsen, Caroline Hersley, Tyler McGathey, Margaret M Racke, Ling Liu, Jirong Lu, Michael J O'Neill, David R Riddell, Andreas Ebneth, Gary J Nabel, Laurent Pradier
Chronic inflammation represents a central component in the pathogenesis of Alzheimer's disease (AD). Recent work suggests that breaking immune tolerance by Programmed cell Death-1 (PD1) checkpoint inhibition produces an IFN-γ-dependent systemic immune response, with infiltration of the brain by peripheral myeloid cells and neuropathological as well as functional improvements even in mice with advanced amyloid pathology (Baruch et al., (): Nature Medicine, 22:135-137). Immune checkpoint inhibition was therefore suggested as potential treatment for neurodegenerative disorders when activation of the immune system is appropriate...
November 14, 2017: Glia
https://www.readbyqxmd.com/read/29133892/er-associated-degradation-regulates-alzheimer-s-amyloid-pathology-and-memory-function-by-modulating-%C3%AE-secretase-activity
#6
Bing Zhu, LuLin Jiang, Timothy Huang, Yingjun Zhao, Tongfei Liu, Yongwang Zhong, Xiaoguang Li, Alexandre Campos, Kenneth Pomeroy, Eliezer Masliah, Dongxian Zhang, Huaxi Xu
Endoplasmic-reticulum-associated degradation (ERAD) is an important protein quality control system which maintains protein homeostasis. Constituents of the ERAD complex and its role in neurodegeneration are not yet fully understood. Here, using proteomic and FRET analyses, we demonstrate that the ER protein membralin is an ERAD component, which mediates degradation of ER luminal and membrane substrates. Interestingly, we identify nicastrin, a key component of the γ-secretase complex, as a membralin binding protein and membralin-associated ERAD substrate...
November 13, 2017: Nature Communications
https://www.readbyqxmd.com/read/29133888/neuronal-hyperactivity-due-to-loss-of-inhibitory-tone-in-apoe4-mice-lacking-alzheimer-s-disease-like-pathology
#7
Tal Nuriel, Sergio L Angulo, Usman Khan, Archana Ashok, Qiuying Chen, Helen Y Figueroa, Sheina Emrani, Li Liu, Mathieu Herman, Geoffrey Barrett, Valerie Savage, Luna Buitrago, Efrain Cepeda-Prado, Christine Fung, Eliana Goldberg, Steven S Gross, S Abid Hussaini, Herman Moreno, Scott A Small, Karen E Duff
The ε4 allele of apolipoprotein E (APOE) is the dominant genetic risk factor for late-onset Alzheimer's disease (AD). However, the reason APOE4 is associated with increased AD risk remains a source of debate. Neuronal hyperactivity is an early phenotype in both AD mouse models and in human AD, which may play a direct role in the pathogenesis of the disease. Here, we have identified an APOE4-associated hyperactivity phenotype in the brains of aged APOE mice using four complimentary techniques-fMRI, in vitro electrophysiology, in vivo electrophysiology, and metabolomics-with the most prominent hyperactivity occurring in the entorhinal cortex...
November 13, 2017: Nature Communications
https://www.readbyqxmd.com/read/29133432/locus-coeruleus-ablation-exacerbates-cognitive-deficits-neuropathology-and-lethality-in-p301s-tau-transgenic-mice
#8
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/29129596/amyloid-toxicity-is-enhanced-after-pharmacological-or-genetic-invalidation-of-the-%C3%AF-1-receptor
#9
Tangui Maurice, Manon Strehaiano, Fanny Duhr, Nathalie Chevallier
The sigma-1 receptor (S1R) is a molecular chaperone which activity modulates several intracellular signals including calcium mobilization at mitochondria-associated endoplasmic reticulum membranes. S1R agonists are potent neuroprotectants against neurodegenerative insults and particularly in rodent models of Alzheimer's disease (AD). We here analyzed whether S1R inactivation modifies vulnerability to amyloid toxicity in AD models. Two strategies were used: (1) amyloid β[25-35] (Aβ25-35) peptide (1, 3, 9nmol) was injected intracerebroventricularly in mice treated repeatedly with the S1R antagonist NE-100 or in S1RKO mice, and (2) WT, APPSweInd, S1RKO, and APPSweInd/S1RKO mice were created and female littermates analyzed at 8 months of age...
November 9, 2017: Behavioural Brain Research
https://www.readbyqxmd.com/read/29128902/overexpression-of-5-lipoxygenase-worsens-the-phenotype-of-a-mouse-model-of-tauopathy
#10
Phillip F Giannopoulos, Domenico Praticò
Brain accumulation of increasing amount of phosphorylated microtubule associated tau protein is one the major hallmark lesions of Alzheimer's disease (AD) and related tauopathies. Consistent evidence from clinical and animal studies has shown that neuroinflammation characterizes these diseases. The 5-lipoxygenase (5LO) is an enzyme protein whose metabolic products are lipids with potent inflammatory actions. Previously, we showed that blockade of 5LO activation ameliorates the phenotype of the htau transgenic mice...
November 11, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/29127580/sigma-1-receptor-agonists-induce-oxidative-stress-in-mitochondria-and-enhance-complex-i-activity-in-physiological-condition-but-protect-against-pathological-oxidative-stress
#11
Nino Goguadze, Elene Zhuravliova, Didier Morin, Davit Mikeladze, Tangui Maurice
The sigma1 receptor (σ1R) is a chaperone protein residing at mitochondria-associated endoplasmic reticulum (ER) membranes (MAMs), where it modulates Ca(2+) exchange between the ER and mitochondria by interacting with inositol-1,4,5 trisphosphate receptors (IP3Rs). The σ1R is highly expressed in the central nervous system and its activation stimulates neuromodulation and neuroprotection, for instance in Alzheimer's disease (AD) models in vitro and in vivo. σ1R effects on mitochondria pathophysiology and the downstream signaling are still not fully understood...
November 10, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/29126931/phytochemical-allylguaiacol-exerts-a-neuroprotective-effect-on-hippocampal-cells-and-ameliorates-scopolamine-induced-memory-impairment-in-mice
#12
Hye-Sun Lim, Bu-Yeo Kim, Yu Jin Kim, Soo-Jin Jeong
Allylguaiacol is a phytochemical occurring in various plants such as cloves, cinnamon, basil, and nutmeg. Pharmacological effects of allylguaiacol include antimicrobial, anti-inflammatory, anticancer, antioxidant, and neuroprotective activity. Although allylguaiacol is considered to have neuroprotective effects, there is no report on its regulatory mechanisms at the molecular level. In the present study, we investigated the mechanisms of allylguaiacol as an antioxidant and neuroprotective agent using hydrogen peroxide (H2O2)-treated HT22 hippocampal cells...
November 7, 2017: Behavioural Brain Research
https://www.readbyqxmd.com/read/29125684/magnesium-boosts-the-memory-restorative-effect-of-environmental-enrichment-in-alzheimer-s-disease-mice
#13
Ying Huang, Xian Huang, Ling Zhang, Fang Han, Ke-Liang Pang, Xue Li, Jian-Ying Shen
BACKGROUND: Environmental enrichment (EE) has been shown to enhance cognitive function in mouse models of Alzheimer's disease (AD). Magnesium-L-threonate (MgT) is a compound with a newly discovered effect to rescue learning and memory function in aging and AD mice. AIM: To study the additive therapeutic effect of EE combined with MgT (EM) and the potential mechanism underlying the effects. MATERIALS AND METHODS: APP/PS1 mice were treated with EE, MgT, or combination of EE and MgT (EM) and compared for restored memory function...
November 10, 2017: CNS Neuroscience & Therapeutics
https://www.readbyqxmd.com/read/29124106/gamma-rhythm-low-field-magnetic-stimulation-alleviates-neuropathologic-changes-and-rescues-memory-and-cognitive-impairments-in-a-mouse-model-of-alzheimer-s-disease
#14
Junli Zhen, Yanjing Qian, Xiechuan Weng, Wenting Su, Jianliang Zhang, Lihui Cai, Lin Dong, Haiting An, Ruijun Su, Jiang Wang, Yan Zheng, Xiaomin Wang
Introduction: The abnormal amyloid β (Aβ) accumulation and Aβ-related neural network dysfunction are considered central to the pathogenesis of Alzheimer's disease (AD) at the early stage. Deep-brain reachable low field magnetic stimulation (DMS), a novel noninvasive approach that was designed to intervene the network activity in brains, has been found to alleviate stress-related cognitive impairments. Methods: Amyloid precursor protein/presenilin-1 transgenic mice (5XFAD) were treated with DMS, and cognitive behavior and AD-like pathologic changes in the neurochemical and electrophysiological properties in 5XFAD mice were assessed...
November 2017: Alzheimer's & Dementia: Translational Research & Clinical Interventions
https://www.readbyqxmd.com/read/29123083/identification-of-a-peptide-recognizing-cerebrovascular-changes-in-mouse-models-of-alzheimer-s-disease
#15
Aman P Mann, Pablo Scodeller, Sazid Hussain, Gary B Braun, Tarmo Mölder, Kadri Toome, Rajesh Ambasudhan, Tambet Teesalu, Stuart A Lipton, Erkki Ruoslahti
Cerebrovascular changes occur in Alzheimer's disease (AD). Using in vivo phage display, we searched for molecular markers of the neurovascular unit, including endothelial cells and astrocytes, in mouse models of AD. We identified a cyclic peptide, CDAGRKQKC (DAG), that accumulates in the hippocampus of hAPP-J20 mice at different ages. Intravenously injected DAG peptide homes to neurovascular unit endothelial cells and to reactive astrocytes in mouse models of AD. We identified connective tissue growth factor (CTGF), a matricellular protein that is highly expressed in the brain of individuals with AD and in mouse models, as the target of the DAG peptide...
November 10, 2017: Nature Communications
https://www.readbyqxmd.com/read/29122977/a%C3%AE-inhibits-srebp-2-activation-through-akt-inhibition
#16
Amany Mohamed, Anissa Viveiros, Kathleen Williams, Elena Posse de Chaves
We previously demonstrated that oligomeric Aβ42 (oAβ42 ) inhibits the mevalonate pathway impairing cholesterol synthesis and protein prenylation. Enzymes of the mevalonate pathway are regulated by the transcription factor sterol regulatory element binding protein (SREBP) 2. Here, we show that in several neuronal types challenged with o Aβ42, SREBP-2 activation is reduced. Moreover, SREBP-2 activation is also decreased in brain cortex of the Alzheimer's disease (AD) mouse model TgCRND8, suggesting that SREBP-2 may be affected in vivo during disease...
November 9, 2017: Journal of Lipid Research
https://www.readbyqxmd.com/read/29121962/direct-interaction-with-14-3-3%C3%AE-promotes-surface-expression-of-best1-channel-in-astrocyte
#17
Soo-Jin Oh, Junsung Woo, Young-Sun Lee, Minhee Cho, Eunju Kim, Nam-Chul Cho, Jae-Yong Park, Ae Nim Pae, C Justin Lee, Eun Mi Hwang
BACKGROUND: Bestrophin-1 (Best1) is a calcium-activated anion channel (CAAC) that is expressed broadly in mammalian tissues including the brain. We have previously reported that Best1 is expressed in hippocampal astrocytes at the distal peri-synaptic regions, called microdomains, right next to synaptic junctions, and that it disappears from the microdomains in Alzheimer's disease mouse model. Although Best1 appears to be dynamically regulated, the mechanism of its regulation and modulation is poorly understood...
November 9, 2017: Molecular Brain
https://www.readbyqxmd.com/read/29116812/x-ray-characterization-and-structure-based-optimization-of-striatal-enriched-protein-tyrosine-phosphatase-inhibitors
#18
Michael R Witten, Lisa Wissler, Melanie Snow, Stefan Geschwindner, Jon A Read, Nicholas J Brandon, Angus C Nairn, Paul J Lombroso, Helena Käck, Jonathan A Ellman
Excessive activity of striatal-enriched protein tyrosine phosphatase (STEP) in the brain has been detected in numerous neuropsychiatric disorders including Alzheimer's disease. Notably, knockdown of STEP in an Alzheimer mouse model effected an increase in the phosphorylation levels of downstream STEP substrates and a significant reversal in the observed cognitive and memory deficits. These data point to the promising potential of STEP as a target for drug discovery in Alzheimer's treatment. We previously reported a substrate-based approach to the development of low molecular weight STEP inhibitors with Ki values as low as 7...
November 8, 2017: Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/29116174/activation-of-g-protein-gated-inwardly-rectifying-potassium-kir3-girk-channels-rescues-hippocampal-functions-in-a-mouse-model-of-early-amyloid-%C3%AE-pathology
#19
Irene Sánchez-Rodríguez, Sara Temprano-Carazo, Alberto Nájera, Souhail Djebari, Javier Yajeya, Agnès Gruart, José M Delgado-García, Lydia Jiménez-Díaz, Juan D Navarro-López
The hippocampus plays a critical role in learning and memory. Its correct performance relies on excitatory/inhibitory synaptic transmission balance. In early stages of Alzheimer's disease (AD), neuronal hyperexcitability leads to network dysfunction observed in cortical regions such as the hippocampus. G-protein-gated potassium (GirK) channels induce neurons to hyperpolarize, contribute to the resting membrane potential and could compensate any excesses of excitation. Here, we have studied the relationship between GirK channels and hippocampal function in a mouse model of early AD pathology...
November 7, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29113959/age-related-epigenetic-changes-in-hippocampal-subregions-of-four-animal-models-of-alzheimer-s-disease
#20
Roy Lardenoije, Daniël L A van den Hove, Monique Havermans, Anne van Casteren, Kevin X Le, Roberta Palmour, Cynthia A Lemere, Bart P F Rutten
Both aging and Alzheimer's disease (AD) are associated with widespread epigenetic changes, with most evidence suggesting global hypomethylation in AD. It is, however, unclear how these age-related epigenetic changes are linked to molecular aberrations as expressed in animal models of AD. Here, we investigated age-related changes of epigenetic markers of DNA methylation and hydroxymethylation in a range of animal models of AD, and their correlations with amyloid plaque load. Three transgenic mouse models, including the J20, APP/PS1dE9 and 3xTg-AD models, as well as Caribbean vervets (a non-transgenic non-human primate model of AD) were investigated...
November 4, 2017: Molecular and Cellular Neurosciences
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