keyword
MENU ▼
Read by QxMD icon Read
search

Mouse modell for alzheimers disease

keyword
https://www.readbyqxmd.com/read/28818766/design-synthesis-and-in%C3%A2-vivo-study-of-novel-pyrrolidine-based-11%C3%AE-hsd1-inhibitors-for-age-related-cognitive-dysfunction
#1
Rosana Leiva, Christian Griñan-Ferré, Constantí Seira, Elena Valverde, Andrew McBride, Margaret Binnie, Belén Pérez, F Javier Luque, Mercè Pallàs, Axel Bidon-Chanal, Scott P Webster, Santiago Vázquez
Recent findings suggest that treatment with 11β-HSD1 inhibitors provides a novel approach to deal with age-related cognitive dysfunctions, including Alzheimer's disease. In this work we report potent 11β-HSD1 inhibitors featuring unexplored pyrrolidine-based polycyclic substituents. A selected candidate administered to 12-month-old SAMP8 mice for four weeks prevented memory deficits and displayed a neuroprotective action. This is the first time that 11β-HSD1 inhibitors have been studied in this broadly-used mouse model of accelerated senescence and late-onset Alzheimer's disease...
August 4, 2017: European Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/28817954/dissecting-amyloid-beta-deposition-using-distinct-strains-of-the-neurotropic-parasite-toxoplasma-gondii-as-a-novel-tool
#2
Carla M Cabral, Kathryn E McGovern, Wes R MacDonald, Jenna Franco, Anita A Koshy
Genetic and pathologic data suggest that amyloid beta (Aβ), produced by processing of the amyloid precursor protein, is a major initiator of Alzheimer's disease (AD). To gain new insights into Aβ modulation, we sought to harness the power of the coevolution between the neurotropic parasite Toxoplasma gondii and the mammalian brain. Two prior studies attributed Toxoplasma-associated protection against Aβ to increases in anti-inflammatory cytokines (TGF-β and IL-10) and infiltrating phagocytic monocytes. These studies only used one Toxoplasma strain making it difficult to determine if the noted changes were associated with Aβ protection or simply infection...
July 2017: ASN Neuro
https://www.readbyqxmd.com/read/28812049/importance-of-adiponectin-activity-in-the-pathogenesis-of-alzheimer-s-disease
#3
REVIEW
Masaaki Waragai, Gilbert Ho, Yoshiki Takamatsu, Kazunari Sekiyama, Shuei Sugama, Takato Takenouchi, Eliezer Masliah, Makoto Hashimoto
A recent study suggested that insulin resistance may play a central role in the pathogenesis of Alzheimer's disease (AD). In this regard, it is of note that upregulation of plasma adiponectin (APN), a benign adipokine that sensitizes the insulin receptor signaling pathway and suppresses inflammation, has recently been associated with the severities of amyloid deposits and cognitive deficits in the elderly, suggesting that APN may enhance the risk of AD. These results are unanticipated because AD has been linked to type II diabetes and other metabolic disorders in which hypoadiponectinemia has been firmly established, and because APN ameliorated neuropathological features in a mouse model of neurodegeneration...
August 2017: Annals of Clinical and Translational Neurology
https://www.readbyqxmd.com/read/28808293/targeting-apolipoprotein-e-amyloid-%C3%AE-binding-by-peptoid-cpo_a%C3%AE-17-21%C3%A2-p-ameliorates-alzheimer-s-disease-related-pathology-and-cognitive-decline
#4
Shan Liu, Shinae Park, Grant Allington, Frances Prelli, Yanjie Sun, Mitchell Martá-Ariza, Henrieta Scholtzova, Goutam Biswas, Bernard Brown, Philip B Verghese, Pankaj D Mehta, Yong-Uk Kwon, Thomas Wisniewski
Inheritance of the apolipoprotein E4 (apoE4) genotype has been identified as the major genetic risk factor for late onset Alzheimer's disease (AD). Studies have shown that apoE, apoE4 in particular, binds to amyloid-β (Aβ) peptides at residues 12-28 of Aβ and this binding modulates Aβ accumulation and disease progression. We have previously shown in several AD transgenic mice lines that blocking the apoE/Aβ interaction with Aβ12-28 P reduced Aβ and tau-related pathology, leading to cognitive improvements in treated AD mice...
August 14, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28808140/amyloid-%C3%AE-and-islet-amyloid-pathologies-link-alzheimer-disease-and-type-2-diabetes-in-a-transgenic-model
#5
Nadeeja Wijesekara, Rosemary Ahrens, Miheer Sabale, Ling Wu, Kathy Ha, Giuseppe Verdile, Paul E Fraser
Alzheimer's disease (AD) and type 2 diabetes (T2D) present a significant risk to each other. AD and T2D are characterized by deposition of cerebral amyloid-β (Aβ) and pancreatic human islet amyloid polypeptide (hIAPP), respectively. We investigated the role of amyloidogenic proteins in the interplay between these diseases. A novel double transgenic mouse model combining T2D and AD was generated and characterized. AD-related amyloid transgenic mice coexpressing hIAPP displayed peripheral insulin resistance, hyperglycemia, and glucose intolerance...
August 14, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28802916/brain-region-and-sex-specific-alterations-in-mitochondrial-function-and-nf-%C3%AE%C2%BAb-signaling-in-the-tgcrnd8-mouse-model-of-alzheimer-s-disease
#6
Jelena Djordjevic, Ella Thomson, Subir Roy Chowdhury, Wanda M Snow, Claudia Perez, Tak Pan Wong, Paul Fernyhough, Benedict C Albensi
Alzheimer's disease (AD) is the most common late onset neurodegenerative disorder with indications that women are disproportionally affected. Mitochondrial dysfunction has been one of the most discussed hypotheses associated with the early onset and progression of AD, and it has been attributed to intraneuronal accumulation of amyloid β (Aβ). It was suggested that one of the possible mediators for Aβ-impaired mitochondrial function is the nuclear factor kappa B (NF-κB) signaling pathway. NF-κB plays important roles in brain inflammation and antioxidant defense, as well as in the regulation of mitochondrial function, and studies have confirmed altered NF-κB signaling in AD brain...
August 9, 2017: Neuroscience
https://www.readbyqxmd.com/read/28799137/ethanol-alters-app-processing-and-aggravates-alzheimer-associated-phenotypes
#7
Daochao Huang, Mengjiao Yu, Shou Yang, Dandan Lou, Weitao Zhou, Lingling Zheng, Zhe Wang, Fang Cai, Weihui Zhou, Tingyu Li, Weihong Song
The majority of Alzheimer's disease (AD) cases are sporadic with unknown causes. Many dietary factors including excessive alcohol intake have been reported to increase the risk to develop AD. The effect of alcohol on cognitive functions and AD pathogenesis remains elusive. In this study, we investigated the relationship between ethanol exposure and Alzheimer's disease. Cell cultures were treated with ethanol at different dosages for different durations up to 48 h and an AD model mouse was fed with ethanol for 4 weeks...
August 10, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28797738/tissue-magnetic-susceptibility-mapping-as-a-marker-of-tau-pathology-in-alzheimer-s-disease
#8
J O'Callaghan, H Holmes, N Powell, J A Wells, O Ismail, I F Harrison, B Siow, R Johnson, Z Ahmed, A Fisher, S Meftah, M J O'Neill, T K Murray, E C Collins, K Shmueli, M F Lythgoe
Alzheimer's disease is connected to a number of other neurodegenerative conditions, known collectively as 'tauopathies', by the presence of aggregated tau protein in the brain. Neuroinflammation and oxidative stress in AD are associated with tau pathology and both the breakdown of axonal sheaths in white matter tracts and excess iron accumulation grey matter brain regions. Despite the identification of myelin and iron concentration as major sources of contrast in quantitative susceptibility maps of the brain, the sensitivity of this technique to tau pathology has yet to be explored...
August 4, 2017: NeuroImage
https://www.readbyqxmd.com/read/28794819/upregulation-of-autophagy-genes-and-the-unfolded-protein-response-in-human-heart-failure
#9
Brian C Jensen, Scott J Bultman, Darcy Holley, Wei Tang, Gustaaf de Ridder, Salvatore Pizzo, Dawn Bowles, Monte S Willis
The cellular environment of the mammalian heart constantly is challenged with environmental and intrinsic pathological insults, which affect the proper folding of proteins in heart failure. The effects of damaged or misfolded proteins on the cell can be profound and result in a process termed "proteotoxicity". While proteotoxicity is best known for its role in mediating the pathogenesis of neurodegenerative diseases such as Alzheimer's disease, its role in human heart failure also has been recognized. The UPR involves three branches, including PERK, ATF6, and IRE1...
2017: International Journal of Clinical and Experimental Medicine
https://www.readbyqxmd.com/read/28793257/the-transcription-factor-sp3-cooperates-with-hdac2-to-regulate-synaptic-function-and-plasticity-in-neurons
#10
Hidekuni Yamakawa, Jemmie Cheng, Jay Penney, Fan Gao, Richard Rueda, Jun Wang, Satoko Yamakawa, Oleg Kritskiy, Elizabeta Gjoneska, Li-Huei Tsai
The histone deacetylase HDAC2, which negatively regulates synaptic gene expression and neuronal plasticity, is upregulated in Alzheimer's disease (AD) patients and mouse models. Therapeutics targeting HDAC2 hold promise for ameliorating AD-related cognitive impairment; however, attempts to generate HDAC2-specific inhibitors have failed. Here, we take an integrative genomics approach to identify proteins that mediate HDAC2 recruitment to synaptic plasticity genes. Functional screening revealed that knockdown of the transcription factor Sp3 phenocopied HDAC2 knockdown and that Sp3 facilitated recruitment of HDAC2 to synaptic genes...
August 8, 2017: Cell Reports
https://www.readbyqxmd.com/read/28776265/traumatic-brain-injury-alters-the-metabolism-and-facilitates-alzheimer-s-disease-in-a-murine-model
#11
Dandan Lou, Yao Du, Daochao Huang, Fang Cai, Yun Zhang, Tinyu Li, Weihui Zhou, Hongchang Gao, Weihong Song
A majority of Alzheimer's disease (AD) cases are sporadic without known cause. People who suffered from traumatic brain injury (TBI) are more likely to develop neurodegeneration and cognitive impairments. However, the role of TBI in pathophysiology of AD remains elusive. The present study intended to explore the effect of TBI on metabolism and its role in AD pathogenesis. We subjected double transgenic AD model mice APP23/PS45 to TBI. We found that TBI promoted β-secretase cleavage of amyloid β precursor protein and amyloid β protein deposition, and exuberated the cognitive impairments in AD mouse models...
August 3, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28771976/hdac3-negatively-regulates-spatial-memory-in-a-mouse-model-of-alzheimer-s-disease
#12
Xiaolei Zhu, Sulei Wang, Linjie Yu, Jiali Jin, Xing Ye, Yi Liu, Yun Xu
The accumulation and deposition of beta-amyloid (Aβ) is a key neuropathological hallmark of Alzheimer's disease (AD). Histone deacetylases (HDACs) are promising therapeutic targets for the treatment of AD, while the specific HDAC isoforms associated with cognitive improvement are poorly understood. In this study, we investigate the role of HDAC3 in the pathogenesis of AD. Nuclear HDAC3 is significantly increased in the hippocampus of 6- and 9-month-old APPswe/PS1dE9 (APP/PS1) mice compared with that in age-matched wild-type C57BL/6 (B6) mice...
August 3, 2017: Aging Cell
https://www.readbyqxmd.com/read/28771492/production-of-an-anti-a%C3%AE-antibody-fragment-in-pichia-pastoris-and-in-vitro-and-in-vivo-validation-of-its-therapeutic-effect
#13
Laia Montoliu-Gaya, Gisela Esquerda-Canals, Silvia Bronsoms, Sandra Villegas
ScFv-h3D6 has been shown as an efficient therapy in the 3xTg-AD mouse model of Alzheimer's Disease. Because one of the major bottlenecks for the therapeutic uses of proteins produced in Escherichia coli is their potential contamination with endotoxins, LPS were extensively removed by a rather low-efficient, expensive, and time-consuming purification step. In addition, disulfide scrambling is favored in the reducing bacterial cytoplasm albeit the use of reductase deficient strains. To overcome these hurdles, as well as to improve the yield, the yeast Pichia pastoris, an endotoxin-free host system for recombinant protein production, has been used to produce scFv-h3D6, both in flask and in a fed-batch bioreactor...
2017: PloS One
https://www.readbyqxmd.com/read/28769761/identification-of-the-role-of-mir-142-5p-in-alzheimer-s-disease-by-comparative-bioinformatics-and-cellular-analysis
#14
Juhyun Song, Young-Kook Kim
Alzheimer's disease (AD) is the most common neurodegenerative disease characterized by the formation of amyloid beta (Aβ) or tau protein aggregates, the hallmark of cognitive decline. MicroRNAs (miRNAs) have emerged as critical factors in neurogenesis and synaptic functions in the central nervous system (CNS). Recent studies have reported alterations in miRNA expression in patients with AD. However, miRNAs associated with AD varied with patient groups or experimental models, suggesting the need for a comparative study to identify miRNAs commonly dysregulated in diverse AD models...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28768718/app-mouse-models-for-alzheimer-s-disease-preclinical-studies
#15
REVIEW
Hiroki Sasaguri, Per Nilsson, Shoko Hashimoto, Kenichi Nagata, Takashi Saito, Bart De Strooper, John Hardy, Robert Vassar, Bengt Winblad, Takaomi C Saido
Animal models of human diseases that accurately recapitulate clinical pathology are indispensable for understanding molecular mechanisms and advancing preclinical studies. The Alzheimer's disease (AD) research community has historically used first-generation transgenic (Tg) mouse models that overexpress proteins linked to familial AD (FAD), mutant amyloid precursor protein (APP), or APP and presenilin (PS). These mice exhibit AD pathology, but the overexpression paradigm may cause additional phenotypes unrelated to AD Second-generation mouse models contain humanized sequences and clinical mutations in the endogenous mouse App gene...
August 1, 2017: EMBO Journal
https://www.readbyqxmd.com/read/28768163/a-protocol-for-quantitative-analysis-of-murine-and-human-amyloid-%C3%AE-1-40-and-1-42
#16
Tomer Illouz, Ravit Madar, Kathleen Griffioen, Eitan Okun
BACKGROUND: Amyloid-β (Aβ), a hallmark of Alzheimer's disease (AD), has long been a focus of basic and translation research in AD. Quantification and dissociation of the Aβ fractions in their soluble and insoluble forms, is a key factor in numerous AD studies. NEW METHOD: Here we provide a generalized sandwich-enzyme-linked-immuno-sorbent-assay (sELISA) protocol for quantification of human and murine Aβ1-40 and Aβ1-42 and dissociation of these peptides to their soluble-oligomeric and insoluble-fibrillar forms...
July 30, 2017: Journal of Neuroscience Methods
https://www.readbyqxmd.com/read/28760945/inactivation-of-nitric-oxide-synthesis-exacerbates-the-development-of-alzheimer-disease-pathology-in-appps1-mice-amyloid-precursor-protein-presenilin-1
#17
Diana Cifuentes, Marine Poittevin, Philippe Bonnin, Anta Ngkelo, Nathalie Kubis, Tatyana Merkulova-Rainon, Bernard I Lévy
The epidemiological link between hypertension and Alzheimer disease is established. We previously reported that hypertension aggravates the Alzheimer-like pathology in APPPS1 mice (amyloid precursor protein/presenilin-1, mouse model of Alzheimer disease) with angiotensin II-induced hypertension, in relation with hypertension and nitric oxide deficiency. To provide further insights into the role of nitric oxide in the hypertension-Alzheimer disease cross-talk, we studied the effects of nitric oxide blockade in APPPS1 mice using N(ω)-nitro-l-arginine methyl ester (l-NAME) alone or in combination with hydralazine, to normalize blood pressure...
July 31, 2017: Hypertension
https://www.readbyqxmd.com/read/28760828/an-acetylation-phosphorylation-switch-that-regulates-tau-aggregation-propensity-and-function
#18
Yari Carlomagno, Dah-Eun Chloe Chung, Mei Yue, Monica Castanedes-Casey, Benjamin J Madden, Judy Dunmore, Jimei Tong, Michael DeTure, Dennis W Dickson, Leonard Petrucelli, Casey Cook
The aberrant accumulation of tau protein is a pathological hallmark of a class of neurodegenerative diseases known as tauopathies, including Alzheimer's disease (AD) and related dementias. On the basis of previous observations that tau is a direct substrate of histone deacetylase 6 (HDAC6), we sought to map all HDAC6-responsive sites in tau and determine how acetylation in a site-specific manner affects tau-s biophysical properties in vitro. Our findings indicate that several acetylation sites on tau are responsive to HDAC6 and that acetylation on Lys-321 (within a KCGS motif) is both essential for acetylation-mediated inhibition of tau aggregation in vitro and a molecular tactic for preventing phosphorylation on the downstream Ser-324 residue...
July 31, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28760697/vision-in-laboratory-rodents-tools-to-measure-it-and-implications-for-behavioral-research
#19
REVIEW
Henri Leinonen, Heikki Tanila
Mice and rats are nocturnal mammals and their vision is specialized for detection of motion and contrast in dim light conditions. These species possess a large proportion of UV-sensitive cones in their retinas and the majority of their optic nerve axons target superior colliculus rather than visual cortex. Therefore, it was a widely held belief that laboratory rodents hardly utilize vision during day-time behavior. This dogma is being questioned as accumulating evidence suggests that laboratory rodents are able to perform complex visual functions, such as perceiving subjective contours, and that declined vision may affect their performance in many behavioral tasks...
July 28, 2017: Behavioural Brain Research
https://www.readbyqxmd.com/read/28760504/protection-against-rage-mediated-neuronal-cell-death-by-srage-secreting-human-mesenchymal-stem-cells-in-5xfad-transgenic-mouse-model
#20
Myeongjoo Son, Seyeon Oh, Hyunjin Park, Hyosang Ahn, Junwon Choi, Hyungho Kim, Hye Sun Lee, Sojung Lee, Hye-Jeong Park, Seung U Kim, Bonghee Lee, Kyunghee Byun
Alzheimer's disease (AD), which is the most commonly encountered neurodegenerative disease, causes synaptic dysfunction and neuronal loss due to various pathological processes that include tau abnormality and amyloid beta (Aβ) accumulation. Aβ stimulates the secretion and the synthesis of Receptor for Advanced Glycation End products (RAGE) ligand by activating microglial cells, and has been reported to cause neuronal cell death in amyloid beta1-42 treated rats and in mice with neurotoxin-induced Parkinson's disease...
July 28, 2017: Brain, Behavior, and Immunity
keyword
keyword
16746
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"