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Showing 1-30 of 32 results for "A5213" within Papers
Chia-Mei Chou et al.
Parasites & vectors, 10(1), 620-620 (2017-12-24)
Toxocariasis is a worldwide zoonotic parasitic disease mainly caused by Toxocara canis. Humans can be infected by accidental ingestion of T. canis embryonated ovum-contaminated food, water, or encapsulated larvae in paratenic hosts' viscera or meat. Since humans and mice are
Tian Tian et al.
Nutrients, 8(9) (2016-09-13)
Alzheimer's disease (AD) is the most common type of dementia. Amyloid-β protein (Aβ) is identified as the core protein of neuritic plaques. Aβ is generated by the sequential cleavage of the amyloid precursor protein (APP) via the APP cleaving enzyme
Hye-Eun Han et al.
PloS one, 5(12), e15645-e15645 (2010-12-29)
The nuclear inclusion a (NIa) protease of turnip mosaic virus (TuMV) is responsible for the processing of the viral polyprotein into functional proteins. NIa was previously shown to possess a relatively strict substrate specificity with a preference for Val-Xaa-His-Gln↓, with
Jessica F Jordão et al.
PloS one, 5(5), e10549-e10549 (2010-05-21)
Immunotherapy for Alzheimer's disease (AD) relies on antibodies directed against toxic amyloid-beta peptide (Abeta), which circulate in the bloodstream and remove Abeta from the brain. In mouse models of AD, the administration of anti-Abeta antibodies directly into the brain, in
Fangfang Qi et al.
Molecular psychiatry (2023-06-07)
Activation of innate immunity in the brain is a prominent feature of Alzheimer's disease (AD). The present study investigated the regulation of innate immunity by wild-type serum injection in a transgenic AD mouse model. We found that treatment with wild-type
Jared Ehrhart et al.
Journal of neuroinflammation, 2, 29-29 (2005-12-14)
Activated microglial cells have been implicated in a number of neurodegenerative disorders, including Alzheimer's disease (AD), multiple sclerosis (MS), and HIV dementia. It is well known that inflammatory mediators such as nitric oxide (NO), cytokines, and chemokines play an important
Effects of Folic Acid on Secretases Involved in Aβ Deposition in APP/PS1 Mice
Tian, T, et al.
Nutrients, 8(9), 556-556 (2016)
Use-dependent effects of amyloidogenic fragments of β-amyloid precursor protein on synaptic plasticity in rat hippocampus in vivo
Kim, J, et al.
The Journal of Neuroscience, 21(4), 1327-1333 (2001)
Kendra L Puig et al.
Scientific reports, 7, 43725-43725 (2017-03-07)
It is well known that mutations in the gene coding for amyloid precursor protein are responsible for autosomal dominant forms of Alzheimer's disease. Proteolytic processing of the protein leads to a number of metabolites including the amyloid beta peptide. Although
Juli Choi et al.
Experimental neurobiology, 30(4), 294-307 (2021-09-07)
Recently we reported that hyperoxygenation treatment reduces amyloid-beta accumulation and rescues cognitive impairment in the Tg-APP/PS1 mouse model of Alzheimer's disease. In the present study, we continue to investigate the mechanism by which hyperoxygenation reduces amyloid-beta deposition in the brain.
Deficits in object-in-place but not relative recency performance in the APPswe/PS1dE9 mouse model of Alzheimer?s disease: Implications for object recognition
Bonardi, C, et al.
Behavioural Brain Research, 313, 71-81 (2016)
Zitian He et al.
Cell death & disease, 11(6), 440-440 (2020-06-10)
Autophagy is a major self-degradative process that maintains cellular homeostasis and function in mammalian cells. Autophagic dysfunction occurs in the early pathogenesis of Alzheimer's disease (AD) and directly regulates amyloid-β (Aβ) metabolism. Although it has been proven that the cytokine
Said AbdAlla et al.
The Journal of biological chemistry, 284(10), 6554-6565 (2008-12-17)
Progressive neurodegeneration and decline of cognitive functions are major hallmarks of Alzheimer disease (AD). Neurodegeneration in AD correlates with dysfunction of diverse signal transduction mechanisms, such as the G-protein-stimulated phosphoinositide hydrolysis mediated by Galphaq/11. We report here that impaired Galphaq/11-stimulated
Abhisarika Patnaik et al.
Scientific reports, 10(1), 13322-13322 (2020-08-10)
Synapse and dendritic spine loss induced by amyloid-β oligomers is one of the main hallmarks of the early phases of Alzheimer's disease (AD) and is directly correlated with the cognitive decline typical of this pathology. The p75 neurotrophin receptor (p75NTR)
Folic acid deficiency enhances aβ accumulation in APP/PS1 mice brain and decreases amyloid-associated miRNAs expression
Liu, H, et al.
The Journal of Nutritional Biochemistry, 26(12), 1502-1508 (2015)
Yunjie Yang et al.
Journal of neuroinflammation, 17(1), 65-65 (2020-02-23)
Alzheimer's disease (AD) is a neurodegenerative disorder strongly correlated with a dysfunctional immune system. Our previous results demonstrated that inactivated influenza vaccine (IIV) facilitates hippocampal neurogenesis and blocks lipopolysaccharide (LPS)-induced cognitive impairment. However, whether IIV improves cognitive deficits in an
Qing-Qing Xu et al.
Journal of neuroinflammation, 20(1), 19-19 (2023-02-01)
Alzheimer's disease (AD) is a chronic neurodegenerative disease characterized by progressive cognitive dysfunctions and behavioral impairments. Patchouli alcohol (PA), isolated from Pogostemonis Herba, exhibits multiple pharmacological properties, including neuroprotective effects. This study aimed to investigate the therapeutic effects of PA
R E Tanzi et al.
Nature, 331(6156), 528-530 (1988-02-11)
Amyloid B-protein/amyloid A4 is a peptide present in the neuritic plaques, neurofibrillary tangles and cerebrovascular deposits in patients with Alzheimer's disease and Down's syndrome (trisomy 21) and may be involved in the pathogenesis of Alzheimer's disease. Recent molecular genetic studies
Chang Qu et al.
Journal of advanced research, 35, 231-243 (2022-01-14)
Honokiol (HO) exerts neuroprotective effects in several animal models of Alzheimer's disease (AD), but the poor dissolution hampers its bioavailability and therapeutic efficacy. A novel honokiol nanoscale drug delivery system (Nano-HO) with smaller size and excellent stability was developed in
Tae-Kyung Kim et al.
Experimental & molecular medicine, 44(8), 492-502 (2012-05-31)
Adequate assessment of plaque deposition levels in the brain of mouse models of Alzheimer disease (AD) is required in many core issues of studies on AD, including studies on the mechanisms underlying plaque pathogenesis, identification of cellular factors modifying plaque
Kavon Rezai-Zadeh et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 25(38), 8807-8814 (2005-09-24)
Alzheimer's disease (AD) is a progressive neurodegenerative disorder pathologically characterized by deposition of beta-amyloid (Abeta) peptides as senile plaques in the brain. Recent studies suggest that green tea flavonoids may be used for the prevention and treatment of a variety
Hendrik Demuth et al.
Frontiers in molecular neuroscience, 16, 1163087-1163087 (2023-05-22)
Alzheimer's disease (AD), is characterized by a gradual cognitive decline associated with the accumulation of Amyloid beta (Aβ)-oligomers, progressive neuronal degeneration and chronic neuroinflammation. Among the receptors shown to bind and possibly transduce the toxic effects of Aβ-oligomers is the
A R Costa et al.
Journal of neuroendocrinology, 28(9) (2016-06-23)
The choroid plexus (CP) epithelium is a unique structure in the brain that forms an interface between the peripheral blood on the basal side and the cerebrospinal fluid (CSF) on the apical side. It is a relevant source of many
Kang-Woo Lee et al.
Journal of neurochemistry, 108(1), 165-175 (2008-11-18)
Alzheimer's disease (AD) is a progressive neurodegenerative disease caused by genetic and non-genetic factors. Most AD cases may be triggered and promoted by non-genetic environmental factors. Clinical studies have reported that patients with AD show enhanced baseline levels of stress
J Kang et al.
Nature, 325(6106), 733-736 (1987-02-19)
Alzheimer's disease is characterized by a widespread functional disturbance of the human brain. Fibrillar amyloid proteins are deposited inside neurons as neurofibrillary tangles and extracellularly as amyloid plaque cores and in blood vessels. The major protein subunit (A4) of the
Neuropathology of Alzheimer's disease
Perl, Daniel P
The Mount Sinai Journal of Medicine, New York, 77(1), 32-42 (2010)
Tae-Shin Park et al.
International journal of molecular medicine, 39(1), 21-30 (2016-12-23)
Humulus japonicus Siebold & Zucc. (HJ) has traditionally been administered to patients with pulmonary disease, skin disease and hypertension in Korea, and it is considered to exert anti-inflammatory, antioxidant, antimicrobial and antimycobacterial effects. However, its effects against Alzheimer's disease (AD) have yet to be
Aneta Stachowicz et al.
International journal of molecular sciences, 18(2) (2017-02-22)
The role of different genotypes of apolipoprotein E (apoE) in the etiology of Alzheimer's disease is widely recognized. It has been shown that altered functioning of apoE may promote 4-hydroxynonenal modification of mitochondrial proteins, which may result in mitochondrial dysfunction
Renato Socodato et al.
Cell reports, 31(12), 107796-107796 (2020-06-25)
Nervous tissue homeostasis requires the regulation of microglia activity. Using conditional gene targeting in mice, we demonstrate that genetic ablation of the small GTPase Rhoa in adult microglia is sufficient to trigger spontaneous microglia activation, producing a neurological phenotype (including
Geng Lin et al.
Frontiers in aging neuroscience, 12, 556008-556008 (2020-11-28)
Human epidemiological evidence and animal experimental data suggest that chronic manganese (Mn) exposure increases the risk of Alzheimer's disease (AD) and amyloid plaques, a hallmark of AD brain pathology, but the underlying mechanisms were not fully understood. Using the transgenic
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