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Amyloid beta tau protein

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https://www.readbyqxmd.com/read/28427866/effect-of-amyloid-%C3%AE-25-35-in-hyperglycemic-and-hyperinsulinemic-rats-effects-on-phosphorylation-and-o-glcnacylation-of-tau-protein
#1
Liliana Lozano, Jorge Guevara, Tony Lefebvre, Ivan Ramos-Martinez, Daniel Limón, Alfonso Díaz, Eduarda Cerón, Edgar Zenteno
Aggregation of the amyloid beta (Aβ) peptide and hyperphosphorylation of tau protein, which are markers of Alzheimer's disease (AD), have been reported also in diabetes mellitus (DM). One regulator of tau phosphorylation is O-GlcNAcylation, whereas for hyperphosphorylation it could be GSK3beta, which is activated in hyperglycemic conditions. With this in mind, both O-GlcNAcylation and phosphorylation of tau protein were evaluated in the brain of rats with streptozotocin (STZ)-induced hyperglycemia and hyperinsulinemia and treated with the Aß25-35 peptide in the hippocampal region CA1...
April 6, 2017: Neuropeptides
https://www.readbyqxmd.com/read/28416393/tdp-43-expression-influences-amyloid%C3%AE-plaque-deposition-and-tau-aggregation
#2
Stephani A Davis, Kok Ann Gan, James A Dowell, Nigel J Cairns, Michael A Gitcho
Although the main focus in Alzheimer's disease (AD) has been an investigation of mechanisms causing Aβ plaque deposition and tau tangle formation, recent studies have shown that phosphorylated TDP-43 pathology is present in up to 50% of sporadic cases. Furthermore, elevated phosphorylated TDP-43 has been associated with more severe AD pathology. Therefore, we hypothesized that TDP-43 may regulate amyloid-beta precursor protein (APP) trafficking and tau phosphorylation/aggregation. In order to examine the role of TDP-43 in AD, we developed a transgenic mouse that overexpresses hippocampal and cortical neuronal TDP-43 in a mouse expressing familial mutations (K595N and M596L) in APP and presenilin 1 (PSEN1ΔE9)...
April 20, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28408165/alterations-in-protein-phosphorylation-in-the-amygdala-of-the-5xfamilial-alzheimer-s-disease-animal-model
#3
Eun-Jeong Yang, Usman Mahmood, Hyunju Kim, Moonseok Choi, Yunjung Choi, Jean-Pyo Lee, Moon-Jeong Chang, Hye-Sun Kim
Alzheimer's disease is the most common disease underlying dementia in humans. Two major neuropathological hallmarks of AD are neuritic plaques primarily composed of amyloid beta peptide and neurofibrillary tangles primarily composed of hyperphosphorylated tau. In addition to impaired memory function, AD patients often display neuropsychiatric symptoms and abnormal emotional states such as confusion, delusion, manic/depressive episodes and altered fear status. Brains from AD patients show atrophy of the amygdala which is involved in fear expression and emotional processing as well as hippocampal atrophy...
March 31, 2017: Journal of Pharmacological Sciences
https://www.readbyqxmd.com/read/28405187/identification-of-cerebral-metal-ion-imbalance-in-the-brain-of-aging-octodon-degus
#4
Nady Braidy, Anne Poljak, Chris Marjo, Helen Rutlidge, Anne Rich, Bat-Erdene Jugder, Tharusha Jayasena, Nibaldo C Inestrosa, Perminder S Sachdev
The accumulation of redox-active transition metals in the brain and metal dyshomeostasis are thought to be associated with the etiology and pathogenesis of several neurodegenerative diseases, and Alzheimer's disease (AD) in particular. As well, distinct biometal imaging and role of metal uptake transporters are central to understanding AD pathogenesis and aging but remain elusive, due inappropriate detection methods. We therefore hypothesized that Octodon degus develop neuropathological abnormalities in the distribution of redox active biometals, and this effect may be due to alterations in the expression of lysosomal protein, major Fe/Cu transporters, and selected Zn transporters (ZnTs and ZIPs)...
2017: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/28400814/neuroprotective-effect-of-the-chinese-medicine-tiantai-no-1-and-its-molecular-mechanism-in-the-senescence-accelerated-mouse-prone-8
#5
Ying-Hong Li, Xu-Sheng Wang, Xiao-Lin Chen, Yu Jin, Hong-Bo Chen, Xiu-Qin Jia, Yong-Feng Zhang, Zheng-Zhi Wu
Tiantai No. 1, a Chinese medicine predominantly composed of powdered Rhizoma Gastrodiae, Radix Ginseng, and Ginkgo leaf at a ratio of 2:1:2 and dissolved in pure water, is neuroprotective in animal models of various cognitive disorders, but its molecular mechanism remains unclear. We administered Tiantai No. 1 intragastrically to senescence-accelerated mouse prone 8 (SAMP8) mice (a model of Alzheimer's disease) at doses of 50, 100 or 150 mg/kg per day for 8 weeks and evaluated their behavior in the Morris water maze and expression of Alzheimer's disease-related proteins in the brain...
February 2017: Neural Regeneration Research
https://www.readbyqxmd.com/read/28392767/early-onset-network-hyperexcitability-in-presymptomatic-alzheimer-s-disease-transgenic-mice-is-suppressed-by-passive-immunization-with-anti-human-app-a%C3%AE-antibody-and-by-mglur5-blockade
#6
Syed F Kazim, Shih-Chieh Chuang, Wangfa Zhao, Robert K S Wong, Riccardo Bianchi, Khalid Iqbal
Cortical and hippocampal network hyperexcitability appears to be an early event in Alzheimer's disease (AD) pathogenesis, and may contribute to memory impairment. It remains unclear if network hyperexcitability precedes memory impairment in mouse models of AD and what are the underlying cellular mechanisms. We thus evaluated seizure susceptibility and hippocampal network hyperexcitability at ~3 weeks of age [prior to amyloid beta (Aβ) plaque deposition, neurofibrillary pathology, and cognitive impairment] in a triple transgenic mouse model of familial AD (3xTg-AD mouse) that harbors mutated human Aβ precursor protein (APP), tau and presenilin 1 (PS1) genes...
2017: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/28382239/mechanical-dilution-of-beta-amyloid-peptide-and-phosphorylated-tau-protein-in-alzheimer-s-disease-too-simple-to-be-true
#7
Manuel Menéndez González
The neuropathology of Alzheimer's disease (AD) is characterized by the widespread accumulation of neuritic plaques and neurofibrillary tangles composed of deposits of beta-amyloid peptide (Aβ) and abnormally phosphorylated tau protein (phospho-tau) respectively. Considerable effort has been expended to identify methods to retard the deposition of these proteins or to enhance their clearance. It is strikingly surprising that until now, very few researchers have attempted to remove these proteins using mechanical procedures...
February 28, 2017: Curēus
https://www.readbyqxmd.com/read/28374012/activation-of-ras-erk-signaling-and-gsk-3-by-amyloid-precursor-protein-and-amyloid-beta-facilitates-neurodegeneration-in-alzheimer-s-disease
#8
Lisa Kirouac, Alexander J Rajic, David H Cribbs, Jaya Padmanabhan
It is widely accepted that amyloid β (Aβ) generated from amyloid precursor protein (APP) oligomerizes and fibrillizes to form neuritic plaques in Alzheimer's disease (AD), yet little is known about the contribution of APP to intracellular signaling events preceding AD pathogenesis. The data presented here demonstrate that APP expression and neuronal exposure to oligomeric Aβ42 enhance Ras/ERK signaling cascade and glycogen synthase kinase 3 (GSK-3) activation. We find that RNA interference (RNAi)-directed knockdown of APP in B103 rat neuroblastoma cells expressing APP inhibits Ras-ERK signaling and GSK-3 activation, indicating that APP acts upstream of these signal transduction events...
March 2017: ENeuro
https://www.readbyqxmd.com/read/28356893/alzheimer-s-toxic-amyloid-beta-oligomers-unwelcome-visitors-to-the-na-k-atpase-alpha3-docking-station
#9
Thomas DiChiara, Nadia DiNunno, Jeffrey Clark, Riana Lo Bu, Erika N Cline, Madeline G Rollins, Yuesong Gong, David L Brody, Stephen G Sligar, Pauline T Velasco, Kirsten L Viola, William L Klein
Toxic amyloid beta oligomers (AβOs) are known to accumulate in Alzheimer's disease (AD) and in animal models of AD. Their structure is heterogeneous, and they are found in both intracellular and extracellular milieu. When given to CNS cultures or injected ICV into non-human primates and other non-transgenic animals, AβOs have been found to cause impaired synaptic plasticity, loss of memory function, tau hyperphosphorylation and tangle formation, synapse elimination, oxidative and ER stress, inflammatory microglial activation, and selective nerve cell death...
March 2017: Yale Journal of Biology and Medicine
https://www.readbyqxmd.com/read/28356048/diagnostic-and-prognostic-potential-of-retinal-biomarkers-in-early-on-set-alzheimer-s-disease
#10
Sahar Shariflou, Dana Georgevsky, Hussein Mansour, Mahdie Rezaeian, Nafiseh Hosseini, Fathima Gani, Vivek Gupta, Nady Braidy, S Mojtaba Golzan
Accumulating evidence suggests that the eye can be used in the assessment of early on-set Alzheimer's disease (AD). The eye offers a natural window to the brain through the retina. The retina and brain share common developmental origins and patho-physiological origins and mechanisms, having been sequestered from it during early development, but retaining its connections with the brain via the optic nerve. Therefore, it is well understood that neurological abnormalities have a direct profound impact on the retina...
March 29, 2017: Current Alzheimer Research
https://www.readbyqxmd.com/read/28298292/cellular-cholesterol-homeostasis-in-alzheimer-s-disease
#11
Ta Yuan Chang, Yoshio Yamauchi, Mazahir Hasan, Catherine Cy Chang
Alzheimer's disease [AD] is the most common form of dementia in older adults. Currently, there is no cure for AD. The hallmark of AD is the accumulation of extracellular amyloid plaques composed of amyloid beta peptides [Abeta; especially Abeta1-42], and neurofibrillary tangles, composed of hyper-phosphorylated tau, accompanied with chronic neuroinflammation. Abeta are derived from the amyloid precursor protein APP. The oligomeric form of Abeta is probably the most neurotoxic species; its accumulation eventually forms the insoluble and aggregated amyloid plaques...
March 15, 2017: Journal of Lipid Research
https://www.readbyqxmd.com/read/28289378/synaptic-dysfunction-in-alzheimer-s-disease-and-glaucoma-from-common-degenerative-mechanisms-toward-neuroprotection
#12
REVIEW
Chiara Criscuolo, Carlotta Fabiani, Elisa Cerri, Luciano Domenici
Alzheimer's disease (AD) and glaucoma are two distinct multifactorial neurodegenerative diseases, primarily affecting the elderly. Common pathophysiological mechanisms have been elucidated in the past decades. First of all both diseases are progressive, with AD leading to dementia and glaucoma inducing blindness. Pathologically, they all feature synaptic dysfunction with changes of neuronal circuitry, progressive accumulation of protein aggregates such as the beta amyloid (Aβ) and intracellular microtubule inclusions containing hyperphosphorylated tau, which belongs to microtubule associated protein family...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28205591/protective-effect-of-17%C3%AE-estradiol-upon-hippocampal-spine-density-and-cognitive-function-in-an-animal-model-of-vascular-dementia
#13
Ying Zhu, Quanguang Zhang, Wenli Zhang, Ning Li, Yongxin Dai, Jingyi Tu, Fang Yang, Darrell W Brann, Ruimin Wang
The current study examined whether the steroid hormone, 17β-estradiol (E2) can exert long-lasting beneficial effects upon axonal health, synaptic plasticity, dementia-related amyloid-beta (Aβ) protein expression, and hippocampal-dependent cognitive function in an animal model of chronic cerebral hypoperfusion and vascular dementia (VaD). Chronic cerebral hypoperfusion and VaD was induced by bilateral common carotid artery occlusion (BCCAO) in adult male Sprague Dawley rats. Low dose E2 administered for the first 3-months after BCCAO exerted long-lasting beneficial effects, including significant neuroprotection of hippocampal CA1 neurons and preservation of hippocampal-dependent cognitive function when examined at 6-months after BCCAO...
February 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28188218/focal-solute-trapping-and-global-glymphatic-pathway-impairment-in-a-murine-model-of-multiple-microinfarcts
#14
Minghuan Wang, Fengfei Ding, SaiYue Deng, Xuequn Guo, Wei Wang, Jeffrey J Iliff, Maiken Nedergaard
Microinfarcts occur commonly in the aging brain as a consequence of diffuse embolic events and are associated with the development of vascular dementia and Alzheimer's disease. However, the manner in which disperse microscopic lesions reduce global cognitive function and increase the risk for Alzheimer's disease is unclear. The glymphatic system, which is a brain-wide perivascular network that supports the recirculation of CSF through the brain parenchyma, facilitates the clearance of interstitial solutes including amyloid β and tau...
March 15, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28183245/ykl-40-as-a-potential-biomarker-and-a-possible-target-in-therapeutic-strategies-of-alzheimer-s-disease
#15
Paweł Muszyński, Magdalena Groblewska, Agnieszka Kulczyńska-Przybik, Alina Kułakowska, Barbara Mroczko
BACKGROUND: Growing body of evidence suggests that pathogenesis of Alzheimer's disease (AD), a progressing neurodegenerative condition, is not limited to the neuronal compartment, but also involves various immunological mechanisms. Insoluble Aβ aggregates in the brain can induce the activation of microglia, resulting in synthesis of proinflammatory mediators, which further can stimulate astrocytic expression of YKL-40. Therefore, the aim of the current review is to present up-to-date data about the role of YKL-40 as a biomarker of AD as well as the possibility of therapeutic strategies targeting neuroinflammation...
February 8, 2017: Current Neuropharmacology
https://www.readbyqxmd.com/read/28181891/-chronic-traumatic-encephalopathy-an-old-acquaintance-in-athletes
#16
E G B Vijverberg, A C M Pijnenburg, P Scheltens, Y A L Pijnenburg
- Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease caused by repetitive head injuries like those seen in sports such as boxing, American football and soccer.- The clinical features of CTE are a range of cognitive, psychiatric and motor symptoms, and histopathology involves deposits of hyperphosphorylated tau protein and the presence of TAR DNA-binding protein (TDP-43) with relatively little beta-amyloid.- CTE is difficult to differentiate clinically from Alzheimer's disease, frontotemporal dementia and psychiatric disorders because of the major symptom overlap between these conditions...
2017: Nederlands Tijdschrift Voor Geneeskunde
https://www.readbyqxmd.com/read/28166276/homovanillic-acid-and-5-hydroxyindole-acetic-acid-as-biomarkers-for-dementia-with-lewy-bodies-and-coincident-alzheimer-s-disease-an-autopsy-confirmed-study
#17
Satoru Morimoto, Masaki Takao, Hiroyuki Hatsuta, Yasushi Nishina, Tadashi Komiya, Renpei Sengoku, Yuta Nakano, Akiko Uchino, Hiroyuki Sumikura, Yuko Saito, Kazutomi Kanemaru, Shigeo Murayama
Dementia with Lewy bodies (DLB) and Alzheimer's disease (AD) are the two most common causes of dementia. Both pathologies often coexist, and AD patients with concomitant neocortical LB pathology (referred to as the Lewy body variant of AD) generally show faster cognitive decline and accelerated mortality relative to patients with pure AD. Thus, discriminating among patients with DLB, AD, and coincident DLB and AD is important in clinical practice. We examined levels of homovanillic acid (HVA), 5-hydroxyindole acetic acid (5-HIAA), tau, phosphorylated tau (p-tau), and beta-amyloid (Aβ) 1-42 in cerebrospinal fluid (CSF) to evaluate their viability as biomarkers to discriminate among different forms of dementia...
2017: PloS One
https://www.readbyqxmd.com/read/28140402/glucose-deficit-triggers-tau-pathology-and-synaptic-dysfunction-in-a-tauopathy-mouse-model
#18
E Lauretti, J-G Li, A Di Meco, D Praticò
Clinical investigations have highlighted a biological link between reduced brain glucose metabolism and Alzheimer's disease (AD). Previous studies showed that glucose deprivation may influence amyloid beta formation in vivo but no data are available on the effect that this condition might have on tau protein metabolism. In the current paper, we investigated the effect of glucose deficit on tau phosphorylation, memory and learning, and synaptic function in a transgenic mouse model of tauopathy, the h-tau mice...
January 31, 2017: Translational Psychiatry
https://www.readbyqxmd.com/read/28138104/mechanisms-of-alzheimer-s-disease-pathogenesis-and-prevention-the-brain-neural-pathology-n-methyl-d-aspartate-receptors-tau-protein-and-other-risk-factors
#19
REVIEW
Sayad Kocahan, Zumrut Doğan
The characteristic features of Alzheimer's disease (AD) are the appearance of extracellular amyloid-beta (Aβ) plaques and neurofibrillary tangles in the intracellular environment, neuronal death and the loss of synapses, all of which contribute to cognitive decline in a progressive manner. A number of hypotheses have been advanced to explain AD. Abnormal tau phosphorylation may contribute to the formation of abnormal neurofibrillary structures. Many different structures are susceptible to AD, including the reticular formation, the nuclei in the brain stem (e...
February 28, 2017: Clinical Psychopharmacology and Neuroscience: the Official Scientific Journal of the Korean College of Neuropsychopharmacology
https://www.readbyqxmd.com/read/28111296/management-of-alzheimer-s-disease-an-insight-of-the-enzymatic-and-other-novel-potential-targets
#20
REVIEW
Badar Ul Islam, Shams Tabrez
Alzheimer's disease (AD) is a well-known cause of memory loss and dementia in elderly people all across the world. It is pathophysiologically characterized by the extracellular deposition of amyloid beta (Aβ) proteins and retention of intracellular neurofibrillary tangles (NFTs) of hyperphosphorylated tau proteins. Several enzymes, such as lipoxygenases, acetylcholinesterases, secretases, glycogen synthase kinase 3, caspases, sirtuins have been reported to actively participate in the pathogenesis of AD. Due to the limited drug for the management of AD till now (only memantine and four other acetylcholinesterase inhibitors), there is an urgent need to find out the novel inhibitors that could specifically act against these enzymes or therapeutically important targets, and barricade or decelerate AD progression...
April 2017: International Journal of Biological Macromolecules
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