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Amyloid beta tau protein

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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
#1
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
#2
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. Yet 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 beta and tau...
February 10, 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
#3
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
#4
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
#5
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
#6
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
#7
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
#8
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
https://www.readbyqxmd.com/read/28093567/beta-amyloid-sequelae-in-the-eye-a-critical-review-on-its-diagnostic-significance-and-clinical-relevance-in-alzheimer-s-disease
#9
REVIEW
T M Shah, S M Gupta, P Chatterjee, M Campbell, R N Martins
Alzheimer's disease (AD) is a progressive and fatal neurodegenerative disorder. There is no test for its definitive diagnosis in routine clinical practice. Although phase III clinical trials have failed, only symptomatic treatment is currently available; a possible reason for these failed trials is that intervention commenced at an advanced stage of the disease. The hallmarks of an AD brain include plaques comprising of extracellular beta-amyloid (Aβ) protein aggregates and intracellular hyperphosphorylated neurofibrillary tangles of tau...
March 2017: Molecular Psychiatry
https://www.readbyqxmd.com/read/28093254/risperidone-ameliorated-a%C3%AE-1-42-induced-cognitive-and-hippocampal-synaptic-impairments-in-mice
#10
Lingzhi Wu, Xiaowen Feng, Tingting Li, Baojuan Sun, Muhammad Zahid Khan, Ling He
Alzheimer's disease (AD) is a complex neurodegenerative disorder with cognitive impairment and major neuropathologic hallmark of amyloid-beta (Aβ) peptides. Risperidone, an atypical antipsychotic, can improve concentration and cognitive deficit in schizophrenia patients. In this study, behavior tests including Morris Water Maze test, Step-through passive avoidance test, Open Field test, Step-Down test, Hole-Board test and Novel object recognition test were preformed to examine the effect of Risperidone on Aβ1-42-induced cognitive dysfunction in both long-term and short-term memory...
March 30, 2017: Behavioural Brain Research
https://www.readbyqxmd.com/read/28049401/alzheimer-s-disease-and-natural-products-future-regimens-emerging-from-nature
#11
Md Asiful Islam, Shahad Saif Khandker, Fahmida Alam, Md Ibrahim Khalil, Mohammad Amjad Kamal, Siew Hua Gan
Alzheimer's disease (AD), which largely affects the elderly, has become a global burden. Patients with AD have both short- and long-term memory impairments. The neuronal loss in AD occurs due to abnormally folded amyloid beta proteins and aggregation of hyperphosphorylated tau proteins in the brain. Eventually, amyloid plaques and neurofibrillary tangles are formed, which subsequently disintegrate the neuronal transport system. There are several factors which are involved in AD pathogenesis, including oxidative stress, inflammation and the presence of metal ions...
3, 2017: Current Topics in Medicinal Chemistry
https://www.readbyqxmd.com/read/28044060/molecular-interaction-between-type-2-diabetes-and-alzheimer-s-disease-through-cross-seeding-of-protein-misfolding
#12
I Moreno-Gonzalez, G Edwards Iii, N Salvadores, M Shahnawaz, R Diaz-Espinoza, C Soto
Numerous epidemiological studies have shown a significantly higher risk for development of Alzheimer's disease (AD) in patients affected by type 2 diabetes (T2D), but the molecular mechanism responsible for this association is presently unknown. Both diseases are considered protein misfolding disorders associated with the accumulation of protein aggregates; amyloid-beta (Aβ) and tau in the brain during AD, and islet amyloid polypeptide (IAPP) in pancreatic islets in T2D. Formation and accumulation of these proteins follows a seeding-nucleation model, where a misfolded aggregate or 'seed' promotes the rapid misfolding and aggregation of the native protein...
January 3, 2017: Molecular Psychiatry
https://www.readbyqxmd.com/read/28043897/natural-products-against-alzheimer-s-disease-pharmaco-therapeutics-and-biotechnological-interventions
#13
REVIEW
Abhijit Dey, Raktim Bhattacharya, Anuradha Mukherjee, Devendra Kumar Pandey
Alzheimer's disease (AD) is a severe, chronic and progressive neurodegenerative disease associated with memory and cognition impairment ultimately leading to death. It is the commonest reason of dementia in elderly populations mostly affecting beyond the age of 65. The pathogenesis is indicated by accumulation of the amyloid-beta (Aβ) plaques and neurofibrillary tangles (NFT) in brain tissues and hyperphosphorylation of tau protein in neurons. The main cause is considered to be the formation of reactive oxygen species (ROS) due to oxidative stress...
December 30, 2016: Biotechnology Advances
https://www.readbyqxmd.com/read/28025562/cannabidiol-modulates-the-expression-of-alzheimer-s-disease-related-genes-in-mesenchymal-stem-cells
#14
Rosaliana Libro, Francesca Diomede, Domenico Scionti, Adriano Piattelli, Gianpaolo Grassi, Federica Pollastro, Placido Bramanti, Emanuela Mazzon, Oriana Trubiani
Mesenchymal stem cells (MSCs) have emerged as a promising tool for the treatment of several neurodegenerative disorders, including Alzheimer's disease (AD). The main neuropathological hallmarks of AD are senile plaques, composed of amyloid beta (Aβ), and neurofibrillary tangles, formed by hyperphosphorylated tau. However, current therapies for AD have shown limited efficacy. In this study, we evaluated whether pre-treatment with cannabidiol (CBD), at 5 μM concentration, modulated the transcriptional profile of MSCs derived from gingiva (GMSCs) in order to improve their therapeutic potential, by performing a transcriptomic analysis by the next-generation sequencing (NGS) platform...
December 23, 2016: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28012089/orexin-and-alzheimer-s-disease
#15
Claudio Liguori
Alzheimer's disease (AD) is the most frequent age-related dementia. It prevalently causes cognitive decline, although it is frequently associated with secondary behavioral disturbances. AD neurodegeneration characteristically produces a remarkable destruction of the sleep-wake cycle, with diurnal napping, nighttime arousals, sleep fragmentation, and REM sleep impairment. It was recently hypothesized that the orexinergic system was involved in AD pathology. Accordingly, recent papers showed the association between orexinergic neurotransmission dysfunction, sleep impairment, and cognitive decline in AD...
December 24, 2016: Current Topics in Behavioral Neurosciences
https://www.readbyqxmd.com/read/28004401/hypoxia-inducible-factors-as-neuroprotective-agent-in-alzheimer-s-disease
#16
REVIEW
Ben Sundra Ashok, Thekkuttuparambil Ananthanarayanan Ajith, Senthilkumar Sivanesan
Beta amyloid (Aβ)-42 peptide and phosphorylated tau protein had been demonstrated as the pathological hallmarks of Alzheimer's disease (AD). A gradual decline of oxygen and glucose supply to the brain during aging or hypoxia was manifested as contributing factors to hypometabolism. The brain regions susceptible to hypometabolism are hippocampus, entorhinal cortex and cognition-associated neocortical regions like parietal, temporal and frontal cortex. In AD patients, the brain regions with hypometabolism can trigger overexpression of amyloid precursor protein and decreased the clearance of Aβ...
December 22, 2016: Clinical and Experimental Pharmacology & Physiology
https://www.readbyqxmd.com/read/27998621/brain-tau-deposition-linked-to-systemic-causes-of-death-in-normal-elderly
#17
Keith A Josephs, Nirubol Tosakulwong, Stephen D Weigand, Melissa E Murray, Jennifer L Whitwell, Joseph E Parisi, Dennis W Dickson, Ronald C Petersen
The relationship between causes of death and 4 major neurodegenerative brain proteins (beta-amyloid, tau, alpha-synuclein, and the TAR DNA-binding protein of 43 kDa (TDP-43) were assessed in 94 cognitively normal elderly participants that died without a neurodegenerative disease. There was an association between tau and causes of death (p = 0.01). Tau in the brain was associated with a reduced likelihood of dying from systemic cancers (p = 0.046), and with an increased likelihood of dying from pulmonary (p = 0...
February 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/27984697/delineating-amyloid-plaque-associated-neuronal-sphingolipids-in-transgenic-alzheimer-s-disease-mice-tgarcswe-using-maldi-imaging-mass-spectrometry
#18
Ibrahim Kaya, Dimitri Brinet, Wojciech Michno, Stina Syvänen, Dag Sehlin, Henrik Zetterberg, Kaj Blennow, Jörg Hanrieder
The major pathological hallmarks of Alzheimer's disease (AD) are the progressive aggregation and accumulation of beta-amyloid (Aβ) and hyperphosphorylated tau protein into neurotoxic deposits. Aβ aggregation has been suggested as the critical early inducer, driving the disease progression. However, the factors that promote neurotoxic Aβ aggregation remain elusive. Imaging mass spectrometry (IMS) is a powerful technique to comprehensively elucidate the spatial distribution patterns of lipids, peptides, and proteins in biological tissue sections...
February 15, 2017: ACS Chemical Neuroscience
https://www.readbyqxmd.com/read/27981642/ginseng-protein-reverses-amyloid-beta-peptide-and-h2-o2-cytotoxicity-in-neurons-and-ameliorates-cognitive-impairment-in-ad-rats-induced-by-a-combination-of-d-galactose-and-alcl3
#19
Hongyan Li, Jie Song, Jianghua Zhang, Tianmin Wang, Yuhui Yan, Zhenyu Tao, Shaoheng Li, Hui Zhang, Tingguo Kang, Jingxian Yang
Ginseng (Panax ginseng C.A. Meyer) is one of the most widely used herbal medicines worldwide. The present study evaluated the neuroprotective effects of ginseng protein (GP) and its possible mechanisms in a cellular and animal model of AD. The results demonstrated that GP (10-100 µg/mL) significantly improved the survival rate of neurons and reduced the cells' apoptosis and the mRNA expression of caspase-3 and Bax/Bcl-2. In addition, GP (0.1 g/kg) significantly shortened the escape latency, prolonged the crossing times and the percentage of residence time; reduced the level of Aβ1-42 and p-tau, the activity of T-NOS and iNOS, and the content of MDA and NO, improved the activity of SOD, the concentration of cAMP and the protein expression of p-PKA/PKA and -CREB/CREB...
February 2017: Phytotherapy Research: PTR
https://www.readbyqxmd.com/read/27895577/fus1-ko-mouse-as-a-model-of-oxidative-stress-mediated-sporadic-alzheimer-s-disease-circadian-disruption-and-long-term-spatial-and-olfactory-memory-impairments
#20
Guillermo Coronas-Samano, Keeley L Baker, Winston J T Tan, Alla V Ivanova, Justus V Verhagen
Insufficient advances in the development of effective therapeutic treatments of sporadic Alzheimer's Disease (sAD) to date are largely due to the lack of sAD-relevant animal models. While the vast majority of models do recapitulate AD's hallmarks of plaques and tangles by virtue of tau and/or beta amyloid overexpression, these models do not reflect the fact that in sAD (unlike familial AD) these genes are not risk factors per se and that other mechanisms like oxidative stress, metabolic dysregulation and inflammation play key roles in AD etiology...
2016: Frontiers in Aging Neuroscience
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