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Amyloid beta tau protein

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https://www.readbyqxmd.com/read/28817311/beta-secretase-inhibitors-in-phase-i-and-phase-ii-clinical-trials-for-alzheimer-s-disease
#1
Charbel E-H Moussa
BACE 1 is a protease that cleaves the transmembrane amyloid precursor protein and generates amyloid-β peptides that accumulate in AD brains. No known mutations are identified in the gene encoding BACE1 in AD. However, enzyme levels are elevated in AD and a single residue mutation in amyloid precursor protein protects against protein cleavage by BACE1, suggesting BACE involvement in disease pathogenesis. Drugs that can inhibit BACE1 would theoretically prevent Aβ accumulation and halt AD onset and progression...
August 17, 2017: Expert Opinion on Investigational Drugs
https://www.readbyqxmd.com/read/28800454/tau-protein-aggregation-in-alzheimer-s-disease-an-attractive-target-for-the-development-of-novel-therapeutic-agents
#2
Marie Jouanne, Sylvain Rault, Anne-Sophie Voisin-Chiret
Alzheimer's Disease (AD) is a neurodegenerative brain disorder in which many biological dysfunctions are involved. Among them, two main types of lesions were discovered and widely studied: the amyloid plaques and the neurofibrillary tangles (NFTs). These two lesions are caused by the dysfunction and the accumulation of two proteins which are, respectively, the beta-amyloid peptide and the tau protein. The process that leads these two proteins to aggregate is complex and is the subject of current studies. After a brief description of the aggregation mechanisms, we will provide an overview of new therapeutic agents targeting the different dysfunctions and toxic species found during aggregation...
July 29, 2017: European Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/28799502/mitochondrial-dynamics-and-proteins-related-to-neurodegenerative-diseases
#3
Athanasios Alexiou, Bilal Nizami, Faez Iqbal Khan, Georgia Soursou, Charalampos Vairaktarakis, Stylianos Chatzichronis, Vasilis Tsiamis, Vasileios Manztavinos, Nagendra Sastry Yarla, Ghulam Md Ashraf
Disruptions in the regulation of mitochondrial dynamics and the occurrence of proteins misfolding lead to neuronal death, resulting in Age-related Dementia and Neurodegenerative diseases as well as Frailty. Functional, neurophysiologic and biochemical alterations within the mitochondrial populations can reveal deficits in brain energy metabolism resulting in Mild Cognitive Impairment, abnormal neural development, autonomic dysfunction and other mitochondrial disorders. Additionally, in cases of Alzheimer's disease or Parkinson's disease, a significant number of proteins seems to form unordered and problematic structures, leading through unknown mechanisms to pathological conditions...
August 10, 2017: Current Protein & Peptide Science
https://www.readbyqxmd.com/read/28774322/tau-accumulation-in-the-retina-promotes-early-neuronal-dysfunction-and-precedes-brain-pathology-in-a-mouse-model-of-alzheimer-s-disease
#4
Marius Chiasseu, Luis Alarcon-Martinez, Nicolas Belforte, Heberto Quintero, Florence Dotigny, Laurie Destroismaisons, Christine Vande Velde, Fany Panayi, Caroline Louis, Adriana Di Polo
BACKGROUND: Tau is an axon-enriched protein that binds to and stabilizes microtubules, and hence plays a crucial role in neuronal function. In Alzheimer's disease (AD), pathological tau accumulation correlates with cognitive decline. Substantial visual deficits are found in individuals affected by AD including a preferential loss of retinal ganglion cells (RGCs), the neurons that convey visual information from the retina to the brain. At present, however, the mechanisms that underlie vision changes in these patients are poorly understood...
August 3, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28771542/a-multivariate-predictive-modeling-approach-reveals-a-novel-csf-peptide-signature-for-both-alzheimer-s-disease-state-classification-and-for-predicting-future-disease-progression
#5
Daniel A Llano, Saurabh Bundela, Raksha A Mudar, Viswanath Devanarayan
To determine if a multi-analyte cerebrospinal fluid (CSF) peptide signature can be used to differentiate Alzheimer's Disease (AD) and normal aged controls (NL), and to determine if this signature can also predict progression from mild cognitive impairment (MCI) to AD, analysis of CSF samples was done on the Alzheimer's Disease Neuroimaging Initiative (ADNI) dataset. The profiles of 320 peptides from baseline CSF samples of 287 subjects over a 3-6 year period were analyzed. As expected, the peptide most able to differentiate between AD vs...
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
#6
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/28760504/protection-against-rage-mediated-neuronal-cell-death-by-srage-secreting-human-mesenchymal-stem-cells-in-5xfad-transgenic-mouse-model
#7
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
https://www.readbyqxmd.com/read/28750656/oligomeric-amyloid-beta-induces-mapk-mediated-activation-of-brain-cytosolic-and-calcium-independent-phospholipase-a2-in-a-spatial-specific-manner
#8
Juan Pablo Palavicini, Chunyan Wang, Linyuan Chen, Kristen Hosang, Jianing Wang, Takami Tomiyama, Hiroshi Mori, Xianlin Han
Alzheimer's disease (AD) is histopathologically characterized by the build-up of fibrillar amyloid beta (Aβ) in the form of amyloid plaques and the development of intraneuronal neurofibrillary tangles consisting of aggregated hyperphosphorylated Tau. Although amyloid fibrils were originally considered responsible for AD pathogenesis, recent convincing evidence strongly implicates soluble oligomeric Aβ as the primary neurotoxic species driving disease progression. A third largely ignored pathological hallmark, originally described by Alois Alzheimer, is the presence of "adipose inclusions", suggestive of aberrant lipid metabolism...
July 27, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28736850/progressive-ataxia-and-palatal-tremor-two-autopsy-cases-of-a-novel-tauopathy
#9
Andrew F Gao, Achinoam Faust-Socher, Maryam Al-Murshed, Marc R Del Bigio, Anthony E Lang, David G Munoz
BACKGROUND: Sporadic progressive ataxia and palatal tremor is a rare syndrome characterized by mid- to late-adult-onset symptomatic palatal tremor and slowly progressive cerebellar ataxia. To date, there has been only one autopsy report, which described a novel 4-repeat tauopathy with hypertrophic olivary degeneration and tau-positive inclusions in olivary neurons and dystrophic neuritic processes termed glomeruloid bodies. We report on 2 additional autopsy cases. METHODS: Sections from selected paraffin-embedded brain regions were stained with hematoxylin and eosin/Luxol fast blue and processed for phosphorylated tau, 3-repeat tau, 4-repeat tau, neurofilament, glial fibrillary acid protein, phosphorylated α-synuclein, phosphorylated TAR DNA-binding protein 43, beta-amyloid, and p62 immunohistochemistry...
July 24, 2017: Movement Disorders: Official Journal of the Movement Disorder Society
https://www.readbyqxmd.com/read/28729832/the-role-of-microglia-in-retinal-neurodegeneration-alzheimer-s-disease-parkinson-and-glaucoma
#10
REVIEW
Ana I Ramirez, Rosa de Hoz, Elena Salobrar-Garcia, Juan J Salazar, Blanca Rojas, Daniel Ajoy, Inés López-Cuenca, Pilar Rojas, Alberto Triviño, José M Ramírez
Microglia, the immunocompetent cells of the central nervous system (CNS), act as neuropathology sensors and are neuroprotective under physiological conditions. Microglia react to injury and degeneration with immune-phenotypic and morphological changes, proliferation, migration, and inflammatory cytokine production. An uncontrolled microglial response secondary to sustained CNS damage can put neuronal survival at risk due to excessive inflammation. A neuroinflammatory response is considered among the etiological factors of the major aged-related neurodegenerative diseases of the CNS, and microglial cells are key players in these neurodegenerative lesions...
2017: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/28726050/a-single-center-study-a%C3%AE-42-p-tau181-csf-ratio-to-discriminate-ad-from-ftd-in-clinical-setting
#11
Andrea Vergallo, Cecilia Carlesi, Cristina Pagni, Filippo Sean Giorgi, Filippo Baldacci, Lucia Petrozzi, Roberto Ceravolo, Gloria Tognoni, Gabriele Siciliano, Ubaldo Bonuccelli
Abnormal levels of beta amyloid (Aβ42) and tau protein concentrations in the cerebral spinal fluid (CSF) have been largely described in Alzheimer's disease (AD). Thus, CSF analysis of these biomarkers has been incorporated in recent AD diagnostic criteria, and it is increasingly performed for neurodegenerative dementia diagnostic workout in clinical setting. Nevertheless, the precise biomarkers CSF features in neurodegenerative dementia, either AD or Frontotemporal dementia (FTD), are still not fully clear today...
July 19, 2017: Neurological Sciences
https://www.readbyqxmd.com/read/28722749/rho-associated-protein-kinases-as-therapeutic-targets-for-both-vascular-and-parenchymal-pathologies-in-alzheimer-s-disease
#12
REVIEW
Aaron Y Lai, JoAnne McLaurin
The causes of late-onset Alzheimer's disease are unclear and likely multifactorial. Rho-associated protein kinases (ROCKs) are ubiquitously expressed signaling messengers that mediate a wide array of cellular processes. Interestingly, they play an important role in several vascular and brain pathologies implicated in Alzheimer's etiology, including hypertension, hypercholesterolemia, blood-brain barrier disruption, oxidative stress, deposition of vascular and parenchymal amyloid-beta peptides, tau hyperphosphorylation, and cognitive decline...
July 19, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28714354/is-cerebral-microbleed-prevalence-relevant-as-a-biomarker-in-amnestic-mild-cognitive-impairment-and-mild-alzheimer-s-disease
#13
Ana Gb Rabelo, Camila Vl Teixeira, Thamires Nc Magalhães, Ana Flávia Mk Carletti-Cassani, Augusto Cs Amato Filho, Helena Pg Joaquim, Leda L Talib, Orestes Forlenza, Patrícia Ao Ribeiro, Rodrigo Secolin, Iscia Lopes-Cendes, Fernando Cendes, Marcio Lf Balthazar
Introduction The search for a reliable neuroimaging biomarker in Alzheimer's disease is a matter of intense research. The presence of cerebral microbleeds seems to be a potential biomarker. However, it is not clear if the presence of microbleeds has clinical usefulness to differentiate mild Alzheimer's disease and amnestic mild cognitive impairment from normal aging. We aimed to verify if microbleed prevalence differs among three groups: mild Alzheimer's disease, amnestic mild cognitive impairment due to Alzheimer's disease, and normal controls...
January 1, 2017: Neuroradiology Journal
https://www.readbyqxmd.com/read/28713158/amyloid-beta-structure-biology-and-structure-based-therapeutic-development
#14
REVIEW
Guo-Fang Chen, Ting-Hai Xu, Yan Yan, Yu-Ren Zhou, Yi Jiang, Karsten Melcher, H Eric Xu
Amyloid beta peptide (Aβ) is produced through the proteolytic processing of a transmembrane protein, amyloid precursor protein (APP), by β- and γ-secretases. Aβ accumulation in the brain is proposed to be an early toxic event in the pathogenesis of Alzheimer's disease, which is the most common form of dementia associated with plaques and tangles in the brain. Currently, it is unclear what the physiological and pathological forms of Aβ are and by what mechanism Aβ causes dementia. Moreover, there are no efficient drugs to stop or reverse the progression of Alzheimer's disease...
July 17, 2017: Acta Pharmacologica Sinica
https://www.readbyqxmd.com/read/28709498/targeting-fyn-kinase-in-alzheimer-s-disease
#15
REVIEW
Haakon B Nygaard
The past decade has brought tremendous progress in unraveling the pathophysiology of Alzheimer's disease (AD). While increasingly sophisticated immunotherapy targeting soluble and aggregated brain amyloid-beta (Aβ) continues to dominate clinical research in AD, a deeper understanding of Aβ physiology has led to the recognition of distinct neuronal signaling pathways linking Aβ to synaptotoxicity and neurodegeneration and to new targets for therapeutic intervention. Identifying specific signaling pathways involving Aβ has allowed for the development of more precise therapeutic interventions targeting the most relevant molecular mechanisms leading to AD...
June 13, 2017: Biological Psychiatry
https://www.readbyqxmd.com/read/28704198/alzheimer-s-disease-as-it-was-in-the-beginning
#16
REVIEW
Stanislav Kozlov, Alexei Afonin, Igor Evsyukov, Andrei Bondarenko
Since Alzheimer's disease was first described in 1907, many attempts have been made to reveal its main cause. Nowadays, two forms of the disease are known, and while the hereditary form of the disease is clearly caused by mutations in one of several genes, the etiology of the sporadic form remains a mystery. Both forms share similar sets of neuropathological and molecular manifestations, including extracellular deposition of amyloid-beta, intracellular accumulation of hyperphosphorylated tau protein, disturbances in both the structure and functions of mitochondria, oxidative stress, metal ion metabolism disorders, impairment of N-methyl-D-aspartate receptor-related signaling pathways, abnormalities of lipid metabolism, and aberrant cell cycle reentry in some neurons...
July 12, 2017: Reviews in the Neurosciences
https://www.readbyqxmd.com/read/28701950/cerebrospinal-fluid-a%C3%AE-43-is-reduced-in-early-onset-compared-to-late-onset-alzheimer-s-disease-but-has-similar-diagnostic-accuracy-to-a%C3%AE-42
#17
Camilla Lauridsen, Sigrid B Sando, Ina Møller, Guro Berge, Precious K Pomary, Gøril R Grøntvedt, Øyvind Salvesen, Geir Bråthen, Linda R White
Background: Amyloid beta 1-43 (Aβ43) may be a useful additional biomarker for diagnosing Alzheimer's disease (AD). We have investigated cerebrospinal fluid (CSF) levels of Aβ43 in patients with early-onset AD in contrast to levels in late-onset AD. For comparison, in addition to the 'core' biomarkers, several other analytes were also determined [YKL-40, neurofilament light (NF-L), glial fibrillary acidic protein (GFAP), and progranulin]. Material and Methods: Cerebrospinal fluid samples were obtained from patients with early-onset AD (age ≤ 62, n = 66), late-onset AD (age ≥ 68, n = 25), and groups of cognitively intact individuals (age ≤ 62, n = 41, age ≥ 68, n = 39)...
2017: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/28696431/synaptic-activity-protects-against-ad-and-ftd-like-pathology-via-autophagic-lysosomal-degradation
#18
Y Akwa, E Gondard, A Mann, E Capetillo-Zarate, E Alberdi, C Matute, S Marty, T Vaccari, A M Lozano, E E Baulieu, D Tampellini
Changes in synaptic excitability and reduced brain metabolism are among the earliest detectable alterations associated with the development of Alzheimer's disease (AD). Stimulation of synaptic activity has been shown to be protective in models of AD beta-amyloidosis. Remarkably, deep brain stimulation (DBS) provides beneficial effects in AD patients, and represents an important therapeutic approach against AD and other forms of dementia. While several studies have explored the effect of synaptic activation on beta-amyloid, little is known about Tau protein...
July 11, 2017: Molecular Psychiatry
https://www.readbyqxmd.com/read/28696204/ltp-and-memory-impairment-caused-by-extracellular-a%C3%AE-and-tau-oligomers-is-app-dependent
#19
Daniela Puzzo, Roberto Piacentini, Mauro Fá, Walter Gulisano, Domenica D Li Puma, Agnes Staniszewski, Hong Zhang, Maria Rosaria Tropea, Sara Cocco, Agostino Palmeri, Paul Fraser, Luciano D'Adamio, Claudio Grassi, Ottavio Arancio
The concurrent application of subtoxic doses of soluble oligomeric forms of human amyloid-beta (oAβ) and Tau (oTau) proteins impairs memory and its electrophysiological surrogate long-term potentiation (LTP), effects that may be mediated by intra-neuronal oligomers uptake. Intrigued by these findings, we investigated whether oAβ and oTau share a common mechanism when they impair memory and LTP in mice. We found that as already shown for oAβ, also oTau can bind to amyloid precursor protein (APP). Moreover, efficient intra-neuronal uptake of oAβ and oTau requires expression of APP...
July 11, 2017: ELife
https://www.readbyqxmd.com/read/28677497/platelets-their-potential-contribution-to-the-generation-of-beta-amyloid-plaques-in-alzheimer-s-disease
#20
Christian Humpel
BACKGROUND: Alzheimer's disease is a severe neurodegenerative brain disorder, showing severe beta-amyloid depositions in the brain (plaques) and in vessels (cerebral amyloid angiopathy, CAA), tau pathology, neurodegeneration (and loss of acetylcholine), inflammation with reactive astrocytes and microglia and cerebrovascular damage, all resulting in memory loss. METHODS AND RESULTS: In this review I present a hypothesis that chronic vascular lesions and bleedings cause platelet overactivation and repair...
July 5, 2017: Current Neurovascular Research
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