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https://www.readbyqxmd.com/read/28729832/the-role-of-microglia-in-retinal-neurodegeneration-alzheimer-s-disease-parkinson-and-glaucoma
#1
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
#2
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
#3
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/28721544/sleep-in-older-adults-and-in-subjects-with-dementia
#4
REVIEW
Helmut Frohnhofen, Jeanina Schlitzer, Nikolaus Netzer
The neuronal structures for the regulation of sleep and wakefulness are located in the brain. This complex network is vulnerable to numerous factors, most importantly neurodegenerative diseases and drugs. The macrostructure and microstructure of sleep change with age. These changes are more pronounced in subjects with dementia. Sleep disorders in subjects with dementia may be independent of dementia or caused by dementia. Furthermore, epidemiological studies reveal that sleep disorders per se may induce dementia by reduction of cerebral clearance of beta-amyloids...
July 18, 2017: Zeitschrift Für Gerontologie und Geriatrie
https://www.readbyqxmd.com/read/28719891/serum-interleukin-10-levels-correlate-with-cerebrospinal-fluid-amyloid-beta-deposition-in-alzheimer-disease-patients
#5
Lucio D'Anna, Samir Abu-Rumeileh, Martina Fabris, Cinzia Pistis, Antonio Baldi, Nova Sanvilli, Francesco Curcio, Gian Luigi Gigli, Sebastiano D'Anna, Mariarosaria Valente
BACKGROUND AND OBJECTIVE: In Alzheimer disease (AD) inflammation becomes evident throughout the course of the disease. However, the association between inflammation, cognitive impairment, and cerebrospinal biomarkers (Aβ42, t-tau, p-tau181, and Aβ42/p-tau181 ratio) is poorly understood. METHODS: A large panel of inflammatory cytokines (interleukin [IL]-1β, IL-1ra, IL-2, IL-4, IL-6, IL-10, IL-17, interferon-γ, tumor necrosis factor-α, and vascular endothelial growth factor) was analyzed using a multiplex immunoassay in 27 patients with a diagnosis of AD dementia and in 18 control subjects...
July 19, 2017: Neuro-degenerative Diseases
https://www.readbyqxmd.com/read/28714403/gsk3-inhibitors-in-the-therapeutic-development-of-diabetes-cancer-and-neurodegeneration-past-present-and-future
#6
Mudasir Maqbool, Nasimul Hoda
GSK3 has gained a considerable attention of researchers in the late 1970s as an inevitable drug target to treat diabetes. Furthermore, it was found to have a key role in the development of diseases like cancer and neurodegeneration (ND). A broad spectrum of GSK3 inhibitors have been discovered from time to time in order to curb these diseases. Inhibition of GSK3 by insulin boosts the dephosphorylation of glycogen synthase, hence its activation to convert UDP glucose into glycogen. Lack of insulin and insulin-resistance is supposed to be the cause of type 2 diabetes (Diabetes mellitus)...
July 14, 2017: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/28714354/is-cerebral-microbleed-prevalence-relevant-as-a-biomarker-in-amnestic-mild-cognitive-impairment-and-mild-alzheimer-s-disease
#7
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
#8
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/28710275/a-ph-dependent-switch-promotes-%C3%AE-synuclein-fibril-formation-via-glutamate-residues
#9
Gina M Moriarty, Michael P Olson, Tamr B Atieh, Maria K Janowska, Sagar D Khare, Jean Baum
Alpha-synuclein (αS) is the primary protein associated with Parkinson's disease, and undergoes aggregation from its intrinsically disordered monomeric form to a cross-β fibrillar form. The closely related homolog beta-synuclein (βS) is essentially fibril resistant under cytoplasmic physiological conditions. Toxic gain of function by βS has been linked to dysfunction, but the aggregation behavior of βS under altered pH is not well understood. In this work, we compare fibril formation of αS and βS at pH 7...
July 14, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28710249/amyloid-precursor-protein-in-pancreatic-islets
#10
Joshua Kulas, Kendra Puig, Colin K Combs
The amyloid precursor protein (APP) has been extensively investigated for its role in the production of amyloid beta (Aβ), a plaque forming peptide in Alzheimer's disease (AD). Epidemiological evidence suggests type 2 diabetes is a risk factor for AD. The pancreas is an essential regulator of blood glucose levels through the secretion of the hormones insulin and glucagon. Pancreatic dysfunction is a well characterized consequence of type 1 and type 2 diabetes. In this study we have examined the expression and processing of pancreatic APP to test the hypothesis that APP may play a role in pancreatic function and the pathophysiology of diabetes...
July 14, 2017: Journal of Endocrinology
https://www.readbyqxmd.com/read/28709849/effects-of-huperzin-a-on-the-beta-amyloid-accumulation-in-the-brain-and-skeletal-muscle-cells-of-a-rat-model-for-alzheimer-s-disease
#11
Cagatay Han Turkseven, Belgin Buyukakilli, Ebru Balli, Derya Yetkin, Mehmet Emin Erdal, Senay Gorucu Yilmaz, Leyla Sahin
AIMS: Alzheimer's Disease (AD) is characterized by a loss of cognitive function and also the accumulation of β-amyloid peptide (βAP) in the brain parenchyma, which plays an important role in this disease. However, it is often also associated with the non-cognitive symptoms such as loss of muscle function (Inclusion-Body Myositis-IBM). MAIN METHODS: Sprague-Dawley rats (13 weeks-n=68) were randomly assigned into five groups: Group C: Control; Group D: d-galactose; Group O+D: Bilateral oophorectomy+d-galactose; Group O: Bilateral oophorectomy; Group O+D+H: Bilateral oophorectomy+d-galactose+Hup-A...
July 11, 2017: Life Sciences
https://www.readbyqxmd.com/read/28709498/targeting-fyn-kinase-in-alzheimer-s-disease
#12
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/28707894/vitamin-d-receptor-regulates-amyloid-beta-1-42-production-with-protein-disulfide-isomerase-a3
#13
Duygu Gezen-Ak, Irem L Atasoy, Esin Candas, Merve Alaylioglu, Selma Yilmazer, Erdinc Dursun
The challenge of understanding the biology of neuronal amyloid processing could provide a basis for understanding the amyloid pathology in Alzheimer's disease (AD). Based on our previous studies we have suggested that AD might be the consequence of a hormonal imbalance in which the critical hormone is vitamin D. The present study primarily focused on the creation of a condition that prevents the genomic or non-genomic action of vitamin D by disrupting vitamin D receptors (VDR or PDIA3/1,25MARRS); the effects of these disruptions on the series of proteins involved in secretases that play a crucial role in amyloid pathology and on amyloid beta (Aβ) production in primary cortical neurons were observed...
July 14, 2017: ACS Chemical Neuroscience
https://www.readbyqxmd.com/read/28704198/alzheimer-s-disease-as-it-was-in-the-beginning
#14
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/28702592/inhibition-of-gnnqqny-prion-peptide-aggregation-by-trehalose-a-mechanistic-view
#15
Nidhi Katyal, Shashank Deep
Deposition of amyloid fibrils is the seminal event in the pathogenesis of numerous neurodegenerative diseases. The formation of this amyloid assembly is the manifestation of a cascade of structural transitions including toxic oligomer formation in the early stages of aggregation. Thus a viable therapeutic strategy involves the use of small molecular ligands to interfere with this assembly. In this perspective, we have explored the kinetics of aggregate formation of the fibril forming GNNQQNY peptide fragment from the yeast prion protein SUP35 using multiple all atom MD simulations with explicit solvent and provided mechanistic insights into the way trehalose, an experimentally known aggregation inhibitor, modulates the aggregation pathway...
July 12, 2017: Physical Chemistry Chemical Physics: PCCP
https://www.readbyqxmd.com/read/28702523/implications-of-peptide-assemblies-in-amyloid-diseases
#16
REVIEW
Pu Chun Ke, Marc-Antonie Sani, Feng Ding, Aleksandr Kakinen, Ibrahim Javed, Frances Separovic, Thomas P Davis, Raffaele Mezzenga
Neurodegenerative disorders and type 2 diabetes are global epidemics compromising the quality of life of millions worldwide, with profound social and economic implications. Despite the significant differences in pathology - much of which are poorly understood - these diseases are commonly characterized by the presence of cross-β amyloid fibrils as well as the loss of neuronal or pancreatic β-cells. In this review, we document research progress on the molecular and mesoscopic self-assembly of amyloid-beta, alpha synuclein, human islet amyloid polypeptide and prions, the peptides and proteins associated with Alzheimer's, Parkinson's, type 2 diabetes and prion diseases...
July 12, 2017: Chemical Society Reviews
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/28698968/inhibition-of-poly-adp-ribose-polymerase-1-enhances-gene-expression-of-selected-sirtuins-and-app-cleaving-enzymes-in-amyloid-beta-cytotoxicity
#18
Przemysław L Wencel, Walter J Lukiw, Joanna B Strosznajder, Robert Piotr Strosznajder
Poly(ADP-ribose) polymerases (PARPs) and sirtuins (SIRTs) are involved in the regulation of cell metabolism, transcription, and DNA repair. Alterations of these enzymes may play a crucial role in Alzheimer's disease (AD). Our previous results indicated that amyloid beta (Aβ) peptides and inflammation led to activation of PARP1 and cell death. This study focused on a role of PARP1 in the regulation of gene expression for SIRTs and beta-amyloid precursor protein (βAPP) cleaving enzymes under Aβ42 oligomers (AβO) toxicity in pheochromocytoma cells (PC12) in culture...
July 12, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28697378/changes-in-phagocytosis-and-potassium-channel-activity-in-microglia-of-5xfad-mice-indicate-alterations-in-purinergic-signaling-in-a-mouse-model-of-alzheimer-s-disease
#19
Stefan Wendt, Meron Maricos, Natascha Vana, Niklas Meyer, Dilansu Guneykaya, Marcus Semtner, Helmut Kettenmann
As the immunocompetent cells of the central nervous system, microglia accumulate at amyloid beta plaques in Alzheimer's disease (AD) and acquire a morphological phenotype of activated microglia. Recent functional studies, however, indicate that in mouse models of amyloidosis and AD, these cells are rather dysfunctional indicated by a reduced phagocytic activity. Here, we report that this reduction in phagocytic activity is associated with perturbed purinergic receptor signaling, since phagocytosis could be stimulated by P2Y6 receptor activation in control, but not in 5xFAD transgenic animals, an animal model of amyloid deposition...
June 8, 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/28696431/synaptic-activity-protects-against-ad-and-ftd-like-pathology-via-autophagic-lysosomal-degradation
#20
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
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