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Alzheimer's etiologies

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https://www.readbyqxmd.com/read/28742084/systematic-tissue-specific-functional-annotation-of-the-human-genome-highlights-immune-related-dna-elements-for-late-onset-alzheimer-s-disease
#1
Qiongshi Lu, Ryan L Powles, Sarah Abdallah, Derek Ou, Qian Wang, Yiming Hu, Yisi Lu, Wei Liu, Boyang Li, Shubhabrata Mukherjee, Paul K Crane, Hongyu Zhao
Continuing efforts from large international consortia have made genome-wide epigenomic and transcriptomic annotation data publicly available for a variety of cell and tissue types. However, synthesis of these datasets into effective summary metrics to characterize the functional non-coding genome remains a challenge. Here, we present GenoSkyline-Plus, an extension of our previous work through integration of an expanded set of epigenomic and transcriptomic annotations to produce high-resolution, single tissue annotations...
July 24, 2017: PLoS Genetics
https://www.readbyqxmd.com/read/28731438/evidence-that-the-human-innate-immune-peptide-ll-37-may-be-a-binding-partner-of%C3%A2-amyloid-%C3%AE-and-inhibitor-of%C3%A2-fibril-assembly
#2
Ersilia De Lorenzi, Marcella Chiari, Raffaella Colombo, Marina Cretich, Laura Sola, Renzo Vanna, Paola Gagni, Federica Bisceglia, Carlo Morasso, Jennifer S Lin, Moonhee Lee, Patrick L McGeer, Annelise E Barron
BACKGROUND: Identifying physiologically relevant binding partners of amyloid-β (Aβ) that modulate in vivo fibril formation may yield new insights into Alzheimer's disease (AD) etiology. Human cathelicidin peptide, LL-37, is an innate immune effector and modulator, ubiquitous in human tissues and expressed in myriad cell types. OBJECTIVE: We present in vitro experimental evidence and discuss findings supporting a novel hypothesis that LL-37 binds to Aβ42 and can modulate Aβ fibril formation...
July 18, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28729832/the-role-of-microglia-in-retinal-neurodegeneration-alzheimer-s-disease-parkinson-and-glaucoma
#3
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/28722749/rho-associated-protein-kinases-as-therapeutic-targets-for-both-vascular-and-parenchymal-pathologies-in-alzheimer-s-disease
#4
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/28721361/role-of-endoplasmic-reticulum-stress-in-learning-and-memory-impairment-and-alzheimer-s-disease-like-neuropathology-in-the-ps19-and-app-swe-mouse-models-of-tauopathy-and-amyloidosis
#5
Denise Isabelle Briggs, Erwin Defensor, Pooneh Memar Ardestani, Bitna Yi, Michelle Halpain, Guy Seabrook, Mehrdad Shamloo
Emerging evidence suggests that endoplasmic reticulum (ER) stress may be involved in the pathogenesis of Alzheimer's disease (AD). Recently, pharmacological modulation of the eukaryotic translation initiation factor-2 (eIF2α) pathway was achieved using an integrated stress response inhibitor (ISRIB). While members of this signaling cascade have been suggested as potential therapeutic targets for neurodegeneration, the biological significance of this pathway has not been comprehensively assessed in animal models of AD...
July 2017: ENeuro
https://www.readbyqxmd.com/read/28720846/physiological-stress-induced-corticosterone-increases-heme-uptake-via-klf4-hcp1-signaling-pathway-in-hippocampus-neurons
#6
Hongxia Li, Caixia Zhang, Hui Shen, Zhilei Shen, Lusha Wu, Fengfeng Mo, Min Li
Iron overload has attracted much attention because of its adverse effect in increasing the risk of developing several neurodegenerative disorders. Under various pathologic conditions, a lot of heme are released. The aggregation of heme is more neurotoxic than that of iron released from the heme breakdown. Our previous studies demonstrated that psychological stress (PS) is a risk factor of cerebral iron metabolism disorders, thus causing iron accumulation in rat brains. In the present study, we found PS could increase heme uptake via heme carrier protein 1 (HCP1) in rat brains...
July 18, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28719622/characterization-of-plasma-metal-profiles-in-alzheimer-s-disease-using-multivariate-statistical-analysis
#7
Chunmei Guan, Rui Dang, Yu Cui, Liyan Liu, Xiaobei Chen, Xiaoyu Wang, Jingli Zhu, Donggang Li, Junwei Li, Decai Wang
The exact cause of Alzheimer's disease (AD) and the role of metals in its etiology remain unclear. We have used an analytical approach, based on inductively coupled plasma mass spectrometry coupled with multivariate statistical analysis, to study the profiles of a wide range of metals in AD patients and healthy controls. AD cannot be cured and the lack of sensitive biomarkers that can be used in the early stages of the disease may contribute to this treatment failure. In the present study, we measured plasma levels of amyloid-β1-42(0...
2017: PloS One
https://www.readbyqxmd.com/read/28717130/polymicrobial-infections-in-brain-tissue-from-alzheimer-s-disease-patients
#8
Diana Pisa, Ruth Alonso, Ana M Fernández-Fernández, Alberto Rábano, Luis Carrasco
Several studies have advanced the idea that the etiology of Alzheimer's disease (AD) could be microbial in origin. In the present study, we tested the possibility that polymicrobial infections exist in tissue from the entorhinal cortex/hippocampus region of patients with AD using immunohistochemistry (confocal laser scanning microscopy) and highly sensitive (nested) PCR. We found no evidence for expression of early (ICP0) or late (ICP5) proteins of herpes simplex virus type 1 (HSV-1) in brain sections. A polyclonal antibody against Borrelia detected structures that appeared not related to spirochetes, but rather to fungi...
July 17, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28714419/design-of-multi-target-agents-for-the-treatment-of-alzheimer-s-disease-based-on-tacrine
#9
Hongzhi Lin, Qi Li, Kai Gu, Jie Zhu, Xueyang Jiang, Yao Chen, Haopeng Sun
Alzheimer's disease (AD) is one of the most common forms of dementia in elderly people. To date, efficacious therapeutic agent for the treatment of AD is still very limited, so it has long been a challenging and attractive task to discover new anti-AD drugs. Considering the multifactorial nature of AD, recently, the concept of multi-target-directed ligands (MTDLs) has emerged as a new strategy for designing therapeutic agents on AD. MTDLs are believed to exert their effects through simultaneously affecting multiple targets which contribute to etiology of AD...
July 17, 2017: Current Topics in Medicinal Chemistry
https://www.readbyqxmd.com/read/28714393/interrelationships-between-gut-microbiota-and-host-paradigms-role-in-neurodegenerative-diseases-and-future-prospects
#10
Javier Caballero-Villarraso, Alberto Galvan, Begoña M Escribano, Isaac Túnez
Advances in the knowledge of the microbiota and concepts related to it have triggered a wake-up call in biomedicine. The development in various scientific areas has enabled a better and broader approach to everything concerning the set of families of microorganisms that coexist with an individual and are able to function as one more organ in its body. Among the aforementioned scientific areas, those worth mentioning are the advances/progress in biotechnological resources and, in particular, molecular biology and related areas...
July 14, 2017: CNS & Neurological Disorders Drug Targets
https://www.readbyqxmd.com/read/28709938/a-cross-sectional-comparison-of-brain-glucose-and-ketone-metabolism-in-cognitively-healthy-older-adults-mild-cognitive-impairment-and-early-alzheimer-s-disease
#11
E Croteau, C A Castellano, M Fortier, C Bocti, T Fulop, N Paquet, S C Cunnane
INTRODUCTION: Deteriorating brain glucose metabolism precedes the clinical onset of Alzheimer's disease (AD) and appears to contribute to its etiology. Ketone bodies, mainly β-hydroxybutyrate and acetoacetate, are the primary alternative brain fuel to glucose. Some reports suggest that brain ketone metabolism is unchanged in AD but, to our knowledge, no such data are available for MCI. OBJECTIVE: To compare brain energy metabolism (glucose and acetoacetate) and some brain morphological characteristics in cognitively healthy older adult controls (CTL), mild cognitive impairment (MCI) and early AD...
July 11, 2017: Experimental Gerontology
https://www.readbyqxmd.com/read/28704198/alzheimer-s-disease-as-it-was-in-the-beginning
#12
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/28699112/brain-under-stress-and-alzheimer-s-disease
#13
REVIEW
Boris Mravec, Lubica Horvathova, Alexandra Padova
Modern society is characterized by the ubiquity of stressors that affect every individual to different extents. Furthermore, experimental, clinical, and epidemiological data have shown that chronic activation of the stress response may participate in the development of various somatic as well as neuropsychiatric diseases. Surprisingly, the role that stress plays in the etiopathogenesis of Alzheimer's disease (AD) has not yet been studied in detail and is therefore not well understood. However, accumulated data have shown that neuroendocrine and behavioral changes accompanying the stress response affect neuronal homeostasis and compromise several key neuronal processes...
July 11, 2017: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/28697887/molecular-origins-of-the-compatibility-between-glycosaminoglycans-and-a%C3%AE-40-amyloid-fibrils
#14
Katie L Stewart, Eleri Hughes, Edwin A Yates, David A Middleton, Sheena E Radford
The Aβ peptide forms extracellular plaques associated with Alzheimer's disease. In addition to protein fibrils, amyloid plaques also contain non-proteinaceous components, including glycosaminoglycans (GAGs). We have shown previously that the GAG low molecular weight heparin (LMWH) binds to Aβ40 fibrils with a three-fold-symmetric (3Q) morphology with higher affinity than Aβ40 fibrils in alternative structures, Aβ42 fibrils, or amyloid fibrils formed from other sequences. Solid-state NMR (SSNMR) analysis of the GAG-3Q fibril complex revealed an interaction site at the corners of the 3Q fibril structure, but the origin of the binding specificity remained obscure...
July 8, 2017: Journal of Molecular Biology
https://www.readbyqxmd.com/read/28694093/functional-analyses-of-major-cancer-related-signaling-pathways-in-alzheimer-s-disease-etiology
#15
REVIEW
Jianping Guo, Ji Cheng, Brian J North, Wenyi Wei
Alzheimer's disease (AD) is an aging-related neurodegenerative disease and accounts for majority of human dementia. The hyper-phosphorylated tau-mediated intracellular neurofibrillary tangle and amyloid β-mediated extracellular senile plaque are characterized as major pathological lesions of AD. Different from the dysregulated growth control and ample genetic mutations associated with human cancers, AD displays damage and death of brain neurons in the absence of genomic alterations. Although various biological processes predominately governing tumorigenesis such as inflammation, metabolic alteration, oxidative stress and insulin resistance have been associated with AD genesis, the mechanistic connection of these biological processes and signaling pathways including mTOR, MAPK, SIRT, HIF, and the FOXO pathway controlling aging and the pathological lesions of AD are not well recapitulated...
July 7, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28671113/implication-of-the-app-gene-in-intellectual-abilities
#16
Craig Myrum, Oleksii Nikolaienko, Clive R Bramham, Jan Haavik, Tetyana Zayats
BACKGROUND: Cognitive functions are highly heritable and polygenic, though the source of this genetic influence is unclear. On the neurobiological level, these functions rely on effective neuroplasticity, in which the activity-regulated cytoskeleton associated protein (ARC) plays and essential role. OBJECTIVES: To examine whether the ARC gene complex may contribute to the genetic components of intellectual function given the crucial role of ARC in brain plasticity and memory formation...
June 27, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28656195/microrna-322-attenuates-aluminum-maltolate-induced-apoptosis-in-the-human-sh-sy5y-neuroblastoma-cell-line
#17
Xinlong Ma, Feng Shang, Qiuxia Zhang, Qingtang Lin, Shuo Han, Yongzhi Shan, Jianxin Du, Feng Ling, Hongqi Zhang, Geng Xu
Aluminum-maltolate (Al‑Malt) is a potent apoptosis inductor, which has been widely reported as an etiologic factor in Alzheimer's disease (AD). MicroRNA-322 (miR‑322) is a vital regulator in various biological processes. The aim of the current study was to identify the role and possible underlying mechanism of miR‑322 in Al‑Malt‑induced apoptosis. Eight concentrations of Al‑Malt were prepared and used for treating the human neuroblastoma cell line, SH‑SY5Y. Subsequent to treatment with Al‑Malt for 3 days, cell viability, apoptosis and the expression levels of apoptosis‑associated factors were measured...
August 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28650335/development-of-ad-like-symptoms-following-co-administration-of-alcl3-and-d-gal-in-rats-a-neurochemical-biochemical-and-behavioural-study
#18
Laraib Liaquat, Saara Ahmad, Sadia Sadir, Zehra Batool, Saima Khaliq, Saiqa Tabassum, Shaista Emad, Syeda Madiha, Sidrah Shahzad, Saida Haider
Alzheimer's disease (AD) is an age-related neurodegenerative disorder associated with neurochemical and neurobehavioural alterations. Aluminium (Al) is considered as a contributing factor in the etiology of several neurodegenerative disorders like AD. D-galactose (D-gal) is a physiological nutrient but over supply induces some neurochemical and biochemical changes that exacerbate natural aging process. In this study, we aimed to develop AD animal model by co-administration of Al and D-gal in rats. Male albino Wistar rats were intraperitoneally injected with AlCl3 and D-gal at a dose of 150mg/kg and 300mg/kg respectively for one week...
March 2017: Pakistan Journal of Pharmaceutical Sciences
https://www.readbyqxmd.com/read/28650319/somatostatin-binds-to-the-human-amyloid-%C3%AE-peptide-and-favors-the-formation-of-distinct-oligomers
#19
Hansen Wang, Lisa D Muiznieks, Punam Ghosh, Declan Williams, Michael Solarski, Andrew Fang, Alejandro Ruiz-Riquelme, Régis Pomès, Joel C Watts, Avi Chakrabartty, Holger Wille, Simon Sharpe, Gerold Schmitt-Ulms
The amyloid β peptide (Aβ) is a key player in the etiology of Alzheimer disease (AD), yet a systematic investigation of its molecular interactions has not been reported. Here we identified by quantitative mass spectrometry proteins in human brain extract that bind to oligomeric Aβ1-42 (oAβ1-42) and/or monomeric Aβ1-42 (mAβ1-42) baits. Remarkably, the cyclic neuroendocrine peptide somatostatin-14 (SST14) was observed to be the most selectively enriched oAβ1-42 binder. The binding interface comprises a central tryptophan within SST14 and the N-terminus of Aβ1-42...
June 26, 2017: ELife
https://www.readbyqxmd.com/read/28648936/diagnostic-pathology-of-alzheimer-s-disease-from-routine-microscopy-to-immunohistochemistry-and-experimental-correlations
#20
Gerard Nuovo, Bernard Paniccia, Louisa Mezache, Maria Quiñónez, James Williams, Paige Vandiver, Paolo Fadda, Vicky Amann
The absence of any histologic correlate for Alzheimer's disease despite its commonness and severe clinical sequelae may offers clues to its etiology. Recent evidence strongly suggests that the central event of this disease is the hyperphosphorylation of neuronal tau protein and not the beta amyloid precipitates. In each case, essential and soluble neuronal proteins derivatives form insoluble aggregates that can readily be detected by immunohistochemistry using antibodies specific for the misfolded proteins...
June 2017: Annals of Diagnostic Pathology
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