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https://www.readbyqxmd.com/read/29332049/free-heme-and-amyloid-%C3%AE-a-fatal-liaison-in-alzheimer-s-disease
#1
Elisabeth Chiziane, Henriette Telemann, Martin Krueger, Juliane Adler, Jürgen Arnhold, A Alia, Jörg Flemmig
While the etiology of Alzheimer's disease (AD) is still unknown, an increased formation of amyloid-β (Aβ) peptide and oxidative processes are major pathological mechanism of the disease. The interaction of Aβ with free heme leads to the formation of peroxidase-active Aβ-heme complexes. However, enzyme-kinetic data and systematic mutational studies are still missing. These aspects were addressed in this study to evaluate the role of Aβ-heme complexes in AD. The enzyme-kinetic measurements showed peroxidase-specific pH- and H2O2-dependencies...
2018: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/29332046/a-novel-antibody-targeting-tau-phosphorylated-at-serine-235-detects-neurofibrillary-tangles
#2
David Brici, Jürgen Götz, Rebecca M Nisbet
Alzheimer's disease is characterized by two main pathological hallmarks in the human brain: the extracellular deposition of amyloid-β as plaques and the intracellular accumulation of the hyperphosphorylated protein tau as neurofibrillary tangles (NFTs). Phosphorylated tau (p-tau) specific-antibodies and silver staining have been used to reveal three morphological stages of NFT formation: pre-NFTs, intraneuronal NFTs (iNFTs), and extraneuronal NFTs (eNFTs). Here we characterize a novel monoclonal antibody, RN235, which is specific for tau phosphorylated at serine 235, and detects iNFTs and eNFTs in brain tissue, suggesting that phosphorylation at this site is indicative of late stage changes in tau...
2018: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/29332042/protective-effects-of-indian-spice-curcumin-against-amyloid-%C3%AE-in-alzheimer-s-disease
#3
P Hemachandra Reddy, Maria Manczak, Xiangling Yin, Mary Catherine Grady, Andrew Mitchell, Sahil Tonk, Chandra Sekhar Kuruva, Jasvinder Singh Bhatti, Ramesh Kandimalla, Murali Vijayan, Subodh Kumar, Rui Wang, Jangampalli Adi Pradeepkiran, Gilbert Ogunmokun, Kavya Thamarai, Kandi Quesada, Annette Boles, Arubala P Reddy
The purpose of our article is to assess the current understanding of Indian spice, curcumin, against amyloid-β (Aβ)-induced toxicity in Alzheimer's disease (AD) pathogenesis. Natural products, such as ginger, curcumin, and gingko biloba have been used as diets and dietary supplements to treat human diseases, including cancer, cardiovascular, respiratory, infectious, diabetes, obesity, metabolic syndromes, and neurological disorders. Products derived from plants are known to have protective effects, including anti-inflammatory, antioxidant, anti-arthritis, pro-healing, and boosting memory cognitive functions...
2018: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/29332040/synthetic-fragment-of-receptor-for-advanced-glycation-end-products-prevents-memory-loss-and-protects-brain-neurons-in-olfactory-bulbectomized-mice
#4
Olga M Volpina, Alexandr N Samokhin, Dmitriy O Koroev, Inna V Nesterova, Tatyana D Volkova, Natalia I Medvinskaya, Pavel V Nekrasov, Olga G Tatarnikova, Anna V Kamynina, Samson M Balasanyants, Tamara A Voronina, Alexey M Kulikov, Natalia V Bobkova
Activation of receptor for advanced glycation end products (RAGE) plays an essential role in the development of Alzheimer's disease (AD). It is known that the soluble isoform of the receptor binds to ligands and prevents negative effects of the receptor activation. We proposed that peptide fragments from RAGE prevent negative effects of the receptor activation during AD neurodegeneration. We have synthesized peptide fragments from surface-exposed regions of RAGE. Peptides were intranasally administrated into olfactory bulbectomized (OBX) mice, which developed some characteristics similar to AD neurodegeneration...
2018: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/29332038/sex-influences-the-accuracy-of-subjective-memory-complaint-reporting-in-older-adults
#5
Erin E Sundermann, Emily C Edmonds, Lisa Delano-Wood, Douglas R Galasko, David P Salmon, Leah H Rubin, Mark W Bondi
Subjective memory complaints (SMC) are required when diagnosing amnestic mild cognitive impairment (aMCI), although their relationship with objective memory performance and Alzheimer's disease (AD) pathology remains unclear. We investigated whether the sex of the patient/participant moderates these associations. Participants were 940 normal control (NC) and aMCI participants from the Alzheimer's Disease Neuroimaging Initiative. SMC were assessed via the memory scale of the Everyday Cognition questionnaire. Discrepancy scores were calculated between self- and informant-reports and categorized into "overestimates," "comparable estimates", and "underestimates" of SMC...
2018: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/29332037/increased-vulnerability-of-the-hippocampus-in-transgenic-mice-overexpressing-app-and-triple-repeat-tau
#6
Andrew Arner, Edward Rockenstein, Michael Mante, Jazmin Florio, Deborah Masliah, Bahar Salehi, Anthony Adame, Cassia Overk, Eliezer Masliah, Robert A Rissman
 Alzheimer's disease (AD) is the most common tauopathy, characterized by progressive accumulation of amyloid-β (Aβ) and hyperphosphorylated tau. While pathology associated with the 4-repeat (4R) tau isoform is more abundant in corticobasal degeneration and progressive supranuclear palsy, both 3R and 4R tau isoforms accumulate in AD. Many studies have investigated interactions between Aβ and 4R tau in double transgenic mice, but few, if any, have examined the effects of Aβ with 3R tau. To examine this relationship, we crossed our APP751 mutant line with our recently characterized 3R tau mutant model to create a bigenic line (hAPP-3RTau) to model AD neuropathology...
2018: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/29331877/cerebral-changes-and-disrupted-gray-matter-cortical-networks-in-asymptomatic-older-adults-at-risk-for-alzheimer-s-disease
#7
Jose L Cantero, Mercedes Atienza, Pascual Sanchez-Juan, Eloy Rodriguez-Rodriguez, Jose Luis Vazquez-Higuera, Ana Pozueta, Andrea Gonzalez-Suarez, Eduard Vilaplana, Jordi Pegueroles, Victor Montal, Rafael Blesa, Daniel Alcolea, Alberto Lleo, Juan Fortea
The diagnostic value of cerebrospinal fluid (CSF) biomarkers is well established in Alzheimer's disease, but our current knowledge about how abnormal CSF levels affect cerebral integrity, at local and network levels, is incomplete in asymptomatic older adults. Here, we have collected CSF samples and performed structural magnetic resonance imaging scans in cognitively normal elderly as part of a cross-sectional multicenter study (SIGNAL project). To identify group differences in cortical thickness, white matter volume, and properties of structural networks, participants were split into controls (N = 20), positive amyloid-β (Aβ1-42+) (N = 19), and positive phosphorylated tau (N = 18)...
December 20, 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/29331876/app-go-protein-g%C3%AE-%C3%AE-complex-signaling-mediates-a%C3%AE-degeneration-and-cognitive-impairment-in-alzheimer-s-disease-models
#8
Elena Anahi Bignante, Nicolás Eric Ponce, Florencia Heredia, Juliana Musso, María C Krawczyk, Julieta Millán, Gustavo F Pigino, Nibaldo C Inestrosa, Mariano M Boccia, Alfredo Lorenzo
Deposition of amyloid-β (Aβ), the proteolytic product of the amyloid precursor protein (APP), might cause neurodegeneration and cognitive decline in Alzheimer's disease (AD). However, the direct involvement of APP in the mechanism of Aβ-induced degeneration in AD remains on debate. Here, we analyzed the interaction of APP with heterotrimeric Go protein in primary hippocampal cultures and found that Aβ deposition dramatically enhanced APP-Go protein interaction in dystrophic neurites. APP overexpression rendered neurons vulnerable to Aβ toxicity by a mechanism that required Go-Gβγ complex signaling and p38-mitogen-activated protein kinase activation...
December 20, 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/29331212/prion-protein-as-a-toxic-acceptor-of-amyloid-%C3%AE-oligomers
#9
REVIEW
Silvia A Purro, Andrew J Nicoll, John Collinge
The initial report that cellular prion protein (PrPC) mediates toxicity of amyloid-β species linked to Alzheimer's disease was initially treated with scepticism, but growing evidence supports this claim. That there is a high-affinity interaction is now clear, and its molecular basis is being unraveled, while recent studies have identified possible downstream toxic mechanisms. Determination of the clinical significance of such interactions between PrPC and disease-associated amyloid-β species will require experimental medicine studies in humans...
February 15, 2018: Biological Psychiatry
https://www.readbyqxmd.com/read/29330470/%C3%AE-ecdysterone-protects-sh-sy5y-cells-against-%C3%AE-amyloid-induced-apoptosis-via-c-jun-n-terminal-kinase-and-akt-associated-complementary-pathways
#10
Tianjiao Xu, Chengu Niu, Xiaojie Zhang, Miaoxian Dong
Recently, the significantly higher incidence of Alzheimer's disease (AD) in women than in men has been attributed to the loss of neuroprotective estrogen after menopause. Does phytoestrogen have the ability to protect against amyloid-β (Aβ) toxicity? The aim of this study was to evaluate hypothesis that β-ecdysterone (β-Ecd) protects SH-SY5Y cells from Aβ-induced apoptosis by separate signaling pathways involving protein kinase B (Akt) and c-Jun N-terminal kinase (JNK). Here, we demonstrate that phytoestrogen β-Ecd inhibits Aβ-triggered mitochondrial apoptotic pathway, as indicated by Bcl-2/Bax ratio elevation, cytochrome c (cyt c) release reduction, and caspase-9 inactivation...
January 12, 2018: Laboratory Investigation; a Journal of Technical Methods and Pathology
https://www.readbyqxmd.com/read/29330223/the-anti-oxidant-xanthorrhizol-prevents-amyloid-%C3%AE-induced-oxidative-modification-and-inactivation-of-neprilysin
#11
Chol Seung Lim, Jung-Soo Han
Activity of neprilysin (NEP), the major protease which cleaves β-amyloid (Aβ), is reportedly reduced in the brains of patients with Alzheimer's disease (AD). Accumulation of Aβ generates reactive oxygen species (ROS) such as 4-hydroxy nonenal (HNE), and then reduces activities of Aβ-degrading enzymes including NEP. Xanthorrhizol (Xan), a natural sesquiterpenoid, has been reported to possess anti-oxidant and anti-inflammatory properties. The present study examined the effects of Xan on HNE- or oligomeric Aβ42-induced oxidative modification of NEP protein...
January 12, 2018: Bioscience Reports
https://www.readbyqxmd.com/read/29329433/rage-mediates-a%C3%AE-accumulation-in-a-mouse-model-of-alzheimer-s-disease-via-modulation-of-%C3%AE-and-%C3%AE-secretase-activity
#12
Fang Fang, Qing Yu, Ottavio Arancio, Doris Chen, Smruti S Gore, Shi Fang Yan, Shirley ShiDu Yan
Receptor for Advanced Glycation End products (RAGE) has been implicated in amyloid β-peptide (Aβ)-induced perturbation relevant to the pathogenesis of Alzheimer's disease (AD). However, whether and how RAGE regulates Aβ metabolism remains largely unknown. Aβ formation arises from aberrant cleavage of amyloid precursor protein (APP) by β- and γ-secretase. To investigate whether RAGE modulates β- and γ-secretase activity potentiating Aβ formation, we generated mAPP mice with genetic deletion of RAGE (mAPP/RO)...
January 10, 2018: Human Molecular Genetics
https://www.readbyqxmd.com/read/29329059/amyloid-burden-and-incident-depressive-symptoms-in-preclinical-alzheimer-s-disease
#13
Stephanie Perin, Karra D Harrington, Yen Ying Lim, Kathryn Ellis, David Ames, Robert H Pietrzak, Adrian Schembri, Stephanie Rainey-Smith, Olivier Salvado, Simon M Laws, Ralph N Martins, Victor L Villemagne, Christopher C Rowe, Colin L Masters, Paul Maruff
BACKGROUND: Relationships between depression and Alzheimer's disease (AD) may become clearer if studied in preclinical AD where dementia is not present. METHOD: The aim of this study was to evaluate prospectively, relationships between brain amyloid-β (Aβ), depressive symptoms and screen positive depression in cognitively normal (CN) older adults. Depressive symptoms were measured with the Geriatric Depression Inventory (GDS-15) in CN adults from the Australian Imaging Biomarkers and Lifestyle (AIBL) study without depression at baseline and classified as having abnormally high (Aβ+; n = 136) or low (Aβ-; n = 449) Aβ according to positron emission tomography at 18-month intervals over 72 months...
January 3, 2018: Journal of Affective Disorders
https://www.readbyqxmd.com/read/29328927/alzheimer-s-disease-biomarker-guided-diagnostic-workflow-using-the-added-value-of-six-combined-cerebrospinal-fluid-candidates-a%C3%AE-1-42-total-tau-phosphorylated-tau-nfl-neurogranin-and-ykl-40
#14
Harald Hampel, Nicola Toschi, Filippo Baldacci, Henrik Zetterberg, Kaj Blennow, Ingo Kilimann, Stefan J Teipel, Enrica Cavedo, Antonio Melo Dos Santos, Stéphane Epelbaum, Foudil Lamari, Remy Genthon, Bruno Dubois, Roberto Floris, Francesco Garaci, Simone Lista
INTRODUCTION: The diagnostic and classificatory performances of all combinations of three core (amyloid β peptide [i.e., Aβ1-42], total tau [t-tau], and phosphorylated tau) and three novel (neurofilament light chain protein, neurogranin, and YKL-40) cerebrospinal fluid biomarkers of neurodegeneration were compared among individuals with mild cognitive impairment (n = 41), Alzheimer's disease dementia (ADD; n = 35), frontotemporal dementia (FTD; n = 9), and cognitively healthy controls (HC; n = 21), using 10-fold cross-validation...
January 9, 2018: Alzheimer's & Dementia: the Journal of the Alzheimer's Association
https://www.readbyqxmd.com/read/29327503/noncoding-rnas-in-alzheimer-s-disease
#15
REVIEW
M Laura Idda, Rachel Munk, Kotb Abdelmohsen, Myriam Gorospe
Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the main cause of dementia among the elderly worldwide. Despite intense efforts to develop drugs for preventing and treating AD, no effective therapies are available as yet, posing a growing burden at the personal, medical, and socioeconomic levels. AD is characterized by the production and aggregation of amyloid β (Aβ) peptides derived from amyloid precursor protein (APP), the presence of hyperphosphorylated microtubule-associated protein Tau (MAPT), and chronic inflammation leading to neuronal loss...
January 12, 2018: Wiley Interdisciplinary Reviews. RNA
https://www.readbyqxmd.com/read/29325505/the-relationship-between-cholesterol-level-and-alzheimer-s-disease-associated-app-proteolysis-a%C3%AE-metabolism
#16
Chaoqun Wang, Yikai Shou, Jie Pan, Yue Du, Cuiqing Liu, Huanhuan Wang
Globally, Alzheimer's disease (AD) is the most prevalent neurodegenerative disease in the elderly population, the hallmark of which is amyloid β (Aβ) peptide. Energy metabolism and AD pathogenesis are believed to influence one another. Different cholesterol levels are thought to influence various steps in neurotoxic Aβ generation, including amyloid precursor protein (APP) proteolysis and the corresponding activities of α-, β-, and γ-secretases. In addition, cholesterol has been proved to mediate Aβ metabolism, such as its fibrillation, transportation, degradation, and clearance processes...
January 11, 2018: Nutritional Neuroscience
https://www.readbyqxmd.com/read/29324783/sirt3-activator-honokiol-attenuates-%C3%AE-amyloid-by-modulating-amyloidogenic-pathway
#17
Sindhu Ramesh, Manoj Govindarajulu, Tyler Lynd, Gwyneth Briggs, Danielle Adamek, Ellery Jones, Jake Heiner, Mohammed Majrashi, Timothy Moore, Rajesh Amin, Vishnu Suppiramaniam, Muralikrishnan Dhanasekaran
Honokiol (poly-phenolic lignan from Magnolia grandiflora) is a Sirtuin-3 (SIRT3) activator which exhibit antioxidant activity and augment mitochondrial functions in several experimental models. Modern evidence suggests the critical role of SIRT3 in the progression of several metabolic and neurodegenerative diseases. Amyloid beta (Aβ), the precursor to extracellular senile plaques, accumulates in the brains of patients with Alzheimer's disease (AD) and is related to the development of cognitive impairment and neuronal cell death...
2018: PloS One
https://www.readbyqxmd.com/read/29321592/amyloid-%C3%AE-causes-excitation-inhibition-imbalance-through-dopamine-receptor-1-dependent-disruption-of-fast-spiking-gabaergic-input-in-anterior-cingulate-cortex
#18
Si-Qiang Ren, Wen Yao, Jing-Zhi Yan, Chunhui Jin, Jia-Jun Yin, Jianmin Yuan, Shui Yu, Zaohuo Cheng
Alzheimer's disease (AD) is the most common cause of dementia in the elderly. At the early stages of AD development, the soluble β-amyloid (Aβ) induces synaptic dysfunction, perturbs the excitation/inhibition balance of neural circuitries, and in turn alters the normal neural network activity leading to cognitive decline, but the underlying mechanisms are not well established. Here by using whole-cell recordings in acute mouse brain slices, we found that 50 nM Aβ induces hyperexcitability of excitatory pyramidal cells in the cingulate cortex, one of the most vulnerable areas in AD, via depressing inhibitory synaptic transmission...
January 10, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29321566/n-domain-of-angiotensin-converting-enzyme-hydrolyzes-human-and-rat-amyloid-%C3%AE-1-16-peptides-as-arginine-specific-endopeptidase-potentially-enhancing-risk-of-alzheimer-s-disease
#19
Elena V Kugaevskaya, Alexander V Veselovsky, Maria I Indeykina, Nina I Solovyeva, Maria S Zharkova, Igor A Popov, Eugene N Nikolaev, Alexey B Mantsyzov, Alexander A Makarov, Sergey A Kozin
Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder. Amyloid-β (Aβ) aggregation is likely to be the major cause of AD. In contrast to humans and other mammals, that share the same Aβ sequence, rats and mice are invulnerable to AD-like neurodegenerative pathologies, and Aβ of these rodents (ratAβ) has three amino acid substitutions in the metal-binding domain 1-16 (MBD). Angiotensin-converting enzyme (ACE) cleaves Aβ-derived peptide substrates, however, there are contradictions concerning the localization of the cleavage sites within Aβ and the roles of each of the two ACE catalytically active domains in the hydrolysis...
January 10, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29321225/humanized-trem2-mice-reveal-microglia-intrinsic-and-extrinsic-effects-of-r47h-polymorphism
#20
Wilbur M Song, Satoru Joshita, Yingyue Zhou, Tyler K Ulland, Susan Gilfillan, Marco Colonna
Alzheimer's disease (AD) is a neurodegenerative disease that causes late-onset dementia. The R47H variant of the microglial receptor TREM2 triples AD risk in genome-wide association studies. In mouse AD models, TREM2-deficient microglia fail to proliferate and cluster around the amyloid-β plaques characteristic of AD. In vitro, the common variant (CV) of TREM2 binds anionic lipids, whereas R47H mutation impairs binding. However, in vivo, the identity of TREM2 ligands and effect of the R47H variant remain unknown...
January 10, 2018: Journal of Experimental Medicine
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