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https://www.readbyqxmd.com/read/28733960/a-review-of-fluid-biomarkers-for-alzheimer-s-disease-moving-from-csf-to-blood
#1
REVIEW
Kaj Blennow
A set of core cerebrospinal fluid (CSF) biomarkers for Alzheimer's disease (AD) includes total tau (T-tau), phosphorylated tau (P-tau) and β-amyloid 42 (Aβ42). These biomarkers reflect some of the key aspects of AD pathophysiology, including neuronal degeneration, tau phosphorylation with tangle formation, and Aβ aggregation with deposition of the peptide into plaques. The core AD CSF biomarkers have been validated clinically in numerous studies, and found to have a very high diagnostic performance to identify AD, both in the dementia and in the mild cognitive impairment stages of the disease...
July 2017: Neurology and Therapy
https://www.readbyqxmd.com/read/28733667/rtn1-and-rtn3-protein-are-differentially-associated-with-senile-plaques-in-alzheimer-s-brains
#2
Qi Shi, Yingying Ge, Wanxia He, Xiangyou Hu, Riqiang Yan
Reticulon proteins (RTNs), consisting of RTN1 to RTN4, were previously shown to interact with BACE1 by negatively modulating its secretase activity. In RTN3-null mice, RTN1 expression was slightly elevated. To understand the in vivo role of RTN1, we generated RTN1-null mice and compared the effects of RTN1 and RTN3 on BACE1 modulation. We show that RTN1 is mostly expressed by neurons and not by glial cells under normal conditions, similar to the expression of RTN3. However, RTN1 is more localized in dendrites and is an excellent marker for dendrites of Purkinje cells, while RTN3 expression is less evident in dendrites...
July 21, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28729665/identification-of-proteins-that-specifically-recognize-and-bind-protofibrillar-aggregates-of-amyloid-%C3%AE
#3
Elisabet Wahlberg, M Mahafuzur Rahman, Hanna Lindberg, Elin Gunneriusson, Benjamin Schmuck, Christofer Lendel, Mats Sandgren, John Löfblom, Stefan Ståhl, Torleif Härd
Protofibrils of the 42 amino acids long amyloid-β peptide are transient pre-fibrillar intermediates in the process of peptide aggregation into amyloid plaques and are thought to play a critical role in the pathology of Alzheimer's disease. Hence, there is a need for research reagents and potential diagnostic reagents for detection and imaging of such aggregates. Here we describe an in vitro selection of Affibody molecules that bind to protofibrils of Aβ42cc, which is a stable engineered mimic of wild type Aβ42 protofibrils...
July 20, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28729192/butyrylcholinesterase-knockout-reduces-fibrillar-%C3%AE-amyloid-and-conserves-18-fdg-retention-in-5xfad-mouse-model-of-alzheimer-s-disease
#4
D R DeBay, G A Reid, I R Macdonald, G Mawko, S Burrell, E Martin, C V Bowen, S Darvesh
Alzheimer's disease (AD) is the most common neurodegenerative disorder causing dementia. One hallmark of the AD brain is the deposition of β-amyloid (Aβ) plaques. AD is also a state of cholinergic dysfunction and butyrylcholinesterase (BChE) associates with Aβ pathology. A transgenic mouse (5XFAD) is an aggressive amyloidosis model, producing Aβ plaques of which BChE also associates. A derived strain (5XFAD/BChE-KO), with the BChE gene knocked out, has significantly lower fibrillar Aβ than 5XFAD mice at the same age...
July 17, 2017: Brain Research
https://www.readbyqxmd.com/read/28728464/repeat-mild-traumatic-brain-injury-in-adolescent-rats-increases-subsequent-%C3%AE-amyloid-pathogenesis
#5
Daya Alexander Grant, Rebecka Serpa, Cameron R Moattari, Ari Brown, Tiffany Greco, Mayumi Prins, Edmond Teng
Single moderate-to-severe traumatic brain injuries (TBIs) may increase subsequent risk for neurodegenerative disease by facilitating β-amyloid (Aβ) deposition. However, the chronic effects on Aβ pathogenesis of repetitive mild TBIs, which are common in adolescents and young adults, remain uncertain. We examined the effects of repetitive mild TBI sustained during adolescence on subsequent deposition of Aβ pathology in a transgenic APP/PS1 rat model. Transgenic rats received sham or four individual mild TBI (rTBI) separated by either 24- or 72-hour intervals at post-natal day 35 (prior to Aβ plaque deposition)...
July 20, 2017: Journal of Neurotrauma
https://www.readbyqxmd.com/read/28728117/alzheimer-s-disease-markers-in-the-aged-sheep-ovis-aries
#6
Suzanne J Reid, Natasha E Mckean, Kristen Henty, Erik Portelius, Kaj Blennow, Skye R Rudiger, C Simon Bawden, Renee R Handley, Paul J Verma, Richard L M Faull, Henry J Waldvogel, Henrik Zetterberg, Russell G Snell
This study reports the identification and characterization of markers of Alzheimer's disease (AD) in aged sheep (Ovis aries) as a preliminary step toward making a genetically modified large animal model of AD. Importantly, the sequences of key proteins involved in AD pathogenesis are highly conserved between sheep and human. The processing of the amyloid-β (Aβ) protein is conserved between sheep and human, and sheep Aβ1-42/Aβ1-40 ratios in cerebrospinal fluid (CSF) are also very similar to human. In addition, total tau and neurofilament light levels in CSF are comparable with those found in human...
June 24, 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/28726016/amyloid-%C3%AE-derived-from-the-brain-of-the-alzheimer-s-disease-transgenic-mouse-is-resistant-to-proteolytic-digestion-due-to-its-conformation
#7
Baian Chen, Jing Zhang, Shubo Wang, Wen Wang, Zitong Yao, Quan Sun, Yi Wu, Jing Lu
The main pathological feature of Alzheimer's disease (AD) is the formation of abundant amyloid-β (Aβ) plaques in the human brain. Studies have reported that Aβ from the AD brain is resistant to proteolytic digestion, which may explain why Aβ cannot be readily eliminated from this organ. However, there are only a few studies that address this important question. We used the AD transgenic mouse (APP/PS1) model to show that Aβ derived from the brain of the old mouse is resistant to proteolytic digestion. This was in contrast to the proteinase K-sensitive human Aβ peptide, whose amino acid sequence was identical to that of AD mouse-derived Aβ but whose conformation was different (i...
July 19, 2017: Journal of Molecular Neuroscience: MN
https://www.readbyqxmd.com/read/28718623/a-multimodal-spectroscopic-imaging-method-to-characterize-the-metal-and-macromolecular-content-of-proteinaceous-aggregates-amyloid-plaques
#8
Kelly L Summers, Nicholas Fimognari, Ashley Hollings, Mitchell Kiernan, Virginie Lam, Rebecca J Tidy, David Paterson, Mark J Tobin, Ryu Takechi, Graham N George, Ingrid J Pickering, John C Mamo, Hugh H Harris, Mark J Hackett
Alzheimer's disease (AD) is a major international health and economic concern. A key pathological feature of AD is so-called "amyloid-β-plaques", or "Aβ-plaques", which are deposits of aggregated protein, enriched with the Aβ fragment of amyloid precursor protein. Despite their name, the deposits are not pure Aβ and have a heterogeneous, chemically complex composition that can include multiple proteins, lipids, and metal ions (Fe, Cu, or Zn). Despite extensive research, it is still uncertain whether Aβ-plaques are a cause or a consequence of AD pathology...
July 18, 2017: Biochemistry
https://www.readbyqxmd.com/read/28714403/gsk3-inhibitors-in-the-therapeutic-development-of-diabetes-cancer-and-neurodegeneration-past-present-and-future
#9
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/28714390/cdk5-and-mapt-gene-expression-in-alzheimer-s-disease-brain-samples
#10
Josianne Thomazini Fukasawa, Roger Willian de Labio, Lucas Trevizani Rasmussen, Lucieni Conterno de Oliveira, Elizabeth Chen, João Villares, Gustavo Tureck, Marília de Arruda Cardoso Smith, Spencer Luiz Marques Payão
BACKGROUND: Alzheimer's disease (AD) is a neurodegenerative disorder characterized by extracellular amyloid plaque and neurofibrillary tangles in the brain. Studies have shown that neurons are able to re-enter the cell cycle, but not enough to enable full replication. This leads to cell death and consequent neurodegeneration. OBJECTIVE: This study aimed to characterize the expression of the MAPT gene and CDK5 (the gene involved in cell cycle regulation) in brain samples from patients with AD and controls...
July 13, 2017: Current Alzheimer Research
https://www.readbyqxmd.com/read/28713158/amyloid-beta-structure-biology-and-structure-based-therapeutic-development
#11
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/28711595/a%C3%AE-truncated-species-implications-for-brain-clearance-mechanisms-and-amyloid-plaque-deposition
#12
Erwin Cabrera, Paul Mathews, Emiliya Mezhericher, Thomas G Beach, Jingjing Deng, Thomas A Neubert, Agueda Rostagno, Jorge Ghiso
Extensive parenchymal and vascular Aβ deposits are pathological hallmarks of Alzheimer's disease (AD). Besides classic full-length peptides, biochemical analyses of brain deposits have revealed high degree of Aβ heterogeneity likely resulting from the action of multiple proteolytic enzymes. In spite of the numerous studies focusing in Aβ, the relevance of N- and C-terminal truncated species for AD pathogenesis remains largely understudied. In the present work, using novel antibodies specifically recognizing Aβ species N-terminally truncated at position 4 or C-terminally truncated at position 34, we provide a clear assessment of the differential topographic localization of these species in AD brains and transgenic models...
July 12, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28710249/amyloid-precursor-protein-in-pancreatic-islets
#13
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/28707657/-transmission-of-pathogenic-protein-aggregates-in-alzheimer-s-disease
#14
A L Schwarzman, S V Sarantseva
Deposits of amyloid peptide Aβ and intracellular aggregates of hyperphosphorylated tau protein in the brain of patients are major neuropathological features of Alzheimer's disease (AD). For a long time, the possibility of horizontal transmission of Aβ aggregates from cell to cell and from person to person remained hypothetical, since there was no experimental evidence. However, in 1993, the formation of senile plaques was confirmed in the brains of animals after intracerebral injections of AD patient brain homogenates or homogenates of the brain of transgenic mice enriched with Aβ aggregates...
May 2017: Molekuliarnaia Biologiia
https://www.readbyqxmd.com/read/28707599/designing-of-selective-%C3%AE-secretase-inhibitory-benzenesulfonamides-through-comparative-in-vitro-and-in-silico-analysis
#15
Neeraj Masand, Satya P Gupta, Ratan Lal Khosa
BACKGROUND: In Alzheimer's disease (AD), the gene mutations have been identified in the amyloid precursor protein (APP), the presenilin-1 (PS1) and -2 (PS2) genes. APP is a transmembrane protein which gets cleaved by α- and β-secretase enzymes and releases Aβ peptides which forms senile plaques in brain tissue. It contributes for local inflammatory response, subsequent oxidative stress, biochemical changes and neuronal death. Targeting the development of Aβ aggregates in the senile plaques is an important strategy in the treatment of AD...
July 13, 2017: Current Drug Discovery Technologies
https://www.readbyqxmd.com/read/28706768/dna-pk-and-p38-mapk-a-kinase-collusion-in-alzheimer-s-disease
#16
Jyotshna Kanungo
The pathogenesis of Alzheimer's disease (AD), characterized by prevalent neuronal death and extracellular deposit of amyloid plaques, is poorly understood. DNA lesions downstream of reduced DNA repair ability have been reported in AD brains. Neurons predominantly use a mechanism to repair double-strand DNA breaks (DSB), which is non-homologous end joining (NHEJ). NHEJ requires DNA-dependent protein kinase (DNA-PK) activity. DNA-PK is a holoenzyme comprising the p460 kD catalytic subunit (DNA-PKcs) and its activator Ku, a heterodimer of p86 and p70 subunits...
2017: Brain Disorders & Therapy
https://www.readbyqxmd.com/read/28704199/the-role-of-ubiquitin-proteasomal-system-and-autophagy-lysosome-pathway-in-alzheimer-s-disease
#17
Yuan Zhang, Xu Chen, Yanfang Zhao, Murugavel Ponnusamy, Ying Liu
Alzheimer's disease (AD) is the most common neurodegenerative disorder leading to dementia in the elderly population. AD is associated with the buildup of β-amyloid and tau, which aggregate into extracellular plaques and neurofibrillary tangles. Although the exact mechanism of pathological process of AD is unclear, the dysfunction of protein degradation mechanisms has been proposed to play an important role in AD. The cellular degradation of abnormal or misfolded proteins consists of three different mechanisms: the ubiquitin proteasomal system (UPS), autophagy-lysosomal pathway (ALP), and interaction of molecular chaperones with UPS or ALP...
July 12, 2017: Reviews in the Neurosciences
https://www.readbyqxmd.com/read/28702899/complex-antioxidants-in-a-randomized-single-blinded-study-of-memory-in-seniors
#18
William K Summers, Roy L Martin, Yimeng Liu, Bernice Peña, Gary M Marsh
INTRODUCTION: Oxidative injury to the brain and aging are theoretical co-causes of Alzheimer's Disease (AD). Amyloid plaques and tangles are then secondary phenomenon. The preclinical state would then be 'normal' elderly. METHODS: A potent complex antioxidant (antiOx) was tested against a popular one-a-day multivitamin (mV) in a randomized single blind design in 'normal' senior subjects over 6 months. Memory testing was done at baseline, 1, 3, and 6 months. The generalized estimating equation (GEE) approach was used to compare the change score of NLT100 and 20WR between two groups over time...
July 12, 2017: Aging Clinical and Experimental Research
https://www.readbyqxmd.com/read/28702365/abnormal-amyloid-%C3%AE-42-expression-and-increased-oxidative-stress-in-plasma-of-ckd-patients-with-cognitive-dysfunction-a-small-scale-case-control-study-comparison-with-alzheimer-s-disease
#19
G Vinothkumar, C Kedharnath, S Krishnakumar, S Sreedhar, K Preethikrishnan, S Dinesh, A Sundaram, D Balakrishnan, G Shivashekar, Sureshkumar, P Venkataraman
BACKGROUND: Cognitive dysfunction has been increasingly recognized in chronic kidney disease (CKD) patients. Senile plaques are important pathophysiological characteristic of cognitive dysfunction. The major component of plaques is the amyloid β (Aβ) peptide released from proteolytic cleavage of amyloid precursor protein (APP). Plasma Aβ has been a focus of the growing literature on blood based biomarkers for cognitive dysfunction. Oxidative stress is prevalent in CKD and it plays an important role in cognitive dysfunction...
December 2017: BBA Clinical
https://www.readbyqxmd.com/read/28701379/loss-of-clusterin-shifts-amyloid-deposition-to-the-cerebrovasculature-via-disruption-of-perivascular-drainage-pathways
#20
Aleksandra M Wojtas, Silvia S Kang, Benjamin M Olley, Maureen Gatherer, Mitsuru Shinohara, Patricia A Lozano, Chia-Chen Liu, Aishe Kurti, Kelsey E Baker, Dennis W Dickson, Mei Yue, Leonard Petrucelli, Guojun Bu, Roxana O Carare, John D Fryer
Alzheimer's disease (AD) is characterized by amyloid-β (Aβ) peptide deposition in brain parenchyma as plaques and in cerebral blood vessels as cerebral amyloid angiopathy (CAA). CAA deposition leads to several clinical complications, including intracerebral hemorrhage. The underlying molecular mechanisms that regulate plaque and CAA deposition in the vast majority of sporadic AD patients remain unclear. The clusterin (CLU) gene is genetically associated with AD and CLU has been shown to alter aggregation, toxicity, and blood-brain barrier transport of Aβ, suggesting it might play a key role in regulating the balance between Aβ deposition and clearance in both brain and blood vessels...
July 12, 2017: Proceedings of the National Academy of Sciences of the United States of America
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