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amyloid precursor protein

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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
#1
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/29331531/profiles-of-%C3%AE-amyloid-peptides-and-key-secretases-in-brain-autopsy-samples-differ-with-sex-and-apoe-%C3%AE%C2%B54-status-impact-for-risk-and-progression-of-alzheimer-disease
#2
Jennifer N K Nyarko, Maa O Quartey, Paul R Pennington, Ryan M Heistad, Doris Dea, Judes Poirier, Glen B Baker, Darrell D Mousseau
The APOE ε 4 allele was originally reported to contribute to risk of Alzheimer disease (AD) in women, yet male and female AD patient-derived data are routinely pooled. Histopathological hallmarks of AD include neurofibrillary tangles centered on hyperphosphorylated Tau and plaques composed of the β -amyloid (A β) peptide that is derived by sequential secretase-mediated cleavage of the Amyloid Protein Precursor (APP). We chose to examine profiles of A β (1-40), A β (1-42), and N-truncated (i.e. p3-related) fragments in the plaque-associated fraction of autopsied cortical and corresponding hippocampal samples from donors with a diagnosis of early-onset (EOAD) and late-onset (LOAD) AD...
January 10, 2018: Neuroscience
https://www.readbyqxmd.com/read/29330135/apbb2-is-associated-with-amphetamine-use-and-plasma-beta-amyloids-in-patients-receiving-methadone-maintenance-treatment
#3
Chia-Chen Liu, Chiu-Ping Fang, Tung-Hsia Liu, Hsiang-Wei Kuo, Shu Chi Liu, Sheng-Chang Wang, Andrew C H Chen, Yu-Li Liu
APBB2, amyloid beta (A4) precursor protein-binding family B member 2, has been reported to be associated with opioid dependence. In this study, we reported the first time that the genetic variants in the APBB2 gene were associated with use of amphetamine in opioid dependent patients undergoing methadone maintenance treatment (MMT). 344 heroin-dependent patients undergoing MMT were recruited and assessed for use of amphetamine and opioids by urine toxicology, withdrawal severity, and side effects. DNAs were genome-widely genotyped for all patients...
January 9, 2018: Progress in Neuro-psychopharmacology & Biological Psychiatry
https://www.readbyqxmd.com/read/29329714/mutation-burden-profile-in-familial-alzheimer-s-disease-cases-from-india
#4
Adhikarla Syama, Somdatta Sen, Lakshmi Narayanan Kota, Biju Viswanath, Meera Purushottam, Mathew Varghese, Sanjeev Jain, Mitradas M Panicker, Odity Mukherjee
This study attempts to identify coding risk variants in genes previously implicated in Alzheimer's disease (AD) pathways, through whole-exome sequencing of subjects (N = 17) with AD, with a positive family history of dementia (familial AD). We attempted to evaluate the mutation burden in genes encoding amyloid precursor protein metabolism and previously linked to risk of dementias. Novel variants were identified in genes involved in amyloid precursor protein metabolism such as PSEN1 (chr 14:73653575, W161C, tgg > tgT), PLAT (chr 8:42039530,G272R), and SORL1 (chr11:121414373,G601D)...
December 12, 2017: Neurobiology of Aging
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
#5
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/29328367/tumorigenic-proteins-upregulated-in-the-mycn-amplified-imr-32-human-neuroblastoma-cells-promote-proliferation-and-migration
#6
Hayat Zaatiti, Jad Abdallah, Zeina Nasr, George Khazen, Anthony Sandler, Tamara J Abou-Antoun
Childhood neuroblastoma is one of the most common types of extra-cranial cancer affecting children with a clinical spectrum ranging from spontaneous regression to malignant and fatal progression. In order to improve the clinical outcomes of children with high-risk neuroblastoma, it is crucial to understand the tumorigenic mechanisms that govern its malignant behaviors. MYCN proto-oncogene, bHLH transcription factor (MYCN) amplification has been implicated in the malignant, treatment-evasive nature of aggressive, high-risk neuroblastoma...
January 4, 2018: International Journal of Oncology
https://www.readbyqxmd.com/read/29327503/noncoding-rnas-in-alzheimer-s-disease
#7
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
#8
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/29325091/%C3%AE-secretase-adam10-physically-interacts-with-%C3%AE-secretase-bace1-in-neurons-and-regulates-chl1-proteolysis
#9
Xin Wang, Congcong Wang, Gang Pei
α-secretase and β-secretase are known to compete for amyloid precursor protein (APP) processing and thus play a vital role in Alzheimer's disease pathogenesis. A disintegrin and metalloproteinase 10 (ADAM10) and β-site APP cleaving enzyme 1 (BACE1) mediate the major activities of α-secretase and β-secretase in brain and share various common substrates. However, whether they function separately or together is poorly understood. Here, we show that ADAM10 and BACE1 co-localize in the neurites of mouse primary neurons...
January 9, 2018: Journal of Molecular Cell Biology
https://www.readbyqxmd.com/read/29324783/sirt3-activator-honokiol-attenuates-%C3%AE-amyloid-by-modulating-amyloidogenic-pathway
#10
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/29320530/the-amyloid-precursor-protein-derivative-app96-110-is-efficacious-following-intravenous-administration-after-traumatic-brain-injury
#11
Stephanie L Plummer, Frances Corrigan, Emma Thornton, Joshua A Woenig, Robert Vink, Roberto Cappai, Corinna Van Den Heuvel
Following traumatic brain injury (TBI) neurological damage is ongoing through a complex cascade of primary and secondary injury events in the ensuing minutes, days and weeks. The delayed nature of secondary injury provides a valuable window of opportunity to limit the consequences with a timely treatment. Recently, the amyloid precursor protein (APP) and its derivative APP96-110 have shown encouraging neuroprotective activity following TBI following an intracerebroventricular administration. Nevertheless, its broader clinical utility would be enhanced by an intravenous (IV) administration...
2018: PloS One
https://www.readbyqxmd.com/read/29317070/hypothesis-for-the-cause-and-therapy-of-neurodegenerative-diseases
#12
Philip Serwer
The cause and therapy of neurodegenerative diseases remain unsolved puzzles. These diseases are correlated with presence of beta sheet-rich amyloid assemblies. Here, I derive and assemble puzzle pieces to obtain a loose end-tying hypothesis for cause with direct implications for therapy. I use the following extrapolations to find connectable puzzle pieces: (a) the traditional extrapolation that amyloid/amyloid precursors cause disease, (b) a recent extrapolation that amyloid-forming proteins, some of which are virus protein homologs, are components of an empirically obscure innate immune system that counters insults, including those by both viruses and bacteria, (c) a new extrapolation that various insults produce assemblies with structural features in common and that amyloid-forming, innate immune system proteins recognize these features and, then, counter insults by co-assembly, (d, 1) a second new extrapolation that beta sheet is a common structural feature and is extended during insult-neutralizing co-assembly and (d, 2) an appendix, derived from studies of phages T3 and T4, that most insult-produced assemblies are obscure to current biochemical analysis...
January 2018: Medical Hypotheses
https://www.readbyqxmd.com/read/29315575/the-appswe-ps1a246e-mutations-in-an-astrocytic-cell-line-leads-to-increased-vulnerability-to-oxygen-and-glucose-deprivation-ca2-dysregulation-and-mitochondrial-abnormalities
#13
María Dolores Martin-de-Saavedra, Elisa Navarro, Ana J Moreno-Ortega, Mauricio P Cunha, Izaskun Buendia, Pablo Hernansanz-Agustín, Rafael León, María F Cano-Abad, Antonio Martínez-Ruiz, Ricardo Martínez-Murillo, Michael R Duchen, Manuela G López
Growing evidence suggests a close relationship between Alzheimer's Disease (AD) and cerebral hypoxia. Astrocytes play a key role in brain homeostasis and disease states, while some of the earliest changes in AD occur in astrocytes. We have therefore asked whether mutations associated with AD increase astrocyte vulnerability to ischemia. Two astroglioma cell lines derived from APPSWE /PS1A246E (APP, amyloid precursor protein; PS1, presenilin 1) transgenic mice and controls from normal mice were subjected to oxygen and glucose deprivation (OGD), an in vitro model of ischemia...
January 6, 2018: Journal of Neurochemistry
https://www.readbyqxmd.com/read/29315574/palmitate-induced-c-ebp-homologous-protein-activation-leads-to-nf-%C3%AE%C2%BAb-mediated-increase-in-bace1-activity-and-amyloid-beta-genesis
#14
Gurdeep Marwarha, Jared Schommer, Jonah Lund, Trevor Schommer, Othman Ghribi
The etiology of Alzheimer's disease (AD) is egregiously comprehended, but epidemiological studies have posited that diets rich in the saturated fatty acid palmitic acid (palmitate) are a significant risk factor. The production and accumulation of Amyloid-beta peptide (Aβ) is considered the core pathological molecular event in the pathogenesis of AD. The rate limiting step in Aβ genesis from Amyloid-β precursor protein (AβPP) is catalyzed by the enzyme β-site APP cleaving enzyme 1 (BACE1), the expression and enzymatic activity of which is significantly upregulated in the AD brain...
January 6, 2018: Journal of Neurochemistry
https://www.readbyqxmd.com/read/29311640/a-specific-form-of-prefibrillar-aggregates-that-functions-as-a-precursor-of-amyloid-nucleation
#15
Naoki Yamamoto, Shoko Tsuhara, Atsuo Tamura, Eri Chatani
Non-fibrillar protein aggregates that appear in the earlier stages of amyloid fibril formation are sometimes considered to play a key role in amyloid nucleation; however, the structural features of these aggregates currently remain unclear. We herein identified a characteristic pathway of fibril formation by human insulin B chain, in which two major species of prefibrillar aggregates were identified. Based on the time-resolved tracking of this pathway with far-UV circular dichroism (CD) spectroscopy, dynamic light scattering (DLS), and 1H-NMR spectroscopy, the first prefibrillar aggregate with a hydrodynamic diameter of approximately 70 nm accumulated concomitantly with the formation of a β-sheet structure, and the size further evolved to 130 nm with an additional structural development...
January 8, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29298895/endoplasmic-reticulum-stress-responses-in-mouse-models-of-alzheimer-disease-overexpression-paradigm-versus-knock-in-paradigm
#16
Shoko Hashimoto, Ayano Ishii, Naoko Kamano, Naoto Watamura, Takashi Saito, Toshio Oshima, Makoto Yokosuka, Takaomi C Saido
Endoplasmic reticulum (ER) stress is believed to play an important role in the etiology of Alzheimer disease (AD). The accumulation of misfolded proteins and perturbation of intracellular calcium homeostasis are thought to underlie the induction of ER stress, resulting in neuronal dysfunction and cell death. Several reports have shown an increased ER stress response in amyloid precursor protein (APP) and presenilin1 (PS1) double transgenic (Tg) AD mouse models. However, it remains unclear whether the ER stress observed in these mouse models is actually caused by AD pathology...
January 3, 2018: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29288051/acceleration-of-amyloid-fibril-formation-by-carboxyl-terminal-truncation-of-human-serum-amyloid-a
#17
Masafumi Tanaka, Toru Kawakami, Nozomi Okino, Kaoru Sasaki, Kiwako Nakanishi, Hiroka Takase, Toshiyuki Yamada, Takahiro Mukai
Human serum amyloid A (SAA) is a precursor protein of AA amyloidosis. Although the full-length SAA is 104 amino acids long, the C-terminal-truncated SAA lacking mainly residues 77-104 is predominantly deposited in AA amyloidosis. Nevertheless, the amyloid fibril formation of such truncated forms of human SAA has never been investigated. In the present study, we examined the effect of C-terminal truncation on amyloid fibril formation of human SAA induced by heparan sulfate (HS). Circular dichroism (CD) measurements demonstrated that the C-terminal truncation induces a reduced α-helical structure of the SAA molecule...
December 26, 2017: Archives of Biochemistry and Biophysics
https://www.readbyqxmd.com/read/29285117/increased-expression-of-myc-interacting-zinc-finger-protein-1-in-app-ps1-mice
#18
Lu Liu, Yu-Jie Lai, Li-Ge Zhao, Guo-Jun Chen
Myc-interacting zinc-finger protein 1 (Miz1) is a member of the poxvirus and zinc-finger domain/zinc finger transcription factor family. Its transcription activation and repression functions in the nucleus are well elucidated; however its cytoplasmic inflammation function is poorly understood and may be associated with the pathogenesis of Alzheimer's disease (AD). The aim of the present study was to investigate the association between AD and Miz1 expression. In the present study, the expression and distribution of Miz1 in wild-type (WT) and amyloid precursor protein/presenelin-1 (AD) mice was studied using reverse transcription-quantitative polymerase chain reaction, western blot analysis, and immunohistochemical and immunofluorescence staining...
December 2017: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/29283428/structure-related-inhibition-of-enzyme-systems-in-cholinesterases-and-bace1-in-vitro-by-naturally-occurring-naphthopyrone-and-its-glycosides-isolated-from-cassia-obtusifolia
#19
Srijan Shrestha, Su Hui Seong, Pradeep Paudel, Hyun Ah Jung, Jae Sue Choi
Cassia obtusifolia Linn. have been used to improve vision, inflammatory diseases, and as hepatoprotective agents and to promote urination from ancient times. In the present study, we investigated the influence of glycosylation of components of C. obtusifolia and structure-activity relationships (SARs) with respect to the inhibition of acetylcholinesterase (AChE), butyrylcholinesterase (BChE), and β-site amyloid precursor protein (APP)-cleaving enzyme 1 (BACE1), which are related to Alzheimer's disease (AD)...
December 28, 2017: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
https://www.readbyqxmd.com/read/29283047/is-it-all-said-for-nsaids-in-alzheimer-s-disease-role-of-mitochondrial-calcium-uptake
#20
Sara Sanz-Blasco, Maria Calvo-Rodríguez, Erica Caballero, Monica Garcia-Durillo, Lucía Nunez, Carlos Villalobos
Epidemiological data suggest that non-steroidal anti-inflammatory drugs (NSAIDs) may protect against Alzheimer's disease (AD). Unfortunately, recent trials have failed in providing compelling evidence of neuroprotection. Discussion as to why NSAIDs effectivity is uncertain is ongoing. Possible explanations include the view that NSAIDs and other possible disease-modifying drugs should be provided before the patients develop symptoms of AD or cognitive decline. In addition, NSAID targets for neuroprotection are unclear...
December 27, 2017: Current Alzheimer Research
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