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https://www.readbyqxmd.com/read/28801274/mannich-base-approach-to-5-methoxyisatin-3-4-isopropylphenyl-hydrazone-a-water-soluble-prodrug-for-a-multitarget-inhibition-of-cholinesterases-beta-amyloid-fibrillization-and-oligomer-induced-cytotoxicity
#1
Leonardo Pisani, Annalisa De Palma, Nicola Giangregorio, Daniela V Miniero, Paolo Pesce, Orazio Nicolotti, Francesco Campagna, Cosimo D Altomare, Marco Catto
Targeting protein aggregation for the therapy of neurodegenerative diseases remains elusive for medicinal chemists, despite a number of small molecules known to interfere in amyloidogenesis, particularly of amyloid beta (Aβ) protein. Starting from previous findings in the antiaggregating activity of a class of indolin-2-ones inhibiting Aβ fibrillization, 5-methoxyisatin 3-(4-isopropylphenyl)hydrazone 1 was identified as a multitarget inhibitor of Aβ aggregation and cholinesterases with IC50s in the low μM range...
August 8, 2017: European Journal of Pharmaceutical Sciences
https://www.readbyqxmd.com/read/28800454/tau-protein-aggregation-in-alzheimer-s-disease-an-attractive-target-for-the-development-of-novel-therapeutic-agents
#2
Marie Jouanne, Sylvain Rault, Anne-Sophie Voisin-Chiret
Alzheimer's Disease (AD) is a neurodegenerative brain disorder in which many biological dysfunctions are involved. Among them, two main types of lesions were discovered and widely studied: the amyloid plaques and the neurofibrillary tangles (NFTs). These two lesions are caused by the dysfunction and the accumulation of two proteins which are, respectively, the beta-amyloid peptide and the tau protein. The process that leads these two proteins to aggregate is complex and is the subject of current studies. After a brief description of the aggregation mechanisms, we will provide an overview of new therapeutic agents targeting the different dysfunctions and toxic species found during aggregation...
July 29, 2017: European Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/28799502/mitochondrial-dynamics-and-proteins-related-to-neurodegenerative-diseases
#3
Athanasios Alexiou, Bilal Nizami, Faez Iqbal Khan, Georgia Soursou, Charalampos Vairaktarakis, Stylianos Chatzichronis, Vasilis Tsiamis, Vasileios Manztavinos, Nagendra Sastry Yarla, Ghulam Md Ashraf
Disruptions in the regulation of mitochondrial dynamics and the occurrence of proteins misfolding lead to neuronal death, resulting in Age-related Dementia and Neurodegenerative diseases as well as Frailty. Functional, neurophysiologic and biochemical alterations within the mitochondrial populations can reveal deficits in brain energy metabolism resulting in Mild Cognitive Impairment, abnormal neural development, autonomic dysfunction and other mitochondrial disorders. Additionally, in cases of Alzheimer's disease or Parkinson's disease, a significant number of proteins seems to form unordered and problematic structures, leading through unknown mechanisms to pathological conditions...
August 10, 2017: Current Protein & Peptide Science
https://www.readbyqxmd.com/read/28799137/ethanol-alters-app-processing-and-aggravates-alzheimer-associated-phenotypes
#4
Daochao Huang, Mengjiao Yu, Shou Yang, Dandan Lou, Weitao Zhou, Lingling Zheng, Zhe Wang, Fang Cai, Weihui Zhou, Tingyu Li, Weihong Song
The majority of Alzheimer's disease (AD) cases are sporadic with unknown causes. Many dietary factors including excessive alcohol intake have been reported to increase the risk to develop AD. The effect of alcohol on cognitive functions and AD pathogenesis remains elusive. In this study, we investigated the relationship between ethanol exposure and Alzheimer's disease. Cell cultures were treated with ethanol at different dosages for different durations up to 48 h and an AD model mouse was fed with ethanol for 4 weeks...
August 10, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28798235/atomic-resolution-map-of-the-interactions-between-an-amyloid-inhibitor-protein-and-amyloid-beta-a%C3%AE-peptides-in-the-monomer-and-protofibril-states
#5
Moustafa Algamal, Rashik Ahmed, Naeimeh Jafari, Bilal Ahsan, Joaquin Ortega, Giuseppe Melacini
Self-association of amyloid beta (Aβ) peptides is a hallmark of Alzheimer's disease and serves as a general prototype for amyloid formation. A key endogenous inhibitor of Aβ self-association is Human Serum Albumin (HSA), which binds ~90% of plasma Aβ. However, the exact molecular mechanism by which HSA binds Aβ monomers and protofibrils is not fully understood. Here, using dark-state exchange saturation transfer (DEST) NMR and relaxation experiments, complemented by morphological characterization, we mapped the HSA-Aβ interactions at atomic resolution by examining HSA's effects on Aβ monomers and soluble high-molecular weight oligomeric protofibrils...
August 10, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28797721/intact-blood-brain-barrier-transport-of-small-molecular-drugs-in-animal-models-of-amyloid-beta-and-alpha-synuclein-pathology
#6
Sofia Gustafsson, Veronica Lindström, Martin Ingelsson, Margareta Hammarlund-Udenaes, Stina Syvänen
Pathophysiological impairment of the neurovascular unit, including the integrity and dynamics of the blood-brain barrier (BBB), has been denoted both a cause and consequence of neurodegenerative diseases. Pathological impact on BBB drug delivery has also been debated. The aim of the present study was to investigate BBB drug transport, by determining the unbound brain-to-plasma concentration ratio (Kp,uu,brain), in aged AβPP-transgenic mice, α-synuclein transgenic mice, and wild type mice. Mice were dosed with a cassette of five compounds, including digoxin, levofloxacin (1 mg/kg, s...
August 5, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/28796060/candidate-genes-investigation-for-severe-nonalcoholic-fatty-liver-disease-based-on-bioinformatics-analysis
#7
Shan Qi, Changhong Wang, Chunfu Li, Pu Wang, Minghui Liu
BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver condition worldwide. However, its etiology and fundamental pathophysiology for the disease process are poorly understood. In this study, we thus used bioinformatics to identify candidate genes potentially causative of severe NAFLD. METHODS: Gene expression profile data GSE49541 were downloaded from the Gene Expression Omnibus database. Tissues samples from 32 severe and 40 mild NAFLD patients were evaluated to identify differentially expressed genes (DEGs) between the 2 groups, followed by analyses of Gene Ontology (GO) functions and Kyoto Encyclopedia of Genes and Genomes pathways...
August 2017: Medicine (Baltimore)
https://www.readbyqxmd.com/read/28794261/neuroprotective-astrocyte-derived-insulin-igf-1-stimulate-endocytic-processing-and-extracellular-release-of-neuron-bound-a%C3%AE-oligomers
#8
Jason Pitt, Kyle C Wilcox, Vanessa Tortelli, Luan Pereira Diniz, Maira S Oliveira, Cassandra Dobbins, Xiao-Wen Yu, Sathwik Nandamuri, Flávia C A Gomes, Nadia DiNunno, Kirsten L Viola, Fernanda G De Felice, Sergio T Ferreira, William L Klein
Synaptopathy underlying memory deficits in Alzheimer's disease (AD) is increasingly thought to be instigated by toxic oligomers of the amyloid beta peptide (AβOs). Given the long latency and incomplete penetrance of AD dementia with respect to Aβ pathology, we hypothesized that factors present in the CNS may physiologically protect neurons from the deleterious impact of AβOs. Here we employed physically-separated neuron-astrocyte co-cultures to investigate potential non cell-autonomous neuroprotective factors influencing AβO toxicity...
August 9, 2017: Molecular Biology of the Cell
https://www.readbyqxmd.com/read/28790911/plasma-levels-of-a%C3%AE-42-and-tau-identified-probable-alzheimer-s-dementia-findings-in-two-cohorts
#9
Lih-Fen Lue, Marwan N Sabbagh, Ming-Jang Chiu, Naomi Jing, Noelle L Snyder, Christopher Schmitz, Andre Guerra, Christine M Belden, Ta-Fu Chen, Che-Chuan Yang, Shieh-Yueh Yang, Douglas G Walker, Kewei Chen, Eric M Reiman
The utility of plasma amyloid beta (Aβ) and tau levels for the clinical diagnosis of Alzheimer's disease (AD) dementia has been controversial. The main objective of this study was to compare Aβ42 and tau levels measured by the ultra-sensitive immunomagnetic reduction (IMR) assays in plasma samples collected at the Banner Sun Health Institute (BSHRI) (United States) with those from the National Taiwan University Hospital (NTUH) (Taiwan). Significant increase in tau levels were detected in AD subjects from both cohorts, while Aβ42 levels were increased only in the NTUH cohort...
2017: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/28790893/brain-and-peripheral-atypical-inflammatory-mediators-potentiate-neuroinflammation-and-neurodegeneration
#10
REVIEW
Duraisamy Kempuraj, Ramasamy Thangavel, Govindhasamy P Selvakumar, Smita Zaheer, Mohammad E Ahmed, Sudhanshu P Raikwar, Haris Zahoor, Daniyal Saeed, Prashant A Natteru, Shankar Iyer, Asgar Zaheer
Neuroinflammatory response is primarily a protective mechanism in the brain. However, excessive and chronic inflammatory responses can lead to deleterious effects involving immune cells, brain cells and signaling molecules. Neuroinflammation induces and accelerates pathogenesis of Parkinson's disease (PD), Alzheimer's disease (AD) and Multiple sclerosis (MS). Neuroinflammatory pathways are indicated as novel therapeutic targets for these diseases. Mast cells are immune cells of hematopoietic origin that regulate inflammation and upon activation release many proinflammatory mediators in systemic and central nervous system (CNS) inflammatory conditions...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28790139/islet-amyloid-deposits-preferentially-in-the-highly-functional-and-most-blood-perfused-islets
#11
Sara Ullsten, Sara Bohman, Marie E Oskarsson, K Peter R Nilsson, Gunilla Westermark, Per-Ola Carlsson
Islet amyloid and beta cell death in type 2 diabetes are heterogeneous events, where some islets are affected early in the disease process whereas others remain visibly unaffected. This study investigated the possibility that inter-islet functional and vascular differences may explain the propensity for amyloid accumulation in certain islets. Highly blood perfused islets were identified by microspheres in human islet amyloid polypeptide expressing mice fed a high-fat diet for three or 10 months. These highly blood perfused islets had better glucose-stimulated insulin secretion capacity than other islets, and developed more amyloid deposits after 10 months of high-fat diet...
August 8, 2017: Endocrine Connections
https://www.readbyqxmd.com/read/28789837/investigating-the-amyloid-beta-enhancing-effect-of-cgmp-in-neuro2a-cells
#12
Elisa Calcagno, Francesca Caudano, Mario Passalacqua, Maria A Pronzato, Ernesto Fedele, Roberta Ricciarelli
Long-term potentiation (LTP) and the process of memory formation require activation of cyclic guanosine monophosphate (cGMP) and cyclic adenosine monophosphate (cAMP) pathways. Notably, recent evidence indicated that both cyclic nucleotides boost the production of amyloid-beta (Aβ) peptides. In particular, cAMP was shown to favor hippocampal LTP by stimulating the synthesis of the amyloid precursor protein APP, whereas cGMP was found to enhance LTP and to improve memory by increasing Aβ levels without affecting the expression of APP...
August 5, 2017: Mechanisms of Ageing and Development
https://www.readbyqxmd.com/read/28782486/nf-kb-as-a-mediator-of-brain-inflammation-in-ad
#13
Jin Tae Hong
Alzheimer's disease is the most common form of dementia. It is characterized by beta-amyloid peptide fibrils which are extracellular deposition of a specific protein, and is accompanied by extensive neuroinflammation. Various studies show the presence of a number of inflammation markers in the AD brain: elevated inflammatory cytokines and chemokines, and an accumulation of activated microglia in the damaged regions. NF-kB is a redox of transcriptional factors, and it is known to be located in the genes involved in amyloidogenesis and inflammation...
August 7, 2017: CNS & Neurological Disorders Drug Targets
https://www.readbyqxmd.com/read/28782443/cerebral-a%C3%AE-40-and-systemic-hypertension
#14
Hannah M Tayler, Jennifer C Palmer, Taya L Thomas, Patrick G Kehoe, Julian Fr Paton, Seth Love
Mid-life hypertension and cerebral hypoperfusion may be preclinical abnormalities in people who later develop Alzheimer's disease. Although accumulation of amyloid-beta (Aβ) is characteristic of Alzheimer's disease and is associated with upregulation of the vasoconstrictor peptide endothelin-1 within the brain, it is unclear how this affects systemic arterial pressure. We have investigated whether infusion of Aβ40 into ventricular cerebrospinal fluid modulates blood pressure in the Dahl salt-sensitive rat...
January 1, 2017: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/28780367/differential-effects-of-blood-insulin-and-hba1c-on-cerebral-amyloid-burden-and-neurodegeneration-in-nondiabetic-cognitively-normal-older-adults
#15
Min Soo Byun, Hyun Jung Kim, Dahyun Yi, Hyo Jung Choi, Hyewon Baek, Jun Ho Lee, Young Min Choe, Bo Kyung Sohn, Jun-Young Lee, Younghwa Lee, Hyunwoong Ko, Yu Kyeong Kim, Yun-Sang Lee, Chul-Ho Sohn, Jong Inn Woo, Dong Young Lee
We tested the hypothesis that lower insulin or higher glycated hemoglobin (HbA1c) levels in blood are associated with increased cerebral beta amyloid (Aβ) deposition and neurodegeneration in nondiabetic cognitively normal (CN) older adults. A total of 205 nondiabetic CN older adults underwent comprehensive clinical assessment, [(11)C]Pittsburgh compound B (PiB)-positron emission tomography (PET), [(18)F]fluorodeoxyglucose-PET, magnetic resonance imaging, and blood sampling for fasting insulin and HbA1c measurement...
July 20, 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/28774322/tau-accumulation-in-the-retina-promotes-early-neuronal-dysfunction-and-precedes-brain-pathology-in-a-mouse-model-of-alzheimer-s-disease
#16
Marius Chiasseu, Luis Alarcon-Martinez, Nicolas Belforte, Heberto Quintero, Florence Dotigny, Laurie Destroismaisons, Christine Vande Velde, Fany Panayi, Caroline Louis, Adriana Di Polo
BACKGROUND: Tau is an axon-enriched protein that binds to and stabilizes microtubules, and hence plays a crucial role in neuronal function. In Alzheimer's disease (AD), pathological tau accumulation correlates with cognitive decline. Substantial visual deficits are found in individuals affected by AD including a preferential loss of retinal ganglion cells (RGCs), the neurons that convey visual information from the retina to the brain. At present, however, the mechanisms that underlie vision changes in these patients are poorly understood...
August 3, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28771976/hdac3-negatively-regulates-spatial-memory-in-a-mouse-model-of-alzheimer-s-disease
#17
Xiaolei Zhu, Sulei Wang, Linjie Yu, Jiali Jin, Xing Ye, Yi Liu, Yun Xu
The accumulation and deposition of beta-amyloid (Aβ) is a key neuropathological hallmark of Alzheimer's disease (AD). Histone deacetylases (HDACs) are promising therapeutic targets for the treatment of AD, while the specific HDAC isoforms associated with cognitive improvement are poorly understood. In this study, we investigate the role of HDAC3 in the pathogenesis of AD. Nuclear HDAC3 is significantly increased in the hippocampus of 6- and 9-month-old APPswe/PS1dE9 (APP/PS1) mice compared with that in age-matched wild-type C57BL/6 (B6) mice...
August 3, 2017: Aging Cell
https://www.readbyqxmd.com/read/28771542/a-multivariate-predictive-modeling-approach-reveals-a-novel-csf-peptide-signature-for-both-alzheimer-s-disease-state-classification-and-for-predicting-future-disease-progression
#18
Daniel A Llano, Saurabh Bundela, Raksha A Mudar, Viswanath Devanarayan
To determine if a multi-analyte cerebrospinal fluid (CSF) peptide signature can be used to differentiate Alzheimer's Disease (AD) and normal aged controls (NL), and to determine if this signature can also predict progression from mild cognitive impairment (MCI) to AD, analysis of CSF samples was done on the Alzheimer's Disease Neuroimaging Initiative (ADNI) dataset. The profiles of 320 peptides from baseline CSF samples of 287 subjects over a 3-6 year period were analyzed. As expected, the peptide most able to differentiate between AD vs...
2017: PloS One
https://www.readbyqxmd.com/read/28769761/identification-of-the-role-of-mir-142-5p-in-alzheimer-s-disease-by-comparative-bioinformatics-and-cellular-analysis
#19
Juhyun Song, Young-Kook Kim
Alzheimer's disease (AD) is the most common neurodegenerative disease characterized by the formation of amyloid beta (Aβ) or tau protein aggregates, the hallmark of cognitive decline. MicroRNAs (miRNAs) have emerged as critical factors in neurogenesis and synaptic functions in the central nervous system (CNS). Recent studies have reported alterations in miRNA expression in patients with AD. However, miRNAs associated with AD varied with patient groups or experimental models, suggesting the need for a comparative study to identify miRNAs commonly dysregulated in diverse AD models...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28768772/a-computational-combinatorial-approach-identifies-a-protein-inhibitor-of-superoxide-dismutase-1-misfolding-aggregation-and-cytotoxicity
#20
Victor Banerjee, Ofek Oren, Efrat Ben-Zeev, Ran Taube, Stanislav Engel, Niv Papo
Molecular agents that specifically bind and neutralize misfolded and toxic superoxide dismutase 1 (SOD1) mutant proteins may find application in attenuating the disease progression of familial amyotrophic lateral sclerosis (fALS). However, high structural similarities between the wild-type and mutant SOD1 proteins limit the utility of this approach. Here, we addressed this challenge by converting a promiscuous natural human IgG binding domain, the hyperthermophilic variant of protein G (HTB1), into a highly specific aggregation inhibitor (designated HTB1M) of two fALS-linked SOD1 mutants, SOD1G93A and SOD1G85R...
August 2, 2017: Journal of Biological Chemistry
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