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Kyriaki Hatziagapiou, Eleni Kakouri, George I Lambrou, Kostas Bethanis, Petros A Tarantilis
BACKGROUND: Reactive oxygen species and reactive nitrogen species, which are collectively called reactive oxygen nitrogen species, are inevitable by-products of cellular metabolic redox reactions, such as oxidative phosphorylation in the mitochondrial respiratory chain, phagocytosis, reactions of biotransformation of exogenous and endogenous substrata in endoplasmic reticulum, eicosanoid synthesis, and redox reactions in the presence of metal with variable valence. Among medicinal plants there is growing interest in Crocus Sativus L...
March 20, 2018: Current Neuropharmacology
Fikret Türkan, Zübeyir Huyut, Yeliz Demir, Fatma Ertaş, Şükrü Beydemir
BACKGROUND: Glutathione S-transferase (GST) and acetylcholinesterase (AChE) are important enzymes in the metabolism. GSTs are primarily available in phase II metabolism. AChE is vital for neurodegenerative disorders. SUBJECTS AND METHODS: The in vitro and in vivo effects of cefoperazone sodium (CFP), cefuroxime (CXM), and cefazolin (CZO) were investigated on GST and AChE activity in the present study. GST was purified using Glutathione-Agarose affinity chromatography...
March 22, 2018: Archives of Physiology and Biochemistry
Yongping Chen, Bei Cao, Ruwei Ou, Qianqian Wei, Xueping Chen, Bi Zhao, Ying Wu, Wei Song, Hui-Fang Shang
Large-scale meta-analyses of genome-wide association studies have identified several loci linked to sporadic Parkinson's disease (PD). However, the roles of some important loci, such as HNMT Thr105Ile, STK39 rs2390669, and NMD3 rs34016896, have not been clarified in Chinese populations. Accumulating evidence indicates that some common clinicopathological characteristics are shared by different neurodegenerative diseases. Consequently, we conducted a large sample study to investigate associations between these variants and PD, multiple system atrophy (MSA), and amyotrophic lateral sclerosis (ALS) in Chinese populations...
March 21, 2018: Journal of Molecular Neuroscience: MN
Paola Origone, Fabio Gotta, Merit Lamp, Lucia Trevisan, Alessandro Geroldi, Davide Massucco, Matteo Grazzini, Federico Massa, Flavia Ticconi, Matteo Bauckneht, Roberta Marchese, Giovanni Abbruzzese, Emilia Bellone, Paola Mandich
Background: Spinocerebellar ataxia 17 (SCA17) is one of the most heterogeneous forms of autosomal dominant cerebellar ataxias with a large clinical spectrum which can mimic other movement disorders such as Huntington disease (HD), dystonia and parkinsonism. SCA17 is caused by an expansion of CAG/CAA repeat in the Tata binding protein ( TBP ) gene. Normal alleles contain 25 to 40 CAG/CAA repeats, alleles with 50 or greater CAG/CAA repeats are pathological with full penetrance. Alleles with 43 to 49 CAG/CAA repeats were also reported and their penetrance is estimated between 50 and 80%...
2018: Cerebellum & Ataxias
Lianne Hoeijmakers, Anna Amelianchik, Fleur Verhaag, Janssen Kotah, Paul J Lucassen, A Korosi
Life-time experiences are thought to influence the risk to develop the neurodegenerative disorder Alzheimer's disease (AD). In particular, early-life stress (ES) may modulate the onset and progression of AD. There is recent evidence by our group and others that AD-related neuropathological progression and the associated neuroimmune responses are modulated by ES in the classic APPswe/PS1dE9 mouse model for AD. We here extend our previous study on ES mediated modulation of neuropathology and neuroinflammation and address in the same cohort of mice whether ES accelerates and/or aggravates AD-induced cognitive decline and alterations in the process of adult hippocampal neurogenesis (AHN), a form of brain plasticity...
2018: Frontiers in Aging Neuroscience
Ryuta Kikuchi, Kimiharu Ambe, Hideki Kon, Satoshi Takada, Hiroki Watanabe
Localization of the nitric oxide (NO)-producing enzyme, nitric oxide synthase (NOS), and its functions are currently being investigated in several tissues and organs. It has been suggested that NO is involved in nerve cell death and the development of neurodegenerative disease. The purpose of this study was to immunohistochemically investigate expression of NOS to clarify its function in the degeneration and regeneration of transected mouse sciatic nerve. Scattered neuronal NOS (nNOS)-positive Schwann cells observed on the central side of the stump on day 1 after transection showed an increase in number on day 7...
2018: Bulletin of Tokyo Dental College
Meredith M Course, Anna I Scott, Carmen Schoor, Chung-Han Hsieh, Amanda M Papakyrikos, Dominic Winter, Tina M Cowan, Xinnan Wang
PINK1 is a mitochondria-targeted kinase, whose mutations are a cause of Parkinson's disease. We set out to better understand PINK1's effects on mitochondrial proteins in vivo Using an unbiased phosphoproteomic screen in Drosophila , we found that PINK1 mediates the phosphorylation of MCAD, a mitochondrial matrix protein critical to fatty acid metabolism. By mimicking phosphorylation of this protein in a PINK1 null background, we restored PINK1 null's climbing, flight, thorax, and wing deficiencies. Due to MCAD's role in fatty acid metabolism, we examined the metabolic profile of PINK1 null flies, where we uncovered significant disruptions in both acylcarnitines and amino acids...
March 21, 2018: Molecular Biology of the Cell
Lawrence Rajendran, Rosa C Paolicelli
Microglia are emerging as key players in neurodegenerative diseases, such as Alzheimer's disease (AD). Thus far, microglia have rather been known as modulator of neurodegeneration with functions limited to neuroinflammation and release of neurotoxic molecules. However, several recent studies have demonstrated a direct role of microglia in "neuro" degeneration observed in AD by promoting phagocytosis of neuronal, in particular, synaptic structures. While some of the studies address the involvement of the β-amyloid peptides in the process, studies also indicate that this could occur independent of amyloid, further elevating the importance of microglia in AD...
March 21, 2018: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
William M Vanderheyden, Miranda M Lim, Erik S Musiek, Jason R Gerstner
Sleep-wake abnormalities are common in patients with Alzheimer's disease, and can be a major reason for institutionalization. However, an emerging concept is that these sleep-wake disturbances are part of the causal pathway accelerating the neurodegenerative process. Recently, new findings have provided intriguing evidence for a positive feedback loop between sleep-wake dysfunction and β-amyloid (Aβ) aggregation. Studies in both humans and animal models have shown that extended periods of wakefulness increase Aβ levels and aggregation, and accumulation of Aβ causes fragmentation of sleep...
March 21, 2018: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Sayaka Kazami, Shingo Nishiyama, Yuji Kimura, Hiroyasu Itoh, Hideo Tsukada
BCPP compounds have been developed as PET imaging probes for neurodegenerative diseases in the living brain.18 F-BCPP-EF identifies damaged neuronal areas based on the lack of MC-I; however, its underlying mechanisms of action and specificity for MC-I remain unclear. We herein report the effects of BCPP-BF, -EF, -EM on MC-I in respiratory chain complexes using cardiomyocyte SMP. BCPP compounds inhibited the binding of3 H-dihydrorotenone to MC-I and the proton pumping activity of MC-I in a concentration-dependent manner in vitro...
March 18, 2018: Mitochondrion
Lesley Hoyles, Tom Snelling, Umm-Kulthum Umlai, Jeremy K Nicholson, Simon R Carding, Robert C Glen, Simon McArthur
BACKGROUND: Gut microbiota composition and function are symbiotically linked with host health and altered in metabolic, inflammatory and neurodegenerative disorders. Three recognised mechanisms exist by which the microbiome influences the gut-brain axis: modification of autonomic/sensorimotor connections, immune activation, and neuroendocrine pathway regulation. We hypothesised interactions between circulating gut-derived microbial metabolites, and the blood-brain barrier (BBB) also contribute to the gut-brain axis...
March 21, 2018: Microbiome
Ewa Kruminis-Kaszkiel, Judyta Juranek, Wojciech Maksymowicz, Joanna Wojtkiewicz
The clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein-9 nuclease (Cas9) is a genome editing tool that has recently caught enormous attention due to its novelty, feasibility, and affordability. This system naturally functions as a defense mechanism in bacteria and has been repurposed as an RNA-guided DNA editing tool. Unlike zinc-finger nucleases (ZFNs) and transcription activator-like effector nucleases (TALENs), CRISPR/Cas9 takes advantage of an RNA-guided DNA endonuclease enzyme, Cas9, which is able to generate double-strand breaks (DSBs) at specific genomic locations...
March 19, 2018: International Journal of Molecular Sciences
Oksana V Salomatina, Irina I Popadyuk, Alexandra L Zakharenko, Olga D Zakharova, Dmitriy S Fadeev, Nina I Komarova, Jóhannes Reynisson, H John Arabshahi, Raina Chand, Konstantin P Volcho, Nariman F Salakhutdinov, Olga I Lavrik
An Important task in the treatment of oncological and neurodegenerative diseases is the search for new inhibitors of DNA repair system enzymes. Tyrosyl-DNA phosphodiesterase 1 (Tdp1) is one of the DNA repair system enzymes involved in the removal of DNA damages caused by topoisomerase I inhibitors. Thus, reducing the activity of Tdp1 can increase the effectiveness of currently used anticancer drugs. We describe here a new class of semisynthetic small molecule Tdp1 inhibitors based on the bile acid scaffold that were originally identified by virtual screening...
March 17, 2018: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
Ying Yang, Jian-Zhi Wang
Neurodegeneration is defined as the progressive loss of structure or function of the neurons. As the nature of degenerative cell loss is currently not clear, there is no specific molecular marker to measure neurodegeneration. Therefore, researchers have been using apoptotic markers to measure neurodegeneration. However, neurodegeneration is completely different from apoptosis by morphology and time course. Lacking specific molecular marker has been the major hindrance in research of neurodegenerative disorders...
2018: Journal of Alzheimer's Disease: JAD
Maria Bjerke, Sebastiaan Engelborghs
An accurate and early diagnosis of Alzheimer's disease (AD) is important to select optimal patient care and is critical in current clinical trials targeting core AD neuropathological features. The past decades, much progress has been made in the development and validation of cerebrospinal fluid (CSF) biomarkers for the biochemical diagnosis of AD, including standardization and harmonization of (pre-) analytical procedures. This has resulted in three core CSF biomarkers for AD diagnostics, namely the 42 amino acid long amyloid-beta peptide (Aβ1-42), total tau protein (T-tau), and tau phosphorylated at threonine 181 (P-tau181)...
2018: Journal of Alzheimer's Disease: JAD
Paul A Adlard, Ashley I Bush
It is estimated that by the year 2050 there will be more than 1.5 billion people globally over the age of 65 years. Aging is associated with changes to a number of different cellular processes which are driven by a variety of factors that contribute to the characteristic decline in function that is seen across multiple physiological domains/tissues in the elderly (including the brain). Importantly, aging is also the primary risk factor for the development of neurodegenerative disorders such as Alzheimer's disease...
2018: Journal of Alzheimer's Disease: JAD
Tingxiang Yan, Luwen Wang, Ju Gao, Sandra L Siedlak, Mikayla L Huntley, Pichet Termsarasab, George Perry, Shu G Chen, Xinglong Wang
Alzheimer's disease (AD) is the leading cause of dementia in the elderly, characterized by neurofibrillary tangles (NFTs), senile plaques (SPs), and a progressive loss of neuronal cells in selective brain regions. Rab10, a small Rab GTPase involved in vesicular trafficking, has recently been identified as a novel protein associated with AD. Interestingly, Rab10 is a key substrate of leucine-rich repeat kinase 2 (LRRK2), a serine/threonine protein kinase genetically associated with the second most common neurodegenerative disease Parkinson's disease...
March 16, 2018: Journal of Alzheimer's Disease: JAD
Harald Hampel, Nicola Toschi, Claudio Babiloni, Filippo Baldacci, Keith L Black, Arun L W Bokde, René S Bun, Francesco Cacciola, Enrica Cavedo, Patrizia A Chiesa, Olivier Colliot, Cristina-Maria Coman, Bruno Dubois, Andrea Duggento, Stanley Durrleman, Maria-Teresa Ferretti, Nathalie George, Remy Genthon, Marie-Odile Habert, Karl Herholz, Yosef Koronyo, Maya Koronyo-Hamaoui, Foudil Lamari, Todd Langevin, Stéphane Lehéricy, Jean Lorenceau, Christian Neri, Robert Nisticò, Francis Nyasse-Messene, Craig Ritchie, Simone Rossi, Emiliano Santarnecchi, Olaf Sporns, Steven R Verdooner, Andrea Vergallo, Nicolas Villain, Erfan Younesi, Francesco Garaci, Simone Lista
The Precision Neurology development process implements systems theory with system biology and neurophysiology in a parallel, bidirectional research path: a combined hypothesis-driven investigation of systems dysfunction within distinct molecular, cellular, and large-scale neural network systems in both animal models as well as through tests for the usefulness of these candidate dynamic systems biomarkers in different diseases and subgroups at different stages of pathophysiological progression. This translational research path is paralleled by an "omics"-based, hypothesis-free, exploratory research pathway, which will collect multimodal data from progressing asymptomatic, preclinical, and clinical neurodegenerative disease (ND) populations, within the wide continuous biological and clinical spectrum of ND, applying high-throughput and high-content technologies combined with powerful computational and statistical modeling tools, aimed at identifying novel dysfunctional systems and predictive marker signatures associated with ND...
March 16, 2018: Journal of Alzheimer's Disease: JAD
Antonia Gutierrez, Javier Vitorica
The continuing failure to develop an effective treatment for Alzheimer's disease urges a better understanding of the pathogenic mechanisms and the improvement of current animal models to facilitate success for clinical interventions. The transgenic models have been so far designed to recapitulate one, or both, protein lesions found in the brain of patients, the extracellular amyloid plaques and the intraneuronal neurofibrillary tangles. However, in recent years, a third pathogenic component is gaining strength in the onset and progression of this disease, the neuroinflammatory response mediated primarily by the brain's resident immune cells, microglia...
March 16, 2018: Journal of Alzheimer's Disease: JAD
Lucilla Parnetti, Paolo Eusebi
Alzheimer's disease (AD) is the most common neurodegenerative disorder, affecting around 35 million people worldwide. Cerebrospinal fluid (CSF) biomarkers entered the diagnostic criteria as support for early diagnosis. The classical biochemical signature of AD includes total tau (T-tau), phosphorylated tau (P-tau), and the 42 amino acid peptide (Aβ42) of amyloid-β. Recent observations suggest that the use of CSF Aβ42:Aβ40 ratio rather than CSF Aβ42 alone could contribute to reduce inter-laboratory variation in Aβ values and increasing diagnostic performance of the CSF AD biomarkers in routine practice...
March 16, 2018: Journal of Alzheimer's Disease: JAD
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