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Ana M Catafau, Santiago Bullich
Clinical classifications of neurodegenerative disorders are often based on neuropathology. The term "proteinopathies" includes disorders that have in common abnormal proteins as a hallmark, e.g. amyloidoses, tauopathies, synucleopathies, ubiquitinopathies. Different proteins can also co-exist in the same disease. To further complicate the pathophysiology scenario, not only different proteins, but also cells are believed to play an active role in neurodegeneration, in particular those participating in neuroinflammatory processes in the brain, such as activated microglia and astrocytes...
June 20, 2016: Current Alzheimer Research
Giacomo Casella, Livia Garzetti, Alberto T Gatta, Annamaria Finardi, Chiara Maiorino, Francesca Ruffini, Gianvito Martino, Luca Muzio, Roberto Furlan
BACKGROUND: Myeloid cells, such as macrophages and microglia, play a crucial role in neuroinflammation and have been recently identified as a novel therapeutic target, especially for chronic forms. The general aim would be to change the phenotype of myeloid cells from pro- to anti-inflammatory, favoring their tissue-trophic and regenerative functions. Myeloid cells, however, display a number of functional phenotypes, not immediately identifiable as pro- or anti-inflammatory, and associated to ambiguous markers...
2016: Journal of Neuroinflammation
Heather L McConnell, Daniel L Schwartz, Brian E Richardson, Randall L Woltjer, Leslie L Muldoon, Edward A Neuwelt
Ferumoxytol ultrasmall superparamagnetic iron oxide nanoparticles can enhance contrast between neuroinflamed and normal-appearing brain tissue when used as a contrast agent for high-sensitivity magnetic resonance imaging (MRI). Here we used an anti-dextran antibody (Dx1) that binds the nanoparticle's carboxymethyldextran coating to differentiate ferumoxytol from endogenous iron and localize it unequivocally in brain tissue. Intravenous injection of ferumoxytol into immune-competent rats that harbored human tumor xenograft-induced inflammatory brain lesions resulted in heterogeneous and lesion-specific signal enhancement on MRI scans in vivo...
August 2016: Nanomedicine: Nanotechnology, Biology, and Medicine
Maria Jose Perez-Alvarez, Francisco Wandosell
Inflammatory response in the nervous system, called neuroinflammation, is a common process of several neurodegenerative diseases and brain disorders. To understand the underlying mechanism of this brain response to damage would be interesting to identify new common therapy targets to neurodegenerative processes. Ischemic stroke has an important socioeconomic impact being the second cause of mortality and the first cause of long-term disability in the world. Until now, there is not any pharmacological treatment to reduce the brain damage induced...
2016: Current Pharmaceutical Design
Burak Yulug, Lütfü Hanoglu, Ahmet M Tavli, Nesrin H Yılmaz, Ertugrul Kılıc
There are rapidly replicating human data suggesting the therapeutic and neurorestorative role of repetitive transcranial magnetic stimulation (rTMS) in clinical depression. However there are only limited experimental studies in the literature and the neurobiological mechanisms of the technique are still unclear. Studies have suggested that modulating of either excitatory or inhibitory neural circuitry may be responsible for the mechanism of action of rTMS while it is still unclear whether rTMS exerts a neuroprotective effect...
2016: Medicinal Chemistry
R Navanietha Krishnaraj, S S Sreeja Kumari, Sudit Sekhar Mukhopadhyay
Alzheimer's disease (AD) and amyotrophic lateral sclerosis (ALS) are progressive neurodegenerative diseases that affect the neurons in the brain and the spinal cord. Neuroinflamation and apoptosis are key players in the progressive damage of the neurons in AD and ALS. Currently, there is no drug to offer complete cure for both these diseases. Riluzole is the only available drug that can prolong the life time of the ALS patients for nearly 3 months. Molecules that offer good HIT to the molecular targets of ALS will help to treat AD and ALS patients...
2016: Journal of Receptor and Signal Transduction Research
Miroslav Adzic, Jelena Djordjevic, Milos Mitic, Zeljka Brkic, Iva Lukic, Marija Radojcic
Peripheral inflammation induced by lipopolysaccharide (LPS) causes behavioural changes indicative for depression. The possible mechanisms involve the interference with neuroinflammatory, neuroendocrine, and neurotrophic processes. Apart from heterogeneity in the molecular background, sexual context may be another factor relevant to the manifestation of mood disturbances upon an immune challenge. We investigated sex-dependent effects of a 7-day LPS treatment of adult Wistar rats on depressive-like behaviour and their relation with hypothalamic neuroendocrine factor, corticotrophin-releasing hormone (CRH), proplastic brain-derived neurotropic factor (BDNF), pro-inflammatory cyclooxygenase-2 (COX-2) and nuclear factor kappa beta (NFkB)...
September 15, 2015: Behavioural Brain Research
Ibukun Dorcas Akinrinade, Adejoke Elizabeth Memudu, Olalekan Michael Ogundele, Olanrewaju Ibrahim Ajetunmobi
BACKGROUND: Oxidative stress formation is pivotal in the action of environmental agents which trigger the activation of glial cells and neuroinflammation to stimulate compensatory mechanisms aimed at restoring homeostasis. AIM: This study sets to demonstrate the interplay of fluoride (F) and aluminium (Al) in brain metabolism. Specifically, it reveals how oxidative stress impacts the activation of astrocytes (GFAP), mediates proinflammatory responses (microglia and B-cells: CD68 and CD 20 respectively) and shows the pattern of lipid peroxidation in the brain following fluoride and (or) aluminium treatment in vivo...
March 2015: Pathophysiology: the Official Journal of the International Society for Pathophysiology
Olalekan Michael Ogundele, Adams Olalekan Omoaghe, Duyilemi Chris Ajonijebu, Abiodun Ayodele Ojo, Temitope Deborah Fabiyi, Olayemi Joseph Olajide, Deborah Tolulope Falode, Philip Adeyemi Adeniyi
Glia activation and neuroinflamation are major factors implicated in the aetiology of most neurodegenerative diseases (NDDs). Several agents and toxins have been known to be capable of inducing glia activation an inflammatory response; most of which are active substances that can cause oxidative stress by inducing production of reactive oxygen species (ROS). Neurogenesis on the other hand involves metabolic and structural interaction between neurogenic and glia cells of the periventricular zone (PVZ); a region around the third ventricle...
June 2014: Metabolic Brain Disease
Vanesa Sanchez-Guajardo, Christopher J Barnum, Malú G Tansey, Marina Romero-Ramos
The role of neuroinflammation and the adaptive immune system in PD (Parkinson's disease) has been the subject of intense investigation in recent years, both in animal models of parkinsonism and in post-mortem PD brains. However, how these processes relate to and modulate α-syn (α-synuclein) pathology and microglia activation is still poorly understood. Specifically, how the peripheral immune system interacts, regulates and/or is induced by neuroinflammatory processes taking place during PD is still undetermined...
2013: ASN Neuro
Agnieszka Smolinska, Joram M Posma, Lionel Blanchet, Kirsten A M Ampt, Amos Attali, Tinka Tuinstra, Theo Luider, Marek Doskocz, Paul J Michiels, Frederic C Girard, Lutgarde M C Buydens, Sybren S Wijmenga
Because cerebrospinal fluid (CSF) is the biofluid which interacts most closely with the central nervous system, it holds promise as a reporter of neurological disease, for example multiple sclerosis (MScl). To characterize the metabolomics profile of neuroinflammatory aspects of this disease we studied an animal model of MScl-experimental autoimmune/allergic encephalomyelitis (EAE). Because CSF also exchanges metabolites with blood via the blood-brain barrier, malfunctions occurring in the CNS may be reflected in the biochemical composition of blood plasma...
May 2012: Analytical and Bioanalytical Chemistry
Sun Seek Min, Hui Yan Quan, Jinhua Ma, Ki Ho Lee, Seung Keun Back, Heung Seek Na, Seung Ho Han, Jae-Yong Yee, Chan Kim, Jung-Soo Han, Geun Hee Seol
Although deficits in synaptic plasticity have been identified in aged or neuroinflamed animals with memory impairments, few studies have examined the cellular basis of plasticity in such animals. Here, we examined whether chronic neuroinflammation altered long-term depression (LTD) and studied the underlying mechanism of LTD impairment by neuroinflammation. Chronic neuroinflammation was induced by administration of lipopolysaccharide (LPS) to the fourth ventricle. Excitatory postsynaptic potentials were recorded extracellularly in the rat hippocampal CA1 area to examine alterations in synaptic plasticity...
May 22, 2009: Biochemical and Biophysical Research Communications
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