Astrocytes

Publication Title: 
Neurochemical Research

The fruit of Terminalia chebula Retz has been used as a traditional medicine in Asia and contains tannic acid, chebulagic acid, chebulinic acid and corilagin. Extract from T. chebula seeds (TCE) has various biological functions. We observed the neuroprotective effects of TCE against ischemic damage in the hippocampal C1 region (CA1) of the gerbil that had received oral administrations of TCE (100 mg/kg) once a day for 7 days before the induction of transient cerebral ischemia.

Author(s): 
Park, Joon Ha
Joo, Han Seung
Yoo, Ki-Yeon
Shin, Bich Na
Kim, In Hye
Lee, Choong Hyun
Choi, Jung Hoon
Byun, Kyunghee
Lee, Bonghee
Lim, Soon Sung
Kim, Myong Jo
Won, Moo-Ho
Publication Title: 
Experimental & Molecular Medicine

Neural progenitor cells (NPs) have shown several promising benefits for the treatment of neurological disorders. To evaluate the therapeutic potential of human neural progenitor cells (hNPs) in amyotrophic lateral sclerosis (ALS), we transplanted hNPs or growth factor (GF)-expressing hNPs into the central nervous system (CNS) of mutant Cu/Zn superoxide dismutase (SOD1(G93A)) transgenic mice.

Author(s): 
Park, Sungju
Kim, Hyoung-Tae
Yun, Seokkwan
Kim, Il-Sun
Lee, Jiyoon
Lee, Il-Shin
Park, Kook In
Publication Title: 
Neurochemistry International

Age is the leading risk factor for many of the most prevalent and devastating diseases including neurodegenerative diseases. A number of herbal medicines have been used for centuries to ameliorate the deleterious effects of ageing-related diseases and increase longevity. Oxidative stress is believed to play a role in normal ageing as well as in neurodegenerative processes.

Author(s): 
Steele, Megan L.
Truong, John
Govindaraghavan, Suresh
Ooi, Lezanne
Sucher, Nikolaus J.
M¸nch, Gerald
Publication Title: 
PloS One

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that causes progressive paralysis due to motor neuron death. Several lines of published evidence suggested that inhibition of epidermal growth factor receptor (EGFR) signaling might protect neurons from degeneration. To test this hypothesis in vivo, we treated the SOD1 transgenic mouse model of ALS with erlotinib, an EGFR inhibitor clinically approved for oncology indications.

Author(s): 
Le Pichon, Claire E.
Dominguez, Sara L.
Solanoy, Hilda
Ngu, Hai
Lewin-Koh, Nicholas
Chen, Mark
Eastham-Anderson, Jeffrey
Watts, Ryan
Scearce-Levie, Kimberly
Publication Title: 
Neuromolecular Medicine

Emerging lines of evidence suggest a relationship between amyotrophic lateral sclerosis (ALS) and protein sumoylation. Multiple studies have demonstrated that several of the proteins involved in the pathogenesis of ALS, including superoxide dismutase 1, fused in liposarcoma, and TAR DNA-binding protein 43 (TDP-43), are substrates for sumoylation.

Author(s): 
Foran, Emily
Rosenblum, Lauren
Bogush, Alexey I.
Trotti, Davide
Publication Title: 
Biogerontology

Ageing can have profound effects on the post-mitotic organ of behaviour, the brain. As yet the precise causes of these deleterious effects are unknown. However, clear insights into the putative mechanisms and consequences of ageing in the CNS have been achieved through the use of invertebrate models. It is now clear that ageing alters the endogenous properties of neurones, their morphology, the efficacy of the connections that the neurones make with their targets and may even lead to neurone loss.

Author(s): 
Yeoman, M. S.
Faragher, R. G.
Publication Title: 
Glia

Glutamate is the major excitatory neurotransmitter in the CNS that is cleared from the extracellular space by a family of high-affinity glutamate transporters. The astroglial glutamate transporter EAAT2 is thought to carry out the uptake of the vast quantity of glutamate, and dysregulation of EAAT2 expression is involved in the pathogenesis of neurological disorders with marked excitotoxic components. Here, we present a novel epigenetic mechanism by which the human EAAT2 gene is kept in a silent state. Sequence inspection identified a classical CpG island at the EAAT2 promoter.

Author(s): 
Zschocke, J¸rgen
Allritz, Claudia
Engele, J¸rgen
Rein, Theo
Publication Title: 
Archives of General Psychiatry

CONTEXT: Although most of the effort to understand the neurobiology of depressive states and suicide has focused on neuronal processes, recent studies suggest that astroglial dysfunction may play an important role. A truncated variant of the tropomyosin-related kinase B (TrkB.T1) is expressed in astrocytes, and brain-derived neurotrophic factor-TrkB signaling has been linked to mood disorders. OBJECTIVE: To test the hypothesis that TrkB.T1 expression is downregulated in suicide completers and that this downregulation is mediated by an epigenetic process.

Author(s): 
Ernst, Carl
Deleva, Vesselina
Deng, Xiaoming
Sequeira, Adolfo
Pomarenski, Amanda
Klempan, Tim
Ernst, Neil
Quirion, Rémi
Gratton, Alain
Szyf, Moshe
Turecki, Gustavo
Publication Title: 
Schizophrenia Bulletin

Schizophrenia is a highly polygenic brain disorder. The main hypothesis for disease etiology in schizophrenia primarily focuses on the role of dysfunctional synaptic transmission. Previous studies have therefore directed their investigations toward the role of neuronal dysfunction. However, recent studies have shown that apart from neurons, glial cells also play a major role in synaptic transmission. Therefore, we investigated the potential causal involvement of the 3 principle glial cell lineages in risk to schizophrenia.

Author(s): 
Goudriaan, Andrea
de Leeuw, Christiaan
Ripke, Stephan
Hultman, Christina M.
Sklar, Pamela
Sullivan, Patrick F.
Smit, August B.
Posthuma, Danielle
Verheijen, Mark H. G.
Publication Title: 
Current Opinion in Pharmacology

Astrocytes orchestrate arrangement and functions of neuronal circuits and of the blood-brain barrier. Dysfunctional astrocytes characterize mood disorders, here showcased by deregulation of the astrocyte end-feet protein Aquaporin-4 around blood vessels and, hypothetically, of the astrocyte-specific phagocytic protein MEGF10 to shape synapses. Development of mood disorders is often a result of 'gene ◊ environment' interactions, regulated among others by histone modifications and related modulator enzymes, which rapidly promote adaptive responses.

Author(s): 
Jakovcevski, Mira
Akbarian, Schahram
Di Benedetto, Barbara

Pages

Subscribe to RSS - Astrocytes