Neuroglia

Publication Title: 
Neurobiology of Aging

An increasing number of people are living past the age of 100 years, but little is known about what differentiates centenarians from the rest of the population. In this study, brains from female subjects in 3 different age groups, 65-75 years (n = 8), 76-85 years (n = 8), and 94-105 years (n = 7), were examined to estimate the total number of neocortical neurons, astrocytes, oligodendrocytes, and microglia.

Author(s): 
Fabricius, Katrine
Jacobsen, Jette Stub
Pakkenberg, Bente
Publication Title: 
Human Molecular Genetics

Niemann-Pick type C (NPC) disease, an autosomal recessive disorder caused primarily by loss-of-function mutations in NPC1 gene, is characterized neuropathologically by intracellular cholesterol accumulation, gliosis and neuronal loss in selected brain regions. Recent studies have shown that NPC disease exhibits intriguing parallels with Alzheimer's disease (AD), including the presence of tau-positive neurofibrillary tangles (NFTs) and ?-amyloid (A?)-related peptides in vulnerable brain regions. Since enhanced cholesterol level, which acts as a risk factor for AD, can increase A?

Author(s): 
Maulik, Mahua
Ghoshal, Bibaswan
Kim, John
Wang, Yanlin
Yang, Jing
Westaway, David
Kar, Satyabrata
Publication Title: 
Neurobiology of Aging

An increasing number of people are living past the age of 100 years, but little is known about what differentiates centenarians from the rest of the population. In this study, brains from female subjects in 3 different age groups, 65-75 years (n = 8), 76-85 years (n = 8), and 94-105 years (n = 7), were examined to estimate the total number of neocortical neurons, astrocytes, oligodendrocytes, and microglia.

Author(s): 
Fabricius, Katrine
Jacobsen, Jette Stub
Pakkenberg, Bente
Publication Title: 
Neurobiology of Aging

A number of neurological diseases are caused by mutations of RNA metabolism-related genes. A complicating issue is that whether under- or overfunction of such genes is responsible for the phenotype. Polyglutamine tract binding protein-1, a causative gene for X-linked mental retardation, is also involved in RNA metabolism, and both mutation and duplication of the gene were reported in human patients. In this study, we first report a novel phenotype of dPQBP1 (drosophila homolog of Polyglutamine tract binding protein-1)-mutant flies, lifespan shortening.

Author(s): 
Tamura, Takuya
Sone, Masaki
Nakamura, Yoko
Shimamura, Teppei
Imoto, Seiya
Miyano, Satoru
Okazawa, Hitoshi
Publication Title: 
Genetics

Neurodegeneration is a hallmark of the human disease ataxia-telangiectasia (A-T) that is caused by mutation of the A-T mutated (ATM) gene. We have analyzed Drosophila melanogaster ATM mutants to determine the molecular mechanisms underlying neurodegeneration in A-T. Previously, we found that ATM mutants upregulate the expression of innate immune response (IIR) genes and undergo neurodegeneration in the central nervous system. Here, we present evidence that activation of the IIR is a cause of neurodegeneration in ATM mutants.

Author(s): 
Petersen, Andrew J.
Katzenberger, Rebeccah J.
Wassarman, David A.
Publication Title: 
Autophagy

Amyotrophic lateral sclerosis (ALS) is a fatal motoneuron disease with no current effective treatment. Accumulation of abnormal protein inclusions containing SOD1, TARDBP, FUS, among other proteins, is a pathological hallmark of ALS. Autophagy is the major degradation pathway involved in the clearance of damaged organelles and protein aggregates. Although autophagy has been shown to efficiently degrade ALS-linked mutant protein in cell culture models, several studies suggest that autophagy impairment may also contribute to disease pathogenesis.

Author(s): 
Castillo, Karen
Nassif, Melissa
Valenzuela, Vicente
Rojas, Fabiola
Matus, Soledad
Mercado, Gabriela
Court, Felipe A.
van Zundert, Brigitte
Hetz, Claudio
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: 
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: 
Neurobiology of Aging

Alzheimer's disease (AD) is a complex neurodegenerative disorder involving dysregulation of many biological pathways at multiple levels. Classical epigenetic mechanisms, including DNA methylation and histone modifications, and regulation by microRNAs (miRNAs), are among the major regulatory elements that control these pathways at the molecular level, with epigenetic modifications regulating gene expression transcriptionally and miRNAs suppressing gene expression posttranscriptionally.

Author(s): 
Van den Hove, Daniel L.
Kompotis, Konstantinos
Lardenoije, Roy
Kenis, Gunter
Mill, Jonathan
Steinbusch, Harry W.
Lesch, Klaus-Peter
Fitzsimons, Carlos P.
De Strooper, Bart
Rutten, Bart P. F.
Publication Title: 
The American Journal of Psychiatry

Considerable research suggests that suicide involves effects of genes, the environment, and their interaction. Analysis of three independent data sets of post-mortem brains revealed signs of increased methylation in one particular gene, SKA2, a finding that was extended to peripheral blood samples from other cohorts of prospectively followed individuals.

Author(s): 
Guintivano, Jerry
Brown, Tori
Newcomer, Alison
Jones, Marcus
Cox, Olivia
Maher, Brion S.
Eaton, William W.
Payne, Jennifer L.
Wilcox, Holly C.
Kaminsky, Zachary A.

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