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Molecular Neurodegeneration

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https://www.readbyqxmd.com/read/29202785/anti-aggregant-tau-mutant-promotes-neurogenesis
#1
Maria Joseph, Marta Anglada-Huguet, Katharina Paesler, Eckhard Mandelkow, Eva-Maria Mandelkow
BACKGROUND: The microtubule-associated protein Tau plays a role in neurodegeneration as well as neurogenesis. Previous work has shown that the expression of the pro-aggregant mutant Tau repeat domain causes strong aggregation and pronounced neuronal loss in the hippocampus whereas the anti-aggregant form has no deleterious effects. These two proteins differ mainly in their propensity to form ß structure and hence to aggregate. METHODS: To elucidate the basis of these contrasting effects, we analyzed organotypic hippocampal slice cultures (OHSCs) from transgenic mice expressing the repeat domain (RD) of Tau with the anti-aggregant mutation (TauRDΔKPP) and compared them with slices containing pro-aggregant TauRDΔK...
December 4, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29157277/a-validated-antibody-panel-for-the-characterization-of-tau-post-translational-modifications
#2
Ebru Ercan, Sameh Eid, Christian Weber, Alexandra Kowalski, Maria Bichmann, Annika Behrendt, Frank Matthes, Sybille Krauss, Peter Reinhardt, Simone Fulle, Dagmar E Ehrnhoefer
BACKGROUND: Tau is a microtubule-binding protein, which is subject to various post-translational modifications (PTMs) including phosphorylation, methylation, acetylation, glycosylation, nitration, sumoylation and truncation. Aberrant PTMs such as hyperphosphorylation result in tau aggregation and the formation of neurofibrillary tangles, which are a hallmark of Alzheimer's disease (AD). In order to study the importance of PTMs on tau function, antibodies raised against specific modification sites are widely used...
November 21, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29137651/abnormal-dendritic-calcium-activity-and-synaptic-depotentiation-occur-early-in-a-mouse-model-of-alzheimer-s-disease
#3
Yang Bai, Miao Li, Yanmei Zhou, Lei Ma, Qian Qiao, Wanling Hu, Wei Li, Zachary Patrick Wills, Wen-Biao Gan
BACKGROUND: Alzheimer's disease (AD) is characterized by amyloid deposition, tangle formation as well as synapse loss. Synaptic abnormalities occur early in the pathogenesis of AD. Identifying early synaptic abnormalities and their underlying mechanisms is likely important for the prevention and treatment of AD. METHODS: We performed in vivo two-photon calcium imaging to examine the activities of somas, dendrites and dendritic spines of layer 2/3 pyramidal neurons in the primary motor cortex in the APPswe/PS1dE9 mouse model of AD and age-matched wild type control mice...
November 14, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29132391/nadph-oxidases-in-parkinson-s-disease-a-systematic-review
#4
REVIEW
Karim Belarbi, Elodie Cuvelier, Alain Destée, Bernard Gressier, Marie-Christine Chartier-Harlin
Parkinson's disease (PD) is a progressive movement neurodegenerative disease associated with a loss of dopaminergic neurons in the substantia nigra of the brain. Oxidative stress, a condition that occurs due to imbalance in oxidant and antioxidant status, is thought to play an important role in dopaminergic neurotoxicity. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases are multi-subunit enzymatic complexes that generate reactive oxygen species as their primary function. Increased immunoreactivities for the NADPH oxidases catalytic subunits Nox1, Nox2 and Nox4 have been reported in the brain of PD patients...
November 13, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29132389/advances-challenges-and-future-directions-for-stem-cell-therapy-in-amyotrophic-lateral-sclerosis
#5
REVIEW
Yuri Ciervo, Ke Ning, Xu Jun, Pamela J Shaw, Richard J Mead
Amyotrophic lateral sclerosis (ALS) is a rapidly progressive neurodegenerative condition where loss of motor neurons within the brain and spinal cord leads to muscle atrophy, weakness, paralysis and ultimately death within 3-5 years from onset of symptoms. The specific molecular mechanisms underlying the disease pathology are not fully understood and neuroprotective treatment options are minimally effective. In recent years, stem cell transplantation as a new therapy for ALS patients has been extensively investigated, becoming an intense and debated field of study...
November 13, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29126445/ykl-40-in-the-brain-and-cerebrospinal-fluid-of-neurodegenerative-dementias
#6
Franc Llorens, Katrin Thüne, Waqas Tahir, Eirini Kanata, Daniela Diaz-Lucena, Konstantinos Xanthopoulos, Eleni Kovatsi, Catharina Pleschka, Paula Garcia-Esparcia, Matthias Schmitz, Duru Ozbay, Susana Correia, Ângela Correia, Ira Milosevic, Olivier Andréoletti, Natalia Fernández-Borges, Ina M Vorberg, Markus Glatzel, Theodoros Sklaviadis, Juan Maria Torres, Susanne Krasemann, Raquel Sánchez-Valle, Isidro Ferrer, Inga Zerr
BACKGROUND: YKL-40 (also known as Chitinase 3-like 1) is a glycoprotein produced by inflammatory, cancer and stem cells. Its physiological role is not completely understood but YKL-40 is elevated in the brain and cerebrospinal fluid (CSF) in several neurological and neurodegenerative diseases associated with inflammatory processes. Yet the precise characterization of YKL-40 in dementia cases is missing. METHODS: In the present study, we comparatively analysed YKL-40 levels in the brain and CSF samples from neurodegenerative dementias of different aetiologies characterized by the presence of cortical pathology and disease-specific neuroinflammatory signatures...
November 10, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29110684/multiscale-network-modeling-of-oligodendrocytes-reveals-molecular-components-of-myelin-dysregulation-in-alzheimer-s-disease
#7
Andrew T McKenzie, Sarah Moyon, Minghui Wang, Igor Katsyv, Won-Min Song, Xianxiao Zhou, Eric B Dammer, Duc M Duong, Joshua Aaker, Yongzhong Zhao, Noam Beckmann, Pei Wang, Jun Zhu, James J Lah, Nicholas T Seyfried, Allan I Levey, Pavel Katsel, Vahram Haroutunian, Eric E Schadt, Brian Popko, Patrizia Casaccia, Bin Zhang
BACKGROUND: Oligodendrocytes (OLs) and myelin are critical for normal brain function and have been implicated in neurodegeneration. Several lines of evidence including neuroimaging and neuropathological data suggest that Alzheimer's disease (AD) may be associated with dysmyelination and a breakdown of OL-axon communication. METHODS: In order to understand this phenomenon on a molecular level, we systematically interrogated OL-enriched gene networks constructed from large-scale genomic, transcriptomic and proteomic data obtained from human AD postmortem brain samples...
November 6, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29100536/correction-to-gene-environment-interaction-between-lead-and-apolipoprotein-e4-causes-cognitive-behavior-deficits-in-mice
#8
Anna K Engstrom, Jessica M Snyder, Nobuyo Maeda, Zhengui Xia
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November 3, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29100525/modulating-the-catalytic-activity-of-ampk-has-neuroprotective-effects-against-%C3%AE-synuclein-toxicity
#9
Wojciech Bobela, Sameer Nazeeruddin, Graham Knott, Patrick Aebischer, Bernard L Schneider
BACKGROUND: Metabolic perturbations and slower renewal of cellular components associated with aging increase the risk of Parkinson's disease (PD). Declining activity of AMPK, a critical cellular energy sensor, may therefore contribute to neurodegeneration. METHODS: Here, we overexpress various genetic variants of the catalytic AMPKα subunit to determine how AMPK activity affects the survival and function of neurons overexpressing human α-synuclein in vivo. RESULTS: Both AMPKα1 and α2 subunits have neuroprotective effects against human α-synuclein toxicity in nigral dopaminergic neurons...
November 3, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29084565/haplotype-specific-mapt-exon-3-expression-regulated-by-common-intronic-polymorphisms-associated-with-parkinsonian-disorders
#10
Mang Ching Lai, Anne-Laure Bechy, Franziska Denk, Emma Collins, Maria Gavriliouk, Judith B Zaugg, Brent J Ryan, Richard Wade-Martins, Tara M Caffrey
BACKGROUND: Genome wide association studies have identified microtubule associated protein tau (MAPT) H1 haplotype single nucleotide polymorphisms (SNPs) as leading common risk variants for Parkinson's disease, progressive supranuclear palsy and corticobasal degeneration. The MAPT risk variants fall within a large 1.8 Mb region of high linkage disequilibrium, making it difficult to discern the functionally important risk variants. Here, we leverage the strong haplotype-specific expression of MAPT exon 3 to investigate the functionality of SNPs that fall within this H1 haplotype region of linkage disequilibrium...
October 30, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29078813/the-trojan-horse-neuroinflammatory-impact-of-t-cells-in-neurodegenerative-diseases
#11
REVIEW
Annika Sommer, Beate Winner, Iryna Prots
Neuronal degeneration is a common mechanism of many neurological diseases including Parkinson's disease (PD), Alzheimer's disease (AD), and Multiple Sclerosis (MS). While AD and PD are classical neurodegenerative diseases, the primary pathology in MS is driven by autoimmune inflammation, attacking oligodendrocytes and thereby inducing neurodegeneration. In AD and PD, immune cells are also considered to play an important role in the disease progression. While the role of local central nervous system (CNS) innate immune cells is well described, a potential influence of adaptive immune cells in PD and AD is not yet fully understood...
October 27, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29078798/proteomic-profiling-of-neuronal-mitochondria-reveals-modulators-of-synaptic-architecture
#12
Laura C Graham, Samantha L Eaton, Paula J Brunton, Abdelmadjid Atrih, Colin Smith, Douglas J Lamont, Thomas H Gillingwater, Giuseppa Pennetta, Paul Skehel, Thomas M Wishart
BACKGROUND: Neurons are highly polarized cells consisting of three distinct functional domains: the cell body (and associated dendrites), the axon and the synapse. Previously, it was believed that the clinical phenotypes of neurodegenerative diseases were caused by the loss of entire neurons, however it has recently become apparent that these neuronal sub-compartments can degenerate independently, with synapses being particularly vulnerable to a broad range of stimuli. Whilst the properties governing the differential degenerative mechanisms remain unknown, mitochondria consistently appear in the literature, suggesting these somewhat promiscuous organelles may play a role in affecting synaptic stability...
October 27, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29065921/fibroblast-bioenergetics-to-classify-amyotrophic-lateral-sclerosis-patients
#13
Csaba Konrad, Hibiki Kawamata, Kirsten G Bredvik, Andrea J Arreguin, Steven A Cajamarca, Jonathan C Hupf, John M Ravits, Timothy M Miller, Nicholas J Maragakis, Chadwick M Hales, Jonathan D Glass, Steven Gross, Hiroshi Mitsumoto, Giovanni Manfredi
BACKGROUND: The objective of this study was to investigate cellular bioenergetics in primary skin fibroblasts derived from patients with amyotrophic lateral sclerosis (ALS) and to determine if they can be used as classifiers for patient stratification. METHODS: We assembled a collection of unprecedented size of fibroblasts from patients with sporadic ALS (sALS, n = 171), primary lateral sclerosis (PLS, n = 34), ALS/PLS with C9orf72 mutations (n = 13), and healthy controls (n = 91)...
October 24, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29061112/iron-regulatory-protein-irp-iron-responsive-element-ire-signaling-pathway-in-human-neurodegenerative-diseases
#14
REVIEW
Zhi Dong Zhou, Eng-King Tan
The homeostasis of iron is vital to human health, and iron dyshomeostasis can lead to various disorders. Iron homeostasis is maintained by iron regulatory proteins (IRP1 and IRP2) and the iron-responsive element (IRE) signaling pathway. IRPs can bind to RNA stem-loops containing an IRE in the untranslated region (UTR) to manipulate translation of target mRNA. However, iron can bind to IRPs, leading to the dissociation of IRPs from the IRE and altered translation of target transcripts. Recently an IRE is found in the 5'-UTR of amyloid precursor protein (APP) and α-synuclein (α-Syn) transcripts...
October 23, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29037207/trem2-deficiency-exacerbates-tau-pathology-through-dysregulated-kinase-signaling-in-a-mouse-model-of-tauopathy
#15
Shane M Bemiller, Tyler J McCray, Kevin Allan, Shane V Formica, Guixiang Xu, Gina Wilson, Olga N Kokiko-Cochran, Samuel D Crish, Cristian A Lasagna-Reeves, Richard M Ransohoff, Gary E Landreth, Bruce T Lamb
BACKGROUND: Genetic variants of the Triggering Receptor Expressed on Myeloid Cells-2 (TREM2) confer increased risk of developing late-onset Alzheimer's Disease (LOAD) and other neurodegenerative disorders. Recent studies provided insight into the multifaceted roles of TREM2 in regulating extracellular β-amyloid (Aβ) pathology, myeloid cell accumulation, and inflammation observed in AD, yet little is known regarding the role of TREM2 in regulating intracellular microtubule associated protein tau (MAPT; tau) pathology in neurodegenerative diseases and in AD, in particular...
October 16, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29017573/gad67-haploinsufficiency-reduces-amyloid-pathology-and-rescues-olfactory-memory-deficits-in-a-mouse-model-of-alzheimer-s-disease
#16
Yue Wang, Zheng Wu, Yu-Ting Bai, Gang-Yi Wu, Gong Chen
BACKGROUND: Alzheimer's disease (AD) is the most common age-related neurodegenerative disorder, affecting millions of people worldwide. Although dysfunction of multiple neurotransmitter systems including cholinergic, glutamatergic and GABAergic systems has been associated with AD progression the underlying mechanisms remain elusive. We and others have recently found that GABA content is elevated in AD brains and linked to cognitive deficits in AD mouse models. The glutamic acid decarboxylase 67 (GAD67) is the major enzyme converting glutamate into GABA and has been implied in a number of neurological disorders such as epilepsy and schizophrenia...
October 10, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28978354/the-cns-in-inbred-transgenic-models-of-4-repeat-tauopathy-develops-consistent-tau-seeding-capacity-yet-focal-and-diverse-patterns-of-protein-deposition
#17
Ghazaleh Eskandari-Sedighi, Nathalie Daude, Hristina Gapeshina, David W Sanders, Razieh Kamali-Jamil, Jing Yang, Beipei Shi, Holger Wille, Bernardino Ghetti, Marc I Diamond, Christopher Janus, David Westaway
BACKGROUND: MAPT mutations cause neurodegenerative diseases such as frontotemporal dementia but, strikingly, patients with the same mutation may have different clinical phenotypes. METHODS: Given heterogeneities observed in a transgenic (Tg) mouse line expressing low levels of human (2 N, 4R) P301L Tau, we backcrossed founder stocks of mice to C57BL/6Tac, 129/SvEvTac and FVB/NJ inbred backgrounds to discern the role of genetic versus environmental effects on disease-related phenotypes...
October 4, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28969695/together-jun-and-ddit3-chop-control-retinal-ganglion-cell-death-after-axonal-injury
#18
Stephanie B Syc-Mazurek, Kimberly A Fernandes, Michael P Wilson, Peter Shrager, Richard T Libby
BACKGROUND: Optic nerve injury is an important pathological component in neurodegenerative diseases such as traumatic optic neuropathies and glaucoma. The molecular signaling pathway(s) critical for retinal ganglion cell (RGC) death after axonal insult, however, is/are not fully defined. RGC death after axonal injury is known to occur by BAX-dependent apoptosis. Two transcription factors JUN (the canonical target of JNK) and DDIT3 (CHOP; a key mediator of the endoplasmic reticulum stress response) are known to be important apoptotic signaling molecules after axonal injury, including in RGCs...
October 2, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28962651/hexokinases-link-dj-1-to-the-pink1-parkin-pathway
#19
David N Hauser, Adamantios Mamais, Melissa M Conti, Christopher T Primiani, Ravindran Kumaran, Allissa A Dillman, Rebekah G Langston, Alexandra Beilina, Joseph H Garcia, Alberto Diaz-Ruiz, Michel Bernier, Fabienne C Fiesel, Xu Hou, Wolfdieter Springer, Yan Li, Rafael de Cabo, Mark R Cookson
BACKGROUND: Early onset Parkinson's disease is caused by variants in PINK1, parkin, and DJ-1. PINK1 and parkin operate in pathways that preserve mitochondrial integrity, but the function of DJ-1 and how it relates to PINK1 and parkin is poorly understood. METHODS: A series of unbiased high-content screens were used to analyze changes at the protein, RNA, and metabolite level in rodent brains lacking DJ-1. Results were validated using targeted approaches, and cellular assays were performed to probe the mechanisms involved...
September 29, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28934974/blood-hemoglobin-a1c-levels-and-amyotrophic-lateral-sclerosis-survival
#20
Qian-Qian Wei, Yongping Chen, Bei Cao, Ru Wei Ou, Lingyu Zhang, Yanbing Hou, Xiang Gao, Huifang Shang
BACKGROUND: There are inconsistences regarding the correlation between diabetes or fasting blood glucose concentrations and the risk and survival of amyotrophic lateral sclerosis (ALS) in the previous studies. Moreover, the association between hemoglobin A1c (HbA1c) levels, which reflect long-term glycemic status, and ALS survival was not examined. METHODS: A prospective cohort study including 450 Chinese sporadic ALS patients (254 men and 196 women; mean age: 55...
September 21, 2017: Molecular Neurodegeneration
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