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https://www.readbyqxmd.com/read/27878757/targeting-ccr3-to-reduce-amyloid-%C3%AE-production-tau-hyperphosphorylation-and-synaptic-loss-in-a-mouse-model-of-alzheimer-s-disease
#1
Chunyan Zhu, Bing Xu, Xiaohong Sun, Qiwen Zhu, Yi Sui
The majority of Alzheimer's disease (AD) patients have a late onset, and chronic neuroinflammation, characterized by glial activation and secretion of pro-inflammatory cytokines and chemokines, plays a role in the pathogenesis of AD. The chemokine CCL11 has been shown to be a causative factor of cognitive decline in the process of aging, but little is known whether it is involved in the pathogenesis of AD. In the present study, we showed that CCR3, the receptor for CCL11, was expressed by hippocampal neurons and treatment of primary hippocampal neuronal cultures (14 days in vitro) with CCL11 resulted in activation of cyclin-dependent kinase 5 and glycogen synthase kinase-3β, associated with elevated tau phosphorylation at multiple sites...
November 23, 2016: Molecular Neurobiology
https://www.readbyqxmd.com/read/27794462/long-term-depression-associated-signaling-is-required-for-an-in-vitro-model-of-nmda-receptor-dependent-synapse-pruning
#2
Maile A Henson, Charles J Tucker, Meilan Zhao, Serena M Dudek
Activity-dependent pruning of synaptic contacts plays a critical role in shaping neuronal circuitry in response to the environment during postnatal brain development. Although there is compelling evidence that shrinkage of dendritic spines coincides with synaptic long-term depression (LTD), and that LTD is accompanied by synapse loss, whether NMDA receptor (NMDAR)-dependent LTD is a required step in the progression toward synapse pruning is still unknown. Using repeated applications of NMDA to induce LTD in dissociated rat neuronal cultures, we found that synapse density, as measured by colocalization of fluorescent markers for pre- and postsynaptic structures, was decreased irrespective of the presynaptic marker used, post-treatment recovery time, and the dendritic location of synapses...
October 26, 2016: Neurobiology of Learning and Memory
https://www.readbyqxmd.com/read/27697456/prenatal-infection-leads-to-asd-like-behavior-and-altered-synaptic-pruning-in-the-mouse-offspring
#3
Lourdes Fernández de Cossío, Andrea Guzmán, Suzanne van der Veldt, Giamal N Luheshi
Environmental challenges to the maternal immune system during pregnancy have been associated with an increase in the frequency of neurodevelopmental disorders such as Autism Spectrum Disorders (ASD) appearing in the offspring. Microglia, the brain's resident immune-cells, are now known to be critically involved in normal brain development, shaping connections between neurons by pruning superfluous synaptic spines. Our aim was to investigate whether maternal infection during critical stages of gestation compromises the role of microglia in sculpting neuronal circuits...
September 30, 2016: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/27604518/induction-of-hippocampal-long-term-potentiation-increases-the-morphological-dynamics-of-microglial-processes-and-prolongs-their-contacts-with-dendritic-spines
#4
Thomas Pfeiffer, Elena Avignone, U Valentin Nägerl
Recently microglia, the resident immune cells of the brain, have been recognized as multi-tasking talents that are not only essential in the diseased brain, but also actively contribute to synaptic circuit remodeling during normal brain development. It is well established that microglia dynamically scan their environment and thereby establish transient physical contacts with neuronal synapses, which may allow them to sense and influence synaptic function. However, it is unknown whether and how the morphological dynamics of microglia and their physical interactions with synapses are affected by the induction of synaptic plasticity in the adult brain...
2016: Scientific Reports
https://www.readbyqxmd.com/read/27576527/colony-stimulating-factor-1-receptor-blockade-prevents-fractionated-whole-brain-irradiation-induced-memory-deficits
#5
Xi Feng, Timothy D Jopson, Maria Serena Paladini, Sharon Liu, Brian L West, Nalin Gupta, Susanna Rosi
BACKGROUND: Primary central nervous system (CNS) neoplasms and brain metastases are routinely treated with whole-brain radiation. Long-term survival occurs in many patients, but their quality of life is severely affected by the development of cognitive deficits, and there is no treatment to prevent these adverse effects. Neuroinflammation, associated with activation of brain-resident microglia and infiltrating monocytes, plays a pivotal role in loss of neurological function and has been shown to be associated with acute and long-term effects of brain irradiation...
August 30, 2016: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/27571442/whole-body-vibration-induces-pain-and-lumbar-spinal-inflammation-responses-in-the-rat-that-vary-with-the-vibration-profile
#6
Martha E Zeeman, Sonia Kartha, Beth A Winkelstein
Whole-body vibration (WBV) is linked epidemiologically to neck and back pain in humans, and to forepaw mechanical allodynia and cervical neuroinflammation in a rodent model of WBV, but the response of the low back and lumbar spine to WBV is unknown. A rat model of WBV was used to determine the effect of different WBV exposures on hind paw behavioral sensitivity and neuroinflammation in the lumbar spinal cord. Rats were exposed to 30 min of WBV at either 8 or 15 Hz on days 0 and 7, with the lumbar spinal cord assayed using immunohistochemistry at day 14...
August 2016: Journal of Orthopaedic Research: Official Publication of the Orthopaedic Research Society
https://www.readbyqxmd.com/read/27558646/microglia-contact-induces-synapse-formation-in-developing-somatosensory-cortex
#7
Akiko Miyamoto, Hiroaki Wake, Ayako Wendy Ishikawa, Kei Eto, Keisuke Shibata, Hideji Murakoshi, Schuichi Koizumi, Andrew J Moorhouse, Yumiko Yoshimura, Junichi Nabekura
Microglia are the immune cells of the central nervous system that play important roles in brain pathologies. Microglia also help shape neuronal circuits during development, via phagocytosing weak synapses and regulating neurogenesis. Using in vivo multiphoton imaging of layer 2/3 pyramidal neurons in the developing somatosensory cortex, we demonstrate here that microglial contact with dendrites directly induces filopodia formation. This filopodia formation occurs only around postnatal day 8-10, a period of intense synaptogenesis and when microglia have an activated phenotype...
2016: Nature Communications
https://www.readbyqxmd.com/read/27421577/the-endocytic-pathway-in-microglia-during-health-aging-and-alzheimer-s-disease
#8
REVIEW
Santiago Solé-Domènech, Dana L Cruz, Estibaliz Capetillo-Zarate, Frederick R Maxfield
Microglia, the main phagocytes of the central nervous system (CNS), are involved in the surveillance and maintenance of nervous tissue. During normal tissue homeostasis, microglia migrates within the CNS, phagocytose dead cells and tissue debris, and modulate synapse pruning and spine formation via controlled phagocytosis. In the event of an invasion by a foreign body, microglia are able to phagocytose the invading pathogen and process it proteolytically for antigen presentation. Internalized substrates are incorporated and sorted within the endocytic pathway and thereafter transported via complex vesicular routes...
December 2016: Ageing Research Reviews
https://www.readbyqxmd.com/read/27400854/deficient-autophagy-in-microglia-impairs-synaptic-pruning-and-causes-social-behavioral-defects
#9
H-J Kim, M-H Cho, W H Shim, J K Kim, E-Y Jeon, D-H Kim, S-Y Yoon
Autism spectrum disorders (ASDs) are neurodevelopmental disorders caused by various genetic and environmental factors that result in synaptic abnormalities. ASD development is suggested to involve microglia, which have a role in synaptic refinement during development. Autophagy and related pathways are also suggested to be involved in ASDs. However, the precise roles of microglial autophagy in synapses and ASDs are unknown. Here, we show that microglial autophagy is involved in synaptic refinement and neurobehavior regulation...
July 12, 2016: Molecular Psychiatry
https://www.readbyqxmd.com/read/27282914/altered-excitatory-inhibitory-balance-within-somatosensory-cortex-is-associated-with-enhanced-plasticity-and-pain-sensitivity-in-a-mouse-model-of-multiple-sclerosis
#10
Liam E Potter, John W Paylor, Jee Su Suh, Gustavo Tenorio, Jayalakshmi Caliaperumal, Fred Colbourne, Glen Baker, Ian Winship, Bradley J Kerr
BACKGROUND: Chronic neuropathic pain is a common symptom of multiple sclerosis (MS). MOG35-55-induced experimental autoimmune encephalomyelitis (EAE) has been used as an animal model to investigate the mechanisms of pain in MS. Previous studies have implicated sensitization of spinal nociceptive networks in the pathogenesis of pain in EAE. However, the involvement of supraspinal sites of nociceptive integration, such as the primary somatosensory cortex (S1), has not been defined. We therefore examined functional, structural, and immunological alterations in S1 during the early stages of EAE, when pain behaviors first appear...
2016: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/27265783/increased-neuroplasticity-and-hippocampal-microglia-activation-in-a-mice-model-of-rapid-antidepressant-treatment
#11
Luca Muzio, Valentina Brambilla, Lorenza Calcaterra, Patrizia D'Adamo, Gianvito Martino, Francesco Benedetti
The search for biomarkers of antidepressant effects focused on pathways regulating synaptic plasticity, and on activated inflammatory markers. Repeated Sleep Deprivation (SD) provides a model treatment to reverse-translate antidepressant effects from in vivo clinical psychiatry to model organisms. We studied the effects of repeated SD alone (ASD) or combined with exercise on a slow spinning wheel (SSW), in 116 C57BL/6J male mice divided in three groups (ASD, SSW, untreated). Forced Swimming Test (FST) was used to detect antidepressant-like effects...
September 15, 2016: Behavioural Brain Research
https://www.readbyqxmd.com/read/27203137/treatment-of-traumatic-brain-injury-in-rats-with-n-acetyl-seryl-aspartyl-lysyl-proline
#12
Yanlu Zhang, Zheng Gang Zhang, Michael Chopp, Yuling Meng, Li Zhang, Asim Mahmood, Ye Xiong
OBJECTIVE The authors' previous studies have suggested that thymosin beta 4 (Tβ4), a major actin-sequestering protein, improves functional recovery after neural injury. N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) is an active peptide fragment of Tβ4. Its effect as a treatment of traumatic brain injury (TBI) has not been investigated. Thus, this study was designed to determine whether AcSDKP treatment improves functional recovery in rats after TBI. METHODS Young adult male Wistar rats were randomly divided into the following groups: 1) sham group (no injury); 2) TBI + vehicle group (0...
May 20, 2016: Journal of Neurosurgery
https://www.readbyqxmd.com/read/27147660/conversion-of-synthetic-a%C3%AE-to-in-vivo-active-seeds-and-amyloid-plaque-formation-in-a-hippocampal-slice-culture-model
#13
Renata Novotny, Franziska Langer, Jasmin Mahler, Angelos Skodras, Andreas Vlachos, Bettina M Wegenast-Braun, Stephan A Kaeser, Jonas J Neher, Yvonne S Eisele, Marie J Pietrowski, K Peter R Nilsson, Thomas Deller, Matthias Staufenbiel, Bernd Heimrich, Mathias Jucker
UNLABELLED: The aggregation of amyloid-β peptide (Aβ) in brain is an early event and hallmark of Alzheimer's disease (AD). We combined the advantages of in vitro and in vivo approaches to study cerebral β-amyloidosis by establishing a long-term hippocampal slice culture (HSC) model. While no Aβ deposition was noted in untreated HSCs of postnatal Aβ precursor protein transgenic (APP tg) mice, Aβ deposition emerged in HSCs when cultures were treated once with brain extract from aged APP tg mice and the culture medium was continuously supplemented with synthetic Aβ...
May 4, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27109181/amyloid-%C3%AE-plaques-disrupt-axon-initial-segments
#14
Miguel A Marin, Jokubus Ziburkus, Joanna Jankowsky, Matthew N Rasband
UNLABELLED: Amyloid-β (Aβ) plaques are one of the central pathologies of Alzheimer's disease (AD). Plaque formation in animal models of AD coincides with the appearance of synaptic abnormalities, aberrant neuronal excitability, and cognitive decline. Aβ plaques may disrupt neuronal excitability since they have been proposed to be synaptotoxic, to induce axonal varicosities and neurite breakage, and to significantly decrease spine density. Axon initial segments (AIS) also regulate neuronal excitability and help maintain neuronal polarity...
July 2016: Experimental Neurology
https://www.readbyqxmd.com/read/26921617/eliminating-microglia-in-alzheimer-s-mice-prevents-neuronal-loss-without-modulating-amyloid-%C3%AE-pathology
#15
Elizabeth E Spangenberg, Rafael J Lee, Allison R Najafi, Rachel A Rice, Monica R P Elmore, Mathew Blurton-Jones, Brian L West, Kim N Green
In addition to amyloid-β plaque and tau neurofibrillary tangle deposition, neuroinflammation is considered a key feature of Alzheimer's disease pathology. Inflammation in Alzheimer's disease is characterized by the presence of reactive astrocytes and activated microglia surrounding amyloid plaques, implicating their role in disease pathogenesis. Microglia in the healthy adult mouse depend on colony-stimulating factor 1 receptor (CSF1R) signalling for survival, and pharmacological inhibition of this receptor results in rapid elimination of nearly all of the microglia in the central nervous system...
April 2016: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/26847266/dark-microglia-a-new-phenotype-predominantly-associated-with-pathological-states
#16
Kanchan Bisht, Kaushik P Sharma, Cynthia Lecours, Maria Gabriela Sánchez, Hassan El Hajj, Giampaolo Milior, Adrián Olmos-Alonso, Diego Gómez-Nicola, Giamal Luheshi, Luc Vallières, Igor Branchi, Laura Maggi, Cristina Limatola, Oleg Butovsky, Marie-Ève Tremblay
The past decade has witnessed a revolution in our understanding of microglia. These immune cells were shown to actively remodel neuronal circuits, leading to propose new pathogenic mechanisms. To study microglial implication in the loss of synapses, the best pathological correlate of cognitive decline across chronic stress, aging, and diseases, we recently conducted ultrastructural analyses. Our work uncovered the existence of a new microglial phenotype that is rarely present under steady state conditions, in hippocampus, cerebral cortex, amygdala, and hypothalamus, but becomes abundant during chronic stress, aging, fractalkine signaling deficiency (CX3 CR1 knockout mice), and Alzheimer's disease pathology (APP-PS1 mice)...
May 2016: Glia
https://www.readbyqxmd.com/read/26843990/emerging-roles-of-filopodia-and-dendritic-spines-in-motoneuron-plasticity-during-development-and-disease
#17
REVIEW
Refik Kanjhan, Peter G Noakes, Mark C Bellingham
Motoneurons develop extensive dendritic trees for receiving excitatory and inhibitory synaptic inputs to perform a variety of complex motor tasks. At birth, the somatodendritic domains of mouse hypoglossal and lumbar motoneurons have dense filopodia and spines. Consistent with Vaughn's synaptotropic hypothesis, we propose a developmental unified-hybrid model implicating filopodia in motoneuron spinogenesis/synaptogenesis and dendritic growth and branching critical for circuit formation and synaptic plasticity at embryonic/prenatal/neonatal period...
2016: Neural Plasticity
https://www.readbyqxmd.com/read/26708068/long-term-central-pathology-and-cognitive-impairment-are-exacerbated-in-a-mixed-model-of-alzheimer-s-disease-and-type-2-diabetes
#18
Carmen Infante-Garcia, Juan Jose Ramos-Rodriguez, Lucia Galindo-Gonzalez, Monica Garcia-Alloza
Type 2 diabetes (T2D) is a well-characterized risk factor for Alzheimer's disease (AD), the most common cause of dementia. Since both, T2D and dementia are closely related to aging and they chronically coexist in elderly patients, it is of particular relevance to know whether long-term evolution of T2D and dementia interfere with each other years after the onset of the diseases. In order to elucidate this interaction, we have characterized a mixed model of T2D and AD, the APP/PS1xdb/db mouse, at 36 weeks of age, when both diseases have long coexisted and evolved...
March 2016: Psychoneuroendocrinology
https://www.readbyqxmd.com/read/26540615/propagation-of-neuronal-damage-to-embryonic-grafts-transplanted-in-the-hippocampus-of-murine-models-of-alzheimer-s-disease
#19
Mohcene Sadallah, Vivien Labat-Gest, Filippo Tempia
Alzheimer's disease (AD) is the most common form of dementia, characterized by the presence of two principal hallmarks-amyloid plaques and neurofibrillary tangles. The primary cause of the majority of AD cases is not known. Likewise, the mechanisms underlying the propagation of the pathology from affected tissue to neighboring healthy neurons are largely unknown, but knowledge about them could be helpful to design strategies aimed at halting the progression of the disease. To throw light on the mechanisms of propagation of neuronal damage to healthy tissue, wild-type (WT) hippocampal solid tissue chunks derived from green fluorescent protein (GFP)-positive embryos were grafted into the hippocampus of 6-month-old WT and 3xTg-AD mice, a triple-transgenic mouse model that exhibits both amyloid-beta (Aβ) and tau protein pathology...
December 2015: Rejuvenation Research
https://www.readbyqxmd.com/read/26538149/viral-gene-transfer-of-apps%C3%AE-rescues-synaptic-failure-in-an-alzheimer-s-disease-mouse-model
#20
Romain Fol, Jerome Braudeau, Susann Ludewig, Tobias Abel, Sascha W Weyer, Jan-Peter Roederer, Florian Brod, Mickael Audrain, Alexis-Pierre Bemelmans, Christian J Buchholz, Martin Korte, Nathalie Cartier, Ulrike C Müller
Alzheimer's disease (AD) is characterized by synaptic failure, dendritic and axonal atrophy, neuronal death and progressive loss of cognitive functions. It is commonly assumed that these deficits arise due to β-amyloid accumulation and plaque deposition. However, increasing evidence indicates that loss of physiological APP functions mediated predominantly by neurotrophic APPsα produced in the non-amyloidogenic α-secretase pathway may contribute to AD pathogenesis. Upregulation of APPsα production via induction of α-secretase might, however, be problematic as this may also affect substrates implicated in tumorigenesis...
February 2016: Acta Neuropathologica
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