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  • 1
    Language: English
    In: Science (New York, N.Y.), 22 September 2006, Vol.313(5794), pp.1781-4
    Description: Protein aggregation is an established pathogenic mechanism in Alzheimer's disease, but little is known about the initiation of this process in vivo. Intracerebral injection of dilute, amyloid-beta (Abeta)-containing brain extracts from humans with Alzheimer's disease or beta-amyloid precursor protein (APP) transgenic mice induced cerebral beta-amyloidosis and associated pathology in APP transgenic mice in a time- and concentration-dependent manner. The seeding activity of brain extracts was reduced or abolished by Abeta immunodepletion, protein denaturation, or by Abeta immunization of the host. The phenotype of the exogenously induced amyloidosis depended on both the host and the source of the agent, suggesting the existence of polymorphic Abeta strains with varying biological activities reminiscent of prion strains.
    Keywords: Amyloid Beta-Peptides -- Administration & Dosage ; Amyloid Beta-Protein Precursor -- Administration & Dosage ; Amyloidosis -- Metabolism ; Brain Diseases -- Metabolism ; Hippocampus -- Chemistry
    ISSN: 00368075
    E-ISSN: 1095-9203
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  • 2
    Language: English
    In: Trends in Neurosciences, October 2015, Vol.38(10), pp.659-668
    Description: Several recent genome-wide association studies (GWAS) in patients with neurodegenerative disorders have shed new light on the brain immune system, suggesting that it plays a pivotal role in disease pathogenesis. Mononuclear phagocytes are blatantly involved in Alzheimer's disease (AD) of the central nervous system (CNS), but the specific functions of resident microglia, perivascular or meningeal macrophages, and circulating myeloid cells have not yet been fully resolved. Next-generation sequencing, high-throughput immune profiling technologies, and novel genetic tools have recently revolutionized the characterization of innate immune responses during AD. These studies advocate selective and non-redundant roles for myeloid subsets, which could be a target for novel disease-modifying therapies in AD. Myeloid cells differ in their kinetics (long-lived versus short-lived) and localization. This should be taken into account when targeting myeloid cells during neurodegenerative diseases. Microglia are recruited to and cluster around newly formed Aβ plaques, indicating that they are not directly involved in the initial stages of amyloid plaque formation. Microglia are phagocytic cells in the brain equipped with several receptors that play a role in the clearance of Aβ. Downregulation of these immune-receptors results in compromised phagocytotic capacity of microglia. Morphological alterations such as dystrophic (senescent) microglia have been observed in the aged human and AD brain. Emerging data suggest that microglia deteriorate with age and are dysfunctional during AD.
    Keywords: Microglia ; Yolk Sac ; Neurodegeneration ; Cx3cr1 ; Macrophage ; Alzheimer'S Disease ; Medicine ; Anatomy & Physiology
    ISSN: 0166-2236
    E-ISSN: 1878-108X
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  • 3
    In: Nature, 2008, Vol.451(7179), p.720
    Description: Senile plaques accumulate over the course of decades in the brains of patients with Alzheimer's disease. A fundamental tenet of the amyloid hypothesis of Alzheimer's disease is that the deposition of amyloid-beta precedes and induces the neuronal abnormalities that underlie dementia. This idea has been challenged, however, by the suggestion that alterations in axonal trafficking and morphological abnormalities precede and lead to senile plaques. The role of microglia in accelerating or retarding these processes has been uncertain. To investigate the temporal relation between plaque formation and the changes in local neuritic architecture, we used longitudinal in vivo multiphoton microscopy to sequentially image young APPswe/PS1d9xYFP (B6C3-YFP) transgenic mice. Here we show that plaques form extraordinarily quickly, over 24 h. Within 1-2 days of a new plaque's appearance, microglia are activated and recruited to the site. Progressive neuritic changes ensue, leading to increasingly dysmorphic neurites over the next days to weeks. These data establish plaques as a critical mediator of neuritic pathology.
    Keywords: Sciences (General) ; Physics;
    ISSN: 0028-0836
    E-ISSN: 14764687
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  • 4
    In: Journal of Neurochemistry, June 2010, Vol.113(5), pp.1240-1251
    Description: To authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1471-4159.2010.06693.x Keywords: advanced glycation end products; anxiety; copy number variant; depression; high anxiety-related behavior Abstract: J. Neurochem. (2010) 113, 1240-1251. Abstract Methylglyoxal (MG) is a highly reactive metabolite that forms adducts with basic amino acid side chains in proteins. MG is degraded by glyoxalase1 (GLO1), an enzyme shown to be differentially expressed in several mouse models of anxiety-related behavior. As yet, molecular mechanisms by which altered GLO1 expression influences emotionality have not been elucidated. Here we report that both MG concentration and protein modification are altered in brain tissue of a mouse model for trait anxiety, with elevated levels in low anxiety-related behavior relative to high anxiety-related behavior animals. Accordingly, repeated intracerebroventricular injections of MG mediated anxiolysis in inbred high anxiety-related behavior and outbred CD1 mice. We found that anxiolytic-like properties of MG were independent of GLO1 expression. In contrast, antidepressant-like properties of intracerebroventricular MG were suppressed in CD1 mice carrying extra copies of the GLO1 gene. Moreover, MG treatment increased expression of GLO1 only in CD1 mice that did not have extra copies of GLO1. Taken together, these results suggest that the MG levels in brain are negatively correlated with anxiety. Thereby, we identified a novel molecular mechanism for anxiety-related behavior in mice that may help to elucidate genesis of psychiatric disorders in humans. Author Affiliation: (*)Department of Behavioral Neuroendocrinology, Max Planck Institute of Psychiatry, Munich, Germany ([dagger])Department of Medical Technology, Fooyin University, Ta-Liao Hsiang, Kaohsiung Hsien, Taiwan ([double dagger])Department of Neuronal Network Dynamics, Max Planck Institute of Psychiatry, Munich, Germany (s.)Department of Proteomics and Biomarkers, Max Planck Institute of Psychiatry, Munich, Germany Article History: Received January 25, 2010; revised manuscript received March 1, 2010; accepted March 14, 2010. Article note: Address correspondence and reprint requests to Dr Boris Hambsch, Department of Behavioral Neuroendocrinology, Max Planck Institute of Psychiatry, Kraepelinstr.2, 80804 Munich, Germany. E-mail: hambsch@mpipsykl.mpg.de
    Keywords: Advanced Glycation End Products ; Anxiety ; Copy Number Variant ; Depression ; High Anxiety‐Related Behavior
    ISSN: 0022-3042
    E-ISSN: 1471-4159
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  • 5
    Language: English
    In: Frontiers in Cellular Neuroscience, Dec 11, 2018
    Description: Synapse loss has detrimental effects on cellular communication, leading to network disruptions within the central nervous system (CNS) such as in Alzheimer’s disease (AD). AD is characterized by a progressive decline of memory function, cognition, neuronal and synapse loss. The two main neuropathological hallmarks are amyloid-β (Aβ) plaques and neurofibrillary tangles. In the brain of AD patients and in mouse models of AD several morphological and functional changes, such as microgliosis and astrogliosis around Aβ plaques, as well as dendritic and synaptic alterations, are associated with these lesions. In this review article, we will summarize the current literature on synapse loss in mouse models of AD and discuss current and prospective treatments for AD.
    Keywords: Alzheimer'S Disease – Care and Treatment ; Glia – Research ; Laboratory Rats – Models ; Synapses – Research
    ISSN: 1662-5102
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  • 6
    Language: English
    In: Forensic Science International, 10 October 2012, Vol.222(1-3), pp.256-258
    Description: The HSP70 superfamily is a reliable biomarker for hyperthermia, hypothermia and hypoxia. The Enzyme-linked Immunosorbent Assay (ELISA) respectively immunohistochemically staining methods are the typically used techniques for the quantification of those proteins. As the costs for reagents and devices as well as the work schedule of these methods are immense it was the goal of our study to develop an easy and reliable method to quantify the concentration of specific proteins. We established a procedure to measure the relative concentration of proteins fixed on ROTI PVDF membranes via Western blot, calculating the relative protein concentration in dependency to the grey scale index of the normalized and digitalized pictures of the bands on the blots.
    Keywords: Quantification ; Protein ; Grey Scale ; Western Blot ; Hsp70 Superfamily ; Immune Detection ; Public Health
    ISSN: 0379-0738
    E-ISSN: 1872-6283
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  • 7
    Language: English
    In: Acta neuropathologica communications, 31 May 2018, Vol.6(1), pp.44
    Description: Several studies suggest that women have a higher risk to develop Alzheimer's disease (AD) than men. In particular, the number of pregnancies was shown to be a risk factor for AD and women with several pregnancies on average had an earlier onset of the disease, thus making childbearing a risk factor. However, the impact of being pregnant on Aβ plaque pathology and adult neurogenesis still remains elusive. Postmortem analysis revealed that pregnant 5xFAD transgenic mice had significantly more Aβ plaques in the hippocampus from G10 onwards and that the number of Ki67 and DCX positive cells dramatically decreased during the postpartum period. Furthermore, 5 months old 5xFAD transgenic mice that also nursed their offsprings for 4 weeks had a similar Aβ plaque load than merely pregnant mice, indicating that pregnancy alone is sufficient to elevate Aβ plaque levels. Interestingly, housing in an enriched environment reduced the Aβ plaque load and vivified neurogenesis. Our results suggest that pregnancy alters Aβ plaque deposition in 5xFAD transgenic mice and diminishes the generation of newborn neurons. We conclude that pregnancy alone is sufficient to induce this phenotype that can be reversed upon environmental enrichment.
    Keywords: Adult Neurogenesis ; Alzheimer’s Disease ; Amyloid-Β Plaques ; Environmental Enrichment ; Estrogens ; Pregnancy ; Progesterone
    E-ISSN: 2051-5960
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  • 8
    Language: English
    In: Frontiers in Molecular Neuroscience, Oct 2, 2019
    Description: Misfolded proteins can form aggregates and induce a self-perpetuating process leading to the amplification and spreading of pathological protein assemblies. These misfolded protein assemblies act as seeds of aggregation. In an in vivo exogenous seeding model, both the features of seeds and the position at which seeding originates are precisely defined. Ample evidence from studies on intracerebal injection of amyloid-beta (Aβ)-rich brain extracts suggests that Aβ aggregation can be initiated by prion-like seeding. In this mini-review article, we will summarize the past and current literature on Aβ seeding in mouse models of AD and discuss its implementation as a tool to study cerebral amyloidosis and associated pathology.
    Keywords: Medical Research ; Amyloidosis ; Proteins
    ISSN: 1662-5099
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  • 9
    Language: English
    In: Molecular Neurodegeneration, 01 March 2011, Vol.6(1), p.22
    Description: Abstract Background Immunization against amyloid-β (Aβ), the peptide that accumulates in the form of senile plaques and in the cerebrovasculature in Alzheimer's disease (AD), causes a dramatic immune response that prevents plaque formation and clears accumulated Aβ in transgenic mice. In a clinical trial of Aβ immunization, some patients developed meningoencephalitis and hemorrhages. Neuropathological investigations of patients who died after the trial showed clearance of amyloid pathology, but also a powerful immune response involving activated T cells probably underlying the negative effects of the immunization. Results To define the impact of T cells on this inflammatory response we used passive immunization and adoptive transfer to separate the effect of IgG and T cell mediated effects on microhemorrhage in APPPS1 transgenic mice. Neither anti Aβ IgG nor adoptively transferred T cells, alone, led to increased cerebrovascular damage. However, the combination of adoptively transferred T cells and passive immunization led to massive cerebrovascular bleeding that ranged from multiple microhemorrhages in the parenchyma to large hematomas. Conclusions Our results indicate that vaccination can lead to Aβ and T cell induced cerebral micro-hemorrhages and acute hematomas, which are greatly exacerbated by T cell mediated activity.
    Keywords: Anatomy & Physiology
    ISSN: 1750-1326
    E-ISSN: 1750-1326
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  • 10
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 11 January 2005, Vol.102(2), pp.479-84
    Description: Diffusion parameters of the extracellular space (ECS) are changed in many brain pathologies, disturbing synaptic as well as extrasynaptic "volume" transmission, which is based on the diffusion of neuroactive substances in the ECS. Amyloid deposition, neuronal loss, and disturbed synaptic transmission are considered to be the main causes of Alzheimer's disease dementia. We studied diffusion parameters in the cerebral cortex of transgenic APP23 mice, which develop a pathology similar to Alzheimer's disease. The real-time tetramethylammonium (TMA) method and diffusion-weighted MRI were used to measure the ECS volume fraction (alpha = ECS volume/total tissue volume) and the apparent diffusion coefficients (ADCs) of TMA (ADC(TMA)), diffusing exclusively in the ECS and of water (ADC(W)). Measurements were performed in vivo in 6-, 8-, and 17- to 25-month-old hemizygous APP23 male and female mice and age-matched controls. In all 6- to 8-month-old APP23 mice, the mean ECS volume fraction, ADC(TMA), and ADC(W) were not significantly different from age-matched controls (alpha = 0.20 +/- 0.01; ADC(TMA), 580 +/- 16 microm(2).s(-1); ADC(W), 618 +/- 19 microm(2).s(-1)). Aging in 17- to 25-month-old controls was accompanied by a decrease in ECS volume fraction and ADC(W), significantly greater in females than in males, but no changes in ADC(TMA). ECS volume fraction increased (0.22 +/- 0.01) and ADC(TMA) decreased (560 +/- 7 microm(2).s(-1)) in aged APP23 mice. The impaired navigation observed in these animals in the Morris water maze correlated with their plaque load, which was twice as high in females (20%) as in males (10%) and may, together with changed ECS diffusion properties, account for the impaired extrasynaptic transmission and spatial cognition observed in old transgenic females.
    Keywords: Disease Models, Animal ; Alzheimer Disease -- Etiology ; Amyloid Beta-Protein Precursor -- Physiology ; Extracellular Space -- Metabolism
    ISSN: 0027-8424
    E-ISSN: 10916490
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