Fluoro-Jade® B staining as useful tool to identify activated microglia and astrocytes in a mouse transgenic model of Alzheimer's disease

Damjanac, Milena; Bilan, Agnès Rioux; Barrier, Laurence; Pontcharraud, Raymond; Cantereau, Anne; Hugon, Jacques; Page, Guylène

doi:10.1016/j.brainres.2006.05.050

Cited by 86 publications

(62 citation statements)

References 39 publications

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“…39,40 In later stages, the compound also reacted with activated glia, similar to observations in unrelated mouse models (Ref. 53, and refs. therein).…”

Section: Type and Mechanism Of Neurodegenerationsupporting

confidence: 60%

Neurodegeneration and Neuroinflammation in cdk5/p25-Inducible Mice

Muyllaert

Terwel

Kremer

et al. 2008

The American Journal of Pathology

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The cyclin-dependent kinase cdk5 is atypically active in postmitotic neurons and enigmatic among the kinases proposed as molecular actors in neurodegeneration. We generated transgenic mice to express p25, the N-terminally truncated p35 activator of cdk5, in forebrain under tetracycline control (TET-off). Neuronal expression of p25 (p25 ON ) caused high mortality postnatally and early in life. Mortality was completely prevented by administration of doxycycline in the drinking water of pregnant dams and litters until P42, allowing us to study the action of p25 in adult mouse forebrain. Neuronal p25 triggered neurodegeneration and also microgliosis, rapidly and intensely in hippocampus and cortex. Progressive neurodegeneration was severe with marked neuron loss, causing brain atrophy (40% loss at age 5 months) with nearly complete elimination of the hippocampus. Neurodegeneration did not involve phosphorylation of protein tau or generation of amyloid peptide. Degenerating neurons did not stain for terminal deoxynucleotidyl transferase-mediated dUTP nickend labeling or activated caspase-3 but were marked by FluoroJadeB in early stages. Diseased neurons were always closely associated with activated microglia already very early in the disease process. Primary neurons derived from p25 embryos were more prone to apoptosis than wild-type neurons, and they activated microglial cells in co-culture. The inducible p25 mice present as a model for neurodegeneration in hippocampal sclerosis and neocortical degeneration, with important contributions of activated microglia.

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“…39,40 In later stages, the compound also reacted with activated glia, similar to observations in unrelated mouse models (Ref. 53, and refs. therein).…”

Section: Type and Mechanism Of Neurodegenerationsupporting

confidence: 60%

Neurodegeneration and Neuroinflammation in cdk5/p25-Inducible Mice

Muyllaert

Terwel

Kremer

et al. 2008

The American Journal of Pathology

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“…One basic prerequisite is perfused tissue, otherwise erythrocytes will also be highlighted and interfere with signals from degenerating cells. Fluoro-Jade B is an anionic dye reportedly specific for soma and neurites of degenerating neurons under various pathologic conditions, including ischemia (Schmued and Hopkins, 2000), although there are reports that describe labeling of microglia and astrocytes under certain conditions (Damjanac et al, 2007;Saganova et al, 2006). Owing to the high sensitivity of Fluoro-Jade B, detection of degenerating neurons as early as 1.5 hours after a 90-minute MCAO in mice is possible (Liu et al, 2009).…”

Section: Light Microscopy and Macroscopymentioning

confidence: 99%

Visualizing Cell Death in Experimental Focal Cerebral Ischemia: Promises, Problems, and Perspectives

Zille

Farr

Przesdzing

et al. 2011

J Cereb Blood Flow Metab

121

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One of the hallmarks of stroke pathophysiology is the widespread death of many different types of brain cells. As our understanding of the complex disease that is stroke has grown, it is now generally accepted that various different mechanisms can result in cell damage and eventual death. A plethora of techniques is available to identify various pathological features of cell death in stroke; each has its own drawbacks and pitfalls, and most are unable to distinguish between different types of cell death, which partially explains the widespread misuse of many terms. The purpose of this review is to summarize the standard histopathological and immunohistochemical techniques used to identify various pathological features of stroke. We then discuss how these methods should be properly interpreted on the basis of what they are showing, as well as advantages and disadvantages that require consideration. As there is much interest in the visualization of stroke using noninvasive imaging strategies, we also specifically discuss how these techniques can be interpreted within the context of cell death.

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“…FluoroJade B staining reveals both the glial cells and degenerating neurons in ischemia [42] and after single injection of a neurotoxin, kainate [19], [31], [43]. Thus, a lack of Fluoro-Jade B markers on CA1 neurons in our study might be associated either with a regenerative capability of the neurons or with co-localization of the markers and Аβ that produced a "masking" effect [44]. Indeed, a population of morphologically uninjured neurons was increased on day 45 after Aβ25-35 injection (Fig.…”

Section: Discussionmentioning

confidence: 79%

“…9); this may be associated with the reversibility of neurodegenerative processes. On the other hand, given Fluoro-Jade B specificity to stain both reactive astroglia and microglia in neurodegeneration [44] it is reasonable to expect that Aβ25-35 injection was able to initiate inflammation, typical for AD [45], [46].…”

Section: Discussionmentioning

confidence: 99%

Intrahippocampal Pathways Involved in Learning/Memory Mechanisms are Affected by Intracerebral Infusions of Amyloid-β25-35 Peptide and Hydrated Fullerene C60 in Rats

Gordon

Podolski

Макарова

et al. 2017

JAD

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Please note: Changes made as a result of publishing processes such as copy-editing, formatting and page numbers may not be reflected in this version. For the definitive version of this publication, please refer to the published source. You are advised to consult the publisher's version if you wish to cite this paper.This version is being made available in accordance with publisher policies. See http://orca.cf.ac.uk/policies.html for usage policies. Copyright and moral rights for publications made available in ORCA are retained by the copyright holders. known to play a key role in learning and memory mechanisms, it is as yet unclear how its structures are involved in the EC pathology. In this study, changes in memory and neuronal morphology in male Wistar rats intrahippocampally injected with Аβ25-35 were correlated on days 14 and 45 after the injection to reveal specific cognitive -structural associations. The main focus was on the dentate gyrus (DG) and hippocampal areas of CA1 and CA3 because of their involvement in afferent flows from EC to the hippocampus through tri-synaptic (EC  DG  CA3  CA1) and/or mono-synaptic (EC  CA1) pathways. Evident memory impairments were observed at both time points after Аβ25-35 injection. However, on day 14, populations of morphological intact neurons were decreased in CA3 and, drastically, in CA1, and the DG supramedial bundle was significantly damaged. On day 45, this bundle largely and СА1 neurons partially recovered, whereas CA3 neurons remained damaged. We suggest that Аβ25-35 primarily affects the tri-synaptic pathway, destroying the granular cells in the DG supramedial area and neurons in CA3 and, through the Schaffer collaterals, in CA1.Intrahippocampal pretreatment with hydrated fullerene С60 allows the neurons and their connections to survive the amyloidosis, thus supporting the memory mechanisms.

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Fluoro-Jade® B staining as useful tool to identify activated microglia and astrocytes in a mouse transgenic model of Alzheimer's disease

Cited by 86 publications

References 39 publications

Neurodegeneration and Neuroinflammation in cdk5/p25-Inducible Mice

Neurodegeneration and Neuroinflammation in cdk5/p25-Inducible Mice

Visualizing Cell Death in Experimental Focal Cerebral Ischemia: Promises, Problems, and Perspectives

Intrahippocampal Pathways Involved in Learning/Memory Mechanisms are Affected by Intracerebral Infusions of Amyloid-β25-35 Peptide and Hydrated Fullerene C60 in Rats

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