scholarly journals Correction of microtubule defects within Aβ plaque‐associated dystrophic axons results in lowered Aβ release and plaque deposition

2020 ◽  
Vol 16 (10) ◽  
pp. 1345-1357
Author(s):  
Yuemang Yao ◽  
Goodwell Nzou ◽  
Thibault Alle ◽  
Wangchen Tsering ◽  
Shaniya Maimaiti ◽  
...  
Keyword(s):  
Dystrophic Axons ◽  
Plaque Deposition

The Role of Mitochondria in the Genesis of Neuroaxonal Dystrophy in the Brains of Aging Mice

1975 ◽  
Vol 33 ◽  
pp. 372-373
Author(s):  
J.E. Johnson
Keyword(s):  
Electron Microscopy ◽  
Present Report ◽  
Light And Electron Microscopy ◽  
Dorsal Column ◽  
Neuroaxonal Dystrophy ◽  
Nucleus Gracilis ◽  
Dystrophic Axons ◽  
The Brain ◽  
Nucleus Cuneatus

Although neuroaxonal dystrophy (NAD) has been examined by light and electron microscopy for years, the nature of the components in the dystrophic axons is not well understood. The present report examines nucleus gracilis and cuneatus (the dorsal column nuclei) in the brain stem of aging mice.Mice (C57BL/6J) were sacrificed by aldehyde perfusion at ages ranging from 3 months to 23 months. Several brain areas and parts of other organs were processed for electron microscopy.At 3 months of age, very little evidence of NAD can be discerned by light microscopy. At the EM level, a few axons are found to contain dystrophic material. By 23 months of age, the entire nucleus gracilis is filled with dystrophic axons. Much less NAD is seen in nucleus cuneatus by comparison. The most recurrent pattern of NAD is an enlarged profile, in the center of which is a mass of reticulated material (reticulated portion; or RP).

scholarly journals Impact of Gut Microbiome Manipulation in 5xFAD Mice on Alzheimer’s Disease-Like Pathology

2021 ◽  
Vol 9 (4) ◽  
pp. 815
Author(s):  
Malena dos Santos Guilherme ◽  
Vu Thu Thuy Nguyen ◽  
Christoph Reinhardt ◽  
Kristina Endres
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Gut Microbiome ◽  
Microbial Composition ◽  
Aβ Peptides ◽  
Plaque Deposition ◽  
Glycation End Products ◽  
Plaque Load ◽  
5Xfad Mice ◽  
Building Capability

The gut brain axis seems to modulate various psychiatric and neurological disorders such as Alzheimer’s disease (AD). Growing evidence has led to the assumption that the gut microbiome might contribute to or even present the nucleus of origin for these diseases. In this regard, modifiers of the microbial composition might provide attractive new therapeutics. Aim of our study was to elucidate the effect of a rigorously changed gut microbiome on pathological hallmarks of AD. 5xFAD model mice were treated by antibiotics or probiotics (L. acidophilus and L. rhamnosus) for 14 weeks. Pathogenesis was measured by nest building capability and plaque deposition. The gut microbiome was affected as expected: antibiotics significantly reduced viable commensals, while probiotics transiently increased Lactobacillaceae. Nesting score, however, was only improved in antibiotics-treated mice. These animals additionally displayed reduced plaque load in the hippocampus. While various physiological parameters were not affected, blood sugar was reduced and serum glucagon level significantly elevated in the antibiotics-treated animals together with a reduction in the receptor for advanced glycation end products RAGE—the inward transporter of Aβ peptides of the brain. Assumedly, the beneficial effect of the antibiotics was based on their anti-diabetic potential.

Early Bioprosthetic Valve Deterioration After Carcinoid Plaque Deposition

2009 ◽  
Vol 87 (1) ◽  
pp. 321 ◽  
Author(s):  
Javier G. Castillo ◽  
Farzan Filsoufi ◽  
Parwis B. Rahmanian ◽  
Jerome S. Zacks ◽  
Richard R.P. Warner ◽  
...  
Keyword(s):  
Bioprosthetic Valve ◽  
Plaque Deposition

P1-033: Cognitive deficits and plaque deposition in a gene-targeted mouse model of Alzheimer's disease

2009 ◽  
Vol 5 (4S_Part_6) ◽  
pp. P181-P181
Author(s):  
John Ciallella ◽  
Heather Hain ◽  
Bryan Strenkowski ◽  
Michelle Hogga ◽  
Stacey Galvin ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Cognitive Deficits ◽  
Plaque Deposition ◽  
Model Of Alzheimer’S Disease

Laser microdissection reveals regional and cellular differences in GFAP mRNA upregulation following brain injury, axonal denervation, and amyloid plaque deposition

Glia ◽  
2004 ◽  
Vol 48 (1) ◽  
pp. 76-84 ◽  
Author(s):  
Guido J. Burbach ◽  
Doris Dehn ◽  
Domenico Del Turco ◽  
Matthias Staufenbiel ◽  
Thomas Deller
Keyword(s):  
Brain Injury ◽  
Laser Microdissection ◽  
Amyloid Plaque ◽  
Plaque Deposition

scholarly journals Caspase-1/IL-1β represses membrane transport of GluA1 by inhibiting the interaction between Stargazin and GluA1 in Alzheimer’s disease

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Xunhu Gu ◽  
Hanjun Wu ◽  
Yuqin Xie ◽  
Lijun Xu ◽  
Xu Liu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Membrane Transport ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Senile Plaque ◽  
Spatial Learning And Memory ◽  
Memory Ability ◽  
Caspase 1 ◽  
Plaque Deposition

Abstract Background Alzheimer's disease is a neurodegenerative disease. Previous study has reported that caspase-1/IL-1β is closely associated with Alzheimer's disease. However, the biological role of caspase-1/IL-1β in Alzheimer's disease has not been fully elucidated. This study aimed to explore the mechanism of action of caspase-1/IL-1β in Alzheimer's disease. Methods Mouse hippocampal neurones were treated with Aβ1-42 to induce Alzheimer's disease cell model. APP/PS1 mice and Aβ1-42-induced hippocampal neurones were treated with AC-YVAD-CMK (caspase-1 inhibitor). Spatial learning and memory ability of mice were detected by morris water maze. Flow cytometry, TUNEL staining, Thioflavin S staining and immunohistochemistry were performed to examine apoptosis and senile plaque deposition. Enzyme linked immunosorbent assay and western blot were performed to assess the levels of protein or cytokines. Co-Immunoprecipitation was performed to verify the interaction between Stargazin and GluA1. Results AC-YVAD-CMK treatment improved spatial learning and memory ability and reduced senile plaque deposition of APP/PS1 mice. Moreover, AC-YVAD-CMK promoted membrane transport of GluA1 in APP/PS1 mice. In vitro, Aβ1-42-induced hippocampal neurones exhibited an increase in apoptosis and a decrease in the membrane transport of GluA1, which was abolished by AC-YVAD-CMK treatment. In addition, Stargazin interacted with GluA1, which was repressed by caspase-1. Caspase-1/IL-1β inhibited membrane transport of GluA1 by inhibiting the interaction between Stargazin and GluA1. Conclusions Our data demonstrate that caspase-1/IL-1β represses membrane transport of GluA1 by inhibiting the interaction between Stargazin in Alzheimer's disease. Thus, caspase-1/IL-1β may be a target for Alzheimer's disease treatment.

scholarly journals α-1-Antichymotrypsin Promotes β-Sheet Amyloid Plaque Deposition in a Transgenic Mouse Model of Alzheimer's Disease

2001 ◽  
Vol 21 (5) ◽  
pp. 1444-1451 ◽  
Author(s):  
Lars N. G. Nilsson ◽  
Kelly R. Bales ◽  
Giovanni DiCarlo ◽  
Marcia N. Gordon ◽  
Dave Morgan ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Amyloid Plaque ◽  
Transgenic Mouse Model ◽  
Plaque Deposition ◽  
Model Of Alzheimer’S Disease ◽  
Β Sheet

Vaccination with a non-human sequence amyloid oligomer mimic results in improved cognitive function and reduced plaque deposition in Tg2576 mice

2011 ◽  
Vol 71 ◽  
pp. e85-e86
Author(s):  
Suhail Rasool ◽  
Hilda Martinez Coria ◽  
Leonoid Breydo ◽  
Jessica Wu ◽  
Saskia Milton ◽  
...  
Keyword(s):  
Cognitive Function ◽  
Plaque Deposition ◽  
Human Sequence ◽  
Tg2576 Mice ◽  
Amyloid Oligomer
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