| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Katja Scheffler, Jan Stenzel, Markus Krohn, Cathleen Lange, Jacqueline Hofrichter, Toni Schumacher, Thomas Brüning, Anne-Sophie Plath, Lary Walker, Jens Pahnk. Determination of spatial and temporal distribution of microglia by 230nm-high-resolution, high-throughput automated analysis reveals different amyloid plaque populations in an APP/PS1 mouse model of Alzheimer's disease. Current Alzheimer research. vol 8. issue 7. 2012-04-04. PMID:21244350. |
one early and prominent pathologic feature of alzheimer's disease (ad) is the appearance of activated microglia in the vicinity of developing β-amyloid deposits. |
2012-04-04 |
2023-08-12 |
mouse |
| Wenwen Sheng, Yijia Zong, Arwa Mohammad, Deepa Ajit, Jiankun Cui, Dongdong Han, Jennifer L Hamilton, Agnes Simonyi, Albert Y Sun, Zezong Gu, Jau-Shyong Hong, Gary A Weisman, Grace Y Su. Pro-inflammatory cytokines and lipopolysaccharide induce changes in cell morphology, and upregulation of ERK1/2, iNOS and sPLA₂-IIA expression in astrocytes and microglia. Journal of neuroinflammation. vol 8. 2012-03-30. PMID:21943492. |
activation of glial cells, including astrocytes and microglia, has been implicated in the inflammatory responses underlying brain injury and neurodegenerative diseases including alzheimer's and parkinson's diseases. |
2012-03-30 |
2023-08-12 |
mouse |
| Emalick G Njie, Ellen Boelen, Frank R Stassen, Harry W M Steinbusch, David R Borchelt, Wolfgang J Strei. Ex vivo cultures of microglia from young and aged rodent brain reveal age-related changes in microglial function. Neurobiology of aging. vol 33. issue 1. 2012-03-13. PMID:20580465. |
they suggest that microglial aβ phagocytosis results in aβ redistribution rather than biophysical degradation in vivo and thereby provide mechanistic insight to the lack of amyloid burden elimination by parenchymal microglia in aged adults and those suffering from alzheimer's disease. |
2012-03-13 |
2023-08-12 |
mouse |
| Hemachander Capiralla, Valérie Vingtdeux, Haitian Zhao, Roman Sankowski, Yousef Al-Abed, Peter Davies, Philippe Marambau. Resveratrol mitigates lipopolysaccharide- and Aβ-mediated microglial inflammation by inhibiting the TLR4/NF-κB/STAT signaling cascade. Journal of neurochemistry. vol 120. issue 3. 2012-02-24. PMID:22118570. |
activation of microglia, the resident macrophages of the brain, around the amyloid plaques is a key hallmark of alzheimer's disease (ad). |
2012-02-24 |
2023-08-12 |
mouse |
| Min Song, Jingji Jin, Jeong-Eun Lim, Jinghong Kou, Abhinandan Pattanayak, Jamaal A Rehman, Hong-Duck Kim, Kazuki Tahara, Robert Lalonde, Ken-ichiro Fukuch. TLR4 mutation reduces microglial activation, increases Aβ deposits and exacerbates cognitive deficits in a mouse model of Alzheimer's disease. Journal of neuroinflammation. vol 8. 2012-02-23. PMID:21827663. |
amyloid plaques, a pathological hallmark of alzheimer's disease (ad), are accompanied by activated microglia. |
2012-02-23 |
2023-08-12 |
mouse |
| Sang-Ho Choi, Saba Aid, Hyung-Wook Kim, Sharon H Jackson, Francesca Bosett. Inhibition of NADPH oxidase promotes alternative and anti-inflammatory microglial activation during neuroinflammation. Journal of neurochemistry. vol 120. issue 2. 2012-02-09. PMID:22050439. |
moreover, we showed a shift in redox state towards an oxidized milieu and that subpopulations of microglia retain their detrimental phenotype in alzheimer's disease brains. |
2012-02-09 |
2023-08-12 |
mouse |
| Massimiliano M Corsi, Federico Licastro, Elisa Porcellini, Giada Dogliotti, Emanuela Galliera, John L Lamont, Paul J Innocenzi, Stephen P Fitzgeral. Reduced plasma levels of P-selectin and L-selectin in a pilot study from Alzheimer disease: relationship with neuro-degeneration. Biogerontology. vol 12. issue 5. 2012-01-30. PMID:21484243. |
neurodegenerative processes associated with alzheimer's disease (ad) are accompanied by reactive astrogliosis and microglia activation and a role for chronic inflammation in the brain degeneration of these patients has been suggested. |
2012-01-30 |
2023-08-12 |
Not clear |
| Tetsuya Mizuno, Yukiko Doi, Hiroyuki Mizoguchi, Shijie Jin, Mariko Noda, Yoshifumi Sonobe, Hideyuki Takeuchi, Akio Suzumur. Interleukin-34 selectively enhances the neuroprotective effects of microglia to attenuate oligomeric amyloid-β neurotoxicity. The American journal of pathology. vol 179. issue 4. 2012-01-23. PMID:21872563. |
microglia, macrophage-like resident immune cells in the brain, possess both neurotoxic and neuroprotective properties and have a critical role in the development of alzheimer's disease (ad). |
2012-01-23 |
2023-08-12 |
mouse |
| Rea Pihlaja, Jari Koistinaho, Riitta Kauppinen, Jouko Sandholm, Heikki Tanila, Milla Koistinah. Multiple cellular and molecular mechanisms are involved in human Aβ clearance by transplanted adult astrocytes. Glia. vol 59. issue 11. 2012-01-06. PMID:21826742. |
astrocytes and microglia are able to degrade potentially neurotoxic β-amyloid (aβ) deposits typical for alzheimer's disease (ad) pathology. |
2012-01-06 |
2023-08-12 |
mouse |
| Mohammed Kouadir, Lifeng Yang, Jian Tu, Xiaomin Yin, Xiangmei Zhou, Deming Zha. Comparison of mRNA expression patterns of class B scavenger receptors in BV2 microglia upon exposure to amyloidogenic fragments of beta-amyloid and prion proteins. DNA and cell biology. vol 30. issue 11. 2011-12-20. PMID:21631281. |
the inflammatory responses in alzheimer's disease and prion diseases are dominated by microglia activation. |
2011-12-20 |
2023-08-12 |
Not clear |
| Nootchanat Mairuae, James R Connor, Poonlarp Cheepsunthor. Increased cellular iron levels affect matrix metalloproteinase expression and phagocytosis in activated microglia. Neuroscience letters. vol 500. issue 1. 2011-12-14. PMID:21683124. |
regardless of disease-specific etiology, iron accumulation, particularly in activated microglia, is a notable feature associated with a series of neuropathologies, including alzheimer's diseases. |
2011-12-14 |
2023-08-12 |
rat |
| Ashutosh, Wei Kou, Robin Cotter, Kathleen Borgmann, Li Wu, Raisa Persidsky, Namita Sakhuja, Anuja Ghorpad. CXCL8 protects human neurons from amyloid-β-induced neurotoxicity: relevance to Alzheimer's disease. Biochemical and biophysical research communications. vol 412. issue 4. 2011-11-22. PMID:21840299. |
alzheimer's disease (ad) is a neurodegenerative disease characterized by amyloid-β (aβ) deposition in senile plaques colocalized with activated microglia and astrocytes. |
2011-11-22 |
2023-08-12 |
human |
| Hideyuki Takeuchi, Hiroyuki Mizoguchi, Yukiko Doi, Shijie Jin, Mariko Noda, Jianfeng Liang, Hua Li, Yan Zhou, Rarami Mori, Satoko Yasuoka, Endong Li, Bijay Parajuli, Jun Kawanokuchi, Yoshifumi Sonobe, Jun Sato, Koji Yamanaka, Gen Sobue, Tetsuya Mizuno, Akio Suzumur. Blockade of gap junction hemichannel suppresses disease progression in mouse models of amyotrophic lateral sclerosis and Alzheimer's disease. PloS one. vol 6. issue 6. 2011-11-21. PMID:21712989. |
glutamate released by activated microglia induces excitotoxic neuronal death, which likely contributes to non-cell autonomous neuronal death in neurodegenerative diseases, including amyotrophic lateral sclerosis and alzheimer's disease. |
2011-11-21 |
2023-08-12 |
mouse |
| Tom Schilling, Claudia Ede. Amyloid-β-induced reactive oxygen species production and priming are differentially regulated by ion channels in microglia. Journal of cellular physiology. vol 226. issue 12. 2011-11-14. PMID:21321937. |
in summary, our data suggest that in microglia aβ-induced ros production and priming are differentially regulated by ion channels, and that trpv1 cation channels and kv1.3 k(+) channels may provide potential therapeutic targets to reduce microglia-induced oxidative stress in alzheimer's disease. |
2011-11-14 |
2023-08-12 |
Not clear |
| Jelena Skuljec, Hui Sun, Refik Pul, Karelle Bénardais, Daniela Ragancokova, Darius Moharregh-Khiabani, Alexandra Kotsiari, Corinna Trebst, Martin Stange. CCL5 induces a pro-inflammatory profile in microglia in vitro. Cellular immunology. vol 270. issue 2. 2011-10-14. PMID:21620385. |
the chemokine receptors ccr1, ccr2, ccr3, ccr5, and cxcr2 have been found to be expressed on microglia in many neurodegenerative diseases, such as multiple sclerosis and alzheimer's disease. |
2011-10-14 |
2023-08-12 |
rat |
| Alexander Mildner, Bernhard Schlevogt, Katrin Kierdorf, Chotima Böttcher, Daniel Erny, Markus P Kummer, Michael Quinn, Wolfgang Brück, Ingo Bechmann, Michael T Heneka, Josef Priller, Marco Prin. Distinct and non-redundant roles of microglia and myeloid subsets in mouse models of Alzheimer's disease. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 31. issue 31. 2011-10-11. PMID:21813677. |
distinct and non-redundant roles of microglia and myeloid subsets in mouse models of alzheimer's disease. |
2011-10-11 |
2023-08-12 |
mouse |
| Alexander Mildner, Bernhard Schlevogt, Katrin Kierdorf, Chotima Böttcher, Daniel Erny, Markus P Kummer, Michael Quinn, Wolfgang Brück, Ingo Bechmann, Michael T Heneka, Josef Priller, Marco Prin. Distinct and non-redundant roles of microglia and myeloid subsets in mouse models of Alzheimer's disease. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 31. issue 31. 2011-10-11. PMID:21813677. |
mononuclear phagocytes are important modulators of alzheimer's disease (ad), but the specific functions of resident microglia, bone marrow-derived mononuclear cells, and perivascular macrophages have not been resolved. |
2011-10-11 |
2023-08-12 |
mouse |
| Caroline C Rodger. Dental X-ray exposure and Alzheimer's disease: a hypothetical etiological association. Medical hypotheses. vol 77. issue 1. 2011-09-26. PMID:21458164. |
degenerated microglia lose their neuroprotective properties, resulting in the formation of neurofibrillary tau tangles and consequently, the neuronal death that causes alzheimer's dementia. |
2011-09-26 |
2023-08-12 |
human |
| Caroline C Rodger. Dental X-ray exposure and Alzheimer's disease: a hypothetical etiological association. Medical hypotheses. vol 77. issue 1. 2011-09-26. PMID:21458164. |
the hypothesis that alzheimer's is caused specifically by microglia telomere damage would explain the delay of one decade or longer between the presence of alzheimer's brain pathology and symptoms; telomere damage would not cause any change in microglial function, it would just reset the countdown clock so that senescence and apoptosis occurred earlier than they would have without the environmental insult. |
2011-09-26 |
2023-08-12 |
human |
| Caroline C Rodger. Dental X-ray exposure and Alzheimer's disease: a hypothetical etiological association. Medical hypotheses. vol 77. issue 1. 2011-09-26. PMID:21458164. |
if microglia telomere damage is causing alzheimer's disease, self-donated bone marrow or dental pulp stem cell transplants could give rise to new microglia populations that would maintain neuronal health while the original resident microglia population died. |
2011-09-26 |
2023-08-12 |
human |