Literature DB >> 19747160

Microglial activation in Alzheimer's disease.

Johannes C M Schlachetzki1, Michael Hüll.   

Abstract

Alzheimer's disease (AD) is a devastating chronic neurodegenerative disease with currently no available disease modifying treatment. In recent years, the peptide amyloid-beta has been proposed as the major pathogenic force in the development and progression of AD. Microglia, the resident immune and phagocytic cells of the brain, are known to constantly scan brain tissue and to respond to various pathological stimuli. Thus, newly formed plaque composed of A beta seem to activate and recruit microglia in AD transgenic mice. However, the role of microglia is only poorly understood in AD. Microglia may act as a double-edged sword being either detrimental or protective depending on the context. In this mini-review, we discuss the importance of microglia and its receptors in neuroinflammation and plaque clearance. A possible disease modifying role of blood-borne monocytes, which are close relatives of bone-marrow derived microglia, will also be addressed.

Entities:  

Mesh:

Substances:

Year:  2009        PMID: 19747160     DOI: 10.2174/156720509790147179

Source DB:  PubMed          Journal:  Curr Alzheimer Res        ISSN: 1567-2050            Impact factor:   3.498


  37 in total

Review 1.  Microglial priming in Alzheimer's disease.

Authors:  Jun-Wei Li; Yu Zong; Xi-Peng Cao; Lin Tan; Lan Tan
Journal:  Ann Transl Med       Date:  2018-05

Review 2.  Anesthetic modulation of neuroinflammation in Alzheimer's disease.

Authors:  Junxia X Tang; Maryellen F Eckenhoff; Roderic G Eckenhoff
Journal:  Curr Opin Anaesthesiol       Date:  2011-08       Impact factor: 2.706

Review 3.  Purinergic receptors as potential therapeutic targets in Alzheimer's disease.

Authors:  Lucas T Woods; Deepa Ajit; Jean M Camden; Laurie Erb; Gary A Weisman
Journal:  Neuropharmacology       Date:  2015-10-28       Impact factor: 5.250

4.  Optical and SPION-enhanced MR imaging shows that trans-stilbene inhibitors of NF-κB concomitantly lower Alzheimer's disease plaque formation and microglial activation in AβPP/PS-1 transgenic mouse brain.

Authors:  Nathan O Solberg; Ryan Chamberlin; Jenette R Vigil; Lorraine M Deck; John E Heidrich; David C Brown; Christina I Brady; Thomas A Vander Jagt; Michael Garwood; Marco Bisoffi; Virginia Severns; David L Vander Jagt; Laurel O Sillerud
Journal:  J Alzheimers Dis       Date:  2014       Impact factor: 4.472

5.  Selective acetyl- and butyrylcholinesterase inhibitors reduce amyloid-β ex vivo activation of peripheral chemo-cytokines from Alzheimer's disease subjects: exploring the cholinergic anti-inflammatory pathway.

Authors:  Marcella Reale; Marta Di Nicola; Lucia Velluto; Chiara D'Angelo; Erica Costantini; Debomoy K Lahiri; Mohammad A Kamal; Qian-sheng Yu; Nigel H Greig
Journal:  Curr Alzheimer Res       Date:  2014       Impact factor: 3.498

Review 6.  Monocytes and Alzheimer's disease.

Authors:  Yu Feng; Lei Li; Xiao-Hong Sun
Journal:  Neurosci Bull       Date:  2011-04       Impact factor: 5.203

7.  Reduction of β-amyloid deposits by γ-secretase inhibitor is associated with the attenuation of secondary damage in the ipsilateral thalamus and sensory functional improvement after focal cortical infarction in hypertensive rats.

Authors:  Yusheng Zhang; Shihui Xing; Jian Zhang; Jingjing Li; Chuo Li; Zhong Pei; Jinsheng Zeng
Journal:  J Cereb Blood Flow Metab       Date:  2010-08-04       Impact factor: 6.200

8.  SPION-enhanced magnetic resonance imaging of Alzheimer's disease plaques in AβPP/PS-1 transgenic mouse brain.

Authors:  Laurel O Sillerud; Nathan O Solberg; Ryan Chamberlain; Robert A Orlando; John E Heidrich; David C Brown; Christina I Brady; Thomas A Vander Jagt; Michael Garwood; David L Vander Jagt
Journal:  J Alzheimers Dis       Date:  2013       Impact factor: 4.472

9.  Transcriptomic responses in mouse brain exposed to chronic excess of the neurotransmitter glutamate.

Authors:  Xinkun Wang; Xiaodong Bao; Ranu Pal; Abdulbaki Agbas; Elias K Michaelis
Journal:  BMC Genomics       Date:  2010-06-07       Impact factor: 3.969

10.  Neuroinflammation in Lyme neuroborreliosis affects amyloid metabolism.

Authors:  Niklas Mattsson; Daniel Bremell; Rolf Anckarsäter; Kaj Blennow; Henrik Anckarsäter; Henrik Zetterberg; Lars Hagberg
Journal:  BMC Neurol       Date:  2010-06-22       Impact factor: 2.474

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.