Pharmacological approaches to mitigate neuroinflammation in Alzheimer’s disease
•Although neuroinflammation is a hallmark of Alzheimer’s disease, it is unclear whether it is a cause or consequence of this pathology.•Microglia and astroglia are powerful regulators of neuroinflammatory responses in Alzheimer’s disease.•Vorinostat and ORY-2001 are two epigenetic drugs under clinic...
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Veröffentlicht in: | International immunopharmacology 2020-07, Vol.84, p.106479-106479, Article 106479 |
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Sprache: | eng |
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Zusammenfassung: | •Although neuroinflammation is a hallmark of Alzheimer’s disease, it is unclear whether it is a cause or consequence of this pathology.•Microglia and astroglia are powerful regulators of neuroinflammatory responses in Alzheimer’s disease.•Vorinostat and ORY-2001 are two epigenetic drugs under clinical trials to combat Alzheimer’s pathogenesis.
Alzheimer's disease (AD) is one of the most prevalent neurodegenerative diseases characterized by the formation of extracellular amyloid beta (Aβ) plaques and intracellular neurofibrillary tangles (NFTs). Growing evidence suggested that there is an association between neuronal dysfunction and neuroinflammation (NI) in AD, coordinated by the chronic activation of astrocytes and microglial cells along with the subsequent excessive generation of the proinflammatory molecule. Therefore, a better understanding of the relationship between the nervous and immune systems is important in order to delay or avert the neurodegenerative events of AD. The inflammatory/immune pathways and the mechanisms to control these pathways may provide a novel arena to develop new drugs in order to target NI in AD. In this review, we represent the influence of cellular mediators which are involved in the NI process, with regards to the progression of AD. We also discuss the processes and the current status of multiple anti-inflammatory agents which are used in AD and have gone through or going through clinical trials. Moreover, new prospects for targeting NI in the development of AD drugs have also been highlighted. |
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ISSN: | 1567-5769 1878-1705 |
DOI: | 10.1016/j.intimp.2020.106479 |