sr-8278 and Alzheimer-Disease

sr-8278 has been researched along with Alzheimer-Disease* in 1 studies

Other Studies

1 other study(ies) available for sr-8278 and Alzheimer-Disease

Article	Year
Inhibition of REV-ERBs stimulates microglial amyloid-beta clearance and reduces amyloid plaque deposition in the 5XFAD mouse model of Alzheimer's disease. Aging cell, 2020, Volume: 19, Issue:2 A promising new therapeutic target for the treatment of Alzheimer's disease (AD) is the circadian system. Although patients with AD are known to have abnormal circadian rhythms and suffer sleep disturbances, the role of the molecular clock in regulating amyloid-beta (Aβ) pathology is still poorly understood. Here, we explored how the circadian repressors REV-ERBα and β affected Aβ clearance in mouse microglia. We discovered that, at Circadian time 4 (CT4), microglia expressed higher levels of the master clock protein BMAL1 and more rapidly phagocytosed fibrillary Aβ Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; ARNTL Transcription Factors; Cell Line; Circadian Clocks; CLOCK Proteins; Disease Models, Animal; Isoquinolines; Macrophages; Mice; Mice, Knockout; Microglia; Nuclear Receptor Subfamily 1, Group D, Member 1; Plaque, Amyloid; Receptors, Cytoplasmic and Nuclear; Receptors, Purinergic P2Y12; Repressor Proteins; RNA, Small Interfering; Synapses; Thiophenes	2020

Article

Year

Inhibition of REV-ERBs stimulates microglial amyloid-beta clearance and reduces amyloid plaque deposition in the 5XFAD mouse model of Alzheimer's disease.

Aging cell, 2020, Volume: 19, Issue:2

A promising new therapeutic target for the treatment of Alzheimer's disease (AD) is the circadian system. Although patients with AD are known to have abnormal circadian rhythms and suffer sleep disturbances, the role of the molecular clock in regulating amyloid-beta (Aβ) pathology is still poorly understood. Here, we explored how the circadian repressors REV-ERBα and β affected Aβ clearance in mouse microglia. We discovered that, at Circadian time 4 (CT4), microglia expressed higher levels of the master clock protein BMAL1 and more rapidly phagocytosed fibrillary Aβ

Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; ARNTL Transcription Factors; Cell Line; Circadian Clocks; CLOCK Proteins; Disease Models, Animal; Isoquinolines; Macrophages; Mice; Mice, Knockout; Microglia; Nuclear Receptor Subfamily 1, Group D, Member 1; Plaque, Amyloid; Receptors, Cytoplasmic and Nuclear; Receptors, Purinergic P2Y12; Repressor Proteins; RNA, Small Interfering; Synapses; Thiophenes

2020