Intercellular cross-talk curbs Alzheimer’s disease

2021 ◽  
Vol 14 (694) ◽  
pp. eabl7096
Author(s):  
John F. Foley
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Cross Talk ◽  
Model Of Alzheimer’S Disease ◽  
Amyloid Aggregates ◽  
Β Amyloid

Astrocyte-derived IL-3 activates microglia to clear β-amyloid aggregates in a mouse model of Alzheimer’s disease.

scholarly journals P3-270: CHF5074 reduces brain β-amyloid burden and hyperphosphorylated tau in a mouse model of Alzheimer's disease

2009 ◽  
Vol 5 (4S_Part_14) ◽  
pp. P422-P422
Author(s):  
M. Pizzi ◽  
A. Lanzillotta ◽  
B.P. Imbimbo ◽  
B. Hutter-Paier ◽  
G. Villetti ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Hyperphosphorylated Tau ◽  
Amyloid Burden ◽  
Model Of Alzheimer’S Disease ◽  
Β Amyloid

scholarly journals A ketogenic diet improves motor performance but does not affect β-amyloid levels in a mouse model of Alzheimer's Disease

2013 ◽  
Vol 1505 ◽  
pp. 61-67 ◽  
Author(s):  
Tina L. Beckett ◽  
Christa M. Studzinski ◽  
Jeffrey N. Keller ◽  
M. Paul Murphy ◽  
Dana M. Niedowicz
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Ketogenic Diet ◽  
Motor Performance ◽  
Model Of Alzheimer’S Disease ◽  
Β Amyloid

scholarly journals Methionine sulfoxide reductase A affects β-amyloid solubility and mitochondrial function in a mouse model of Alzheimer's disease

2016 ◽  
Vol 310 (6) ◽  
pp. E388-E393 ◽  
Author(s):  
Jackob Moskovitz ◽  
Fang Du ◽  
Connor F. Bowman ◽  
Shirley S. Yan
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Methionine Sulfoxide ◽  
Methionine Sulfoxide Reductase ◽  
Methionine Sulfoxide Reductase A ◽  
Model Of Alzheimer’S Disease ◽  
Amyloid Aβ ◽  
Β Amyloid

Accumulation of oxidized proteins, and especially β-amyloid (Aβ), is thought to be one of the common causes of Alzheimer's disease (AD). The current studies determine the effect of an in vivo methionine sulfoxidation of Aβ through ablation of the methionine sulfoxide reductase A (MsrA) in a mouse model of AD, a mouse that overexpresses amyloid precursor protein (APP) and Aβ in neurons. Lack of MsrA fosters the formation of methionine sulfoxide in proteins, and thus its ablation in the AD-mouse model will increase the formation of methionine sulfoxide in Aβ. Indeed, the novel MsrA-deficient APP mice ( APP+/ MsrAKO) exhibited higher levels of soluble Aβ in brain compared with APP+ mice. Furthermore, mitochondrial respiration and the activity of cytochrome c oxidase were compromised in the APP+/ MsrAKO compared with control mice. These results suggest that lower MsrA activity modifies Aβ solubility properties and causes mitochondrial dysfunction, and augmenting its activity may be beneficial in delaying AD progression.

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