Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid β-protein in both transfected cells and transgenic mice

1997 ◽  
Vol 3 (1) ◽  
pp. 67-72 ◽  
Author(s):  
Martin Citron ◽  
David Westaway ◽  
Weiming Xia ◽  
George Carlson ◽  
Thekla Diehl ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Transfected Cells ◽  
Β Protein

Normal Production of the Amyloid β-Protein and the Pathogenesis of Alzheimer’s Disease

1995 ◽  
pp. 95-97
Author(s):  
Dennis J. Selkoe ◽  
Christian Haass ◽  
Michael Schlossmacher ◽  
Albert Hung ◽  
Martin Citron ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Β Protein ◽  
Normal Production

scholarly journals The Alzheimer's Disease-Associated Amyloid β-Protein Is an Antimicrobial Peptide

PLoS ONE ◽  
2010 ◽  
Vol 5 (3) ◽  
pp. e9505 ◽  
Author(s):  
Stephanie J. Soscia ◽  
James E. Kirby ◽  
Kevin J. Washicosky ◽  
Stephanie M. Tucker ◽  
Martin Ingelsson ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Antimicrobial Peptide ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Β Protein

scholarly journals Amyloid-beta uptake by blood monocytes is reduced with ageing and Alzheimer’s disease

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Si-Han Chen ◽  
Ding-Yuan Tian ◽  
Ying-Ying Shen ◽  
Yuan Cheng ◽  
Dong-Yu Fan ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Blood Levels ◽  
Amyloid Β Protein ◽  
Blood Monocytes ◽  
Cognitively Normal ◽  
Β Protein ◽  
Toll Like Receptor 2 ◽  
Age And Sex

AbstractDeficits in the clearance of amyloid β-protein (Aβ) play a pivotal role in the pathogenesis of sporadic Alzheimer’s disease (AD). The roles of blood monocytes in the development of AD remain unclear. In this study, we sought to investigate the alterations in the Aβ phagocytosis function of peripheral monocytes during ageing and in AD patients. A total of 104 cognitively normal participants aged 22–89 years, 24 AD patients, 25 age- and sex-matched cognitively normal (CN) subjects, 15 Parkinson’s disease patients (PD), and 15 age- and sex-matched CN subjects were recruited. The Aβ uptake by blood monocytes was measured and its alteration during ageing and in AD patients were investigated. Aβ1-42 uptake by monocytes decreased during ageing and further decreased in AD but not in PD patients. Aβ1-42 uptake by monocytes was associated with Aβ1-42 levels in the blood. Among the Aβ uptake-related receptors and enzymes, the expression of Toll-like receptor 2 (TLR2) was reduced in monocytes from AD patients. Our findings suggest that monocytes regulate the blood levels of Aβ and might be involved in the development of AD. The recovery of the Aβ uptake function by blood monocytes represents a potential therapeutic strategy for AD.

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