scholarly journals Genetic Association Study on Colony-Stimulating Factor 1 in Alzheimer’s Disease

2006 ◽  
Vol 3 (6) ◽  
pp. 334-337 ◽  
Author(s):  
M. Axel Wollmer ◽  
Roger M. Nitsch ◽  
Christoph Hock ◽  
Andreas Papassotiropoulos
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Association Study ◽  
Genetic Association ◽  
Genetic Association Study ◽  
Colony Stimulating Factor ◽  
Stimulating Factor

PLCG2 rs72824905 Variant Reduces the Risk of Alzheimer’s Disease and Multiple Sclerosis

2021 ◽  
pp. 1-7
Author(s):  
Fan Chen ◽  
Yan Zhang ◽  
Longcai Wang ◽  
Tao Wang ◽  
Zhifa Han ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Association Study ◽  
Genetic Association ◽  
Genetic Association Study ◽  
Large Scale

We aimed to evaluate the association of PLCG2 rs72824905 variant with Alzheimer’s disease (AD) and multiple sclerosis (MS) using large-scale genetic association study datasets. We selected 50,024 AD cases and 467,330 controls, and 32,367 MS cases and 36,012 controls. We found moderate heterogeneity of rs72824905 in different studies. We found significant association between rs72824905 G allele and reduced AD risk (OR = 0.66, 95% CI 0.59–0.74, p = 5.91E-14). Importantly, rs72824905 G allele could also significantly reduce the risk of MS with OR = 0.94, p = 3.63E-05. Hence, the effects of rs72824905 on AD and MS are consistent.

Cardiovascular risk factors and Alzheimer's disease: a genetic association study in a population aged 85 or over

2000 ◽  
Vol 292 (3) ◽  
pp. 195-198 ◽  
Author(s):  
Liisa Myllykangas ◽  
Tuomo Polvikoski ◽  
Raimo Sulkava ◽  
Auli Verkkoniemi ◽  
Pentti Tienari ◽  
...  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cardiovascular Risk ◽  
Association Study ◽  
Cardiovascular Risk Factors ◽  
Genetic Association ◽  
Genetic Association Study

Ubc9 gene polymorphisms and late-onset Alzheimer's disease in the Korean population: A genetic association study

2009 ◽  
Vol 465 (3) ◽  
pp. 272-275 ◽  
Author(s):  
Kyungsook Ahn ◽  
Ju Hee Song ◽  
Doh Kwan Kim ◽  
Moon Ho Park ◽  
Sangmee A. Jo ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Association Study ◽  
Genetic Association ◽  
Gene Polymorphisms ◽  
Genetic Association Study ◽  
Late Onset ◽  
Korean Population

P3-204: Genetic association study to the amyloid plaque-associated protein gene COL25A1 in Alzheimer's disease

2008 ◽  
Vol 4 ◽  
pp. T580-T580
Author(s):  
Behnosh F. Bjork ◽  
Charlotte Forsell ◽  
Lena Lilius ◽  
Karin Axelman ◽  
Susanne Froelich Fabre ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Association Study ◽  
Genetic Association ◽  
Genetic Association Study ◽  
Protein Gene ◽  
Amyloid Plaque

Amyloid β Protein Deposition in Osteopetrotic (op/op) Mice Is Reduced by Injections of Macrophage Colony Stimulating Factor

2005 ◽  
Vol 33 (6) ◽  
pp. 654-660 ◽  
Author(s):  
T Kawata ◽  
K Tsutsui ◽  
S Kohno ◽  
M Kaku ◽  
T Fujita ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Microglial Cell ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Colony Stimulating Factor ◽  
Β Protein ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

The deposition of amyloid β (Aβ) protein is a neuropathological change that characterizes Alzheimer's disease. Animals with the osteopetrosis (op/op) mutation suffer from a general skeletal sclerosis, a significantly reduced number of macrophages and osteoclasts in various tissues, and have no systemic macrophage colony stimulating factor (M-CSF). This study examined the effect that M-CSF injections had on Aβ deposition and microglial cell distribution in the brains of normal and op/op mice. Aβ-positive plaques were detected in the cerebral cortex of op/op mice, but not in normal mice. M-CSF reduced the numbers of Aβ-positive plaques in op/op mice. The microglial cell population was reduced in op/op mice compared with normal mice, and M-CSF increased the numbers to 65.8% of that observed in normal mice. Our results suggest that a clearer understanding of the role that microglial cells play in Aβ deposition may help determine the mechanisms involved in the pathogenesis of Alzheimer's disease.

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