scholarly journals Platelet APP‐ratio correlates with CSF levels of Aβ1‐42 in Alzheimer’s disease patients

2020 ◽  
Vol 16 (S5) ◽  
Author(s):  
Tamires Alves Sarno ◽  
Leda Leme Talib ◽  
Helena Passarelli Giroud Joaquim ◽  
Marcia Radanovic ◽  
Jessyka Maria de França Bram ◽  
...  
2020 ◽  
Vol 16 (S4) ◽  
Author(s):  
Francois Mouton‐Liger ◽  
Julien Dumurgier ◽  
Emmanuel Cognat ◽  
Claire Hourregue ◽  
Henrik Zetterberg ◽  
...  

2008 ◽  
Vol 4 ◽  
pp. T543-T543
Author(s):  
Sandra D. Mulder ◽  
Hans A. Heijst ◽  
Cees Mulder ◽  
Hilde M. Dijstelbloem ◽  
C. Erik Hack ◽  
...  

2009 ◽  
Vol 24 (3) ◽  
pp. 183-190 ◽  
Author(s):  
Heike Kölsch ◽  
Dieter Lütjohann ◽  
Frank Jessen ◽  
Julius Popp ◽  
Frank Hentschel ◽  
...  

AbstractBackgroundCholesterol 24S-hydroxylase (CYP46) catalyzes the conversion of cholesterol to 24S-hydroxycholesterol, the primary cerebral cholesterol elimination product. Only few gene variations in CYP46 gene (CYP46A1) have been investigated for their relevance as genetic risk factors of Alzheimer’s disease (AD) and results are contradictory.MethodsWe performed a gene variability screening in CYP46A1 and investigated the effect of gene variants on the risk of AD and on CSF levels of cholesterol and 24S-hydroxycholesterol.ResultsTwo of the identified 16 SNPs in CYP46A1 influenced AD risk in our study (rs7157609: p = 0.016; rs4900442: p = 0.019). The interaction term of both SNPs was also associated with an increased risk of AD (p = 0.006). Haplotypes including both SNPs were calculated and haplotype G–C was identified to influence the risk of AD (p = 0.005). AD patients and non-demented controls, who were carriers of the G–C haplotype, presented with reduced CSF levels of 24S-hydroxycholesterol (p = 0.001) and cholesterol (p < 0.001).ConclusionOur results suggest that CYP46A1 gene variations might act as risk factor for AD via an influence on brain cholesterol metabolism.


2010 ◽  
Vol 22 (3) ◽  
pp. 861-871 ◽  
Author(s):  
Mouhammad Motawaj ◽  
Katell Peoc'h ◽  
Jacques Callebert ◽  
Jean-Michel Arrang

2020 ◽  
Vol 21 (14) ◽  
pp. 5110
Author(s):  
Tiziana Casoli ◽  
Cinzia Giuli ◽  
Marta Balietti ◽  
Paolo Fabbietti ◽  
Fiorenzo Conti

In patients with Alzheimer’s disease (AD), synaptic plasticity seems to be involved in cognitive improvement induced by cognitive training. The platelet amyloid precursor protein (APP) ratio (APPr), i.e., the ratio between two APP isoforms, may be a useful peripheral biomarker to investigate synaptic plasticity pathways. This study evaluates the changes in neuropsychological/cognitive performance and APPr induced by cognitive training in AD patients participating in the “My Mind Project”. Neuropsychological/cognitive variables and APPr were evaluated in the trained group (n = 28) before a two-month experimental protocol, immediately after its termination at follow-up 1 (FU1), after 6 months at follow-up 2 (FU2), and after 24 months at follow-up 3 (FU3). The control group (n = 31) received general psychoeducational training for two months. Some memory and attention parameters were significantly improved in trained vs. control patients at FU1 and FU2 compared to baseline (Δ values). At FU3, APPr and Mini Mental State Examination (MMSE) scores decreased in trained patients. Δ APPr correlated significantly with the Δ scores of (i) MMSE at FU1, (ii) the prose memory test at FU2, and (iii) Instrumental Activities of Daily Living (IADL), the semantic word fluency test, Clinical Dementia Rating (CDR), and the attentive matrices test at FU3. Our data demonstrate that the platelet APPr correlates with key clinical variables, thereby proving that it may be a reliable biomarker of brain function in AD patients.


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