Mass spectrometric identification of citrullination sites and immunohistochemical detection of citrullinated glial fibrillary acidic protein in Alzheimer's disease brains

2015 ◽  
Vol 93 (11) ◽  
pp. 1664-1674 ◽  
Author(s):  
Akihito Ishigami ◽  
Hirofumi Masutomi ◽  
Setsuko Handa ◽  
Megumi Nakamura ◽  
Shuuichi Nakaya ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Glial Fibrillary Acidic Protein ◽  
Mass Spectrometric ◽  
Acidic Protein ◽  
Immunohistochemical Detection ◽  
Spectrometric Identification ◽  
Mass Spectrometric Identification

scholarly journals Glial fibrillary acidic protein isoform expression in plaque related astrogliosis in Alzheimer's disease

2014 ◽  
Vol 35 (3) ◽  
pp. 492-510 ◽  
Author(s):  
Willem Kamphuis ◽  
Jinte Middeldorp ◽  
Lieneke Kooijman ◽  
Jacqueline A. Sluijs ◽  
Evert-Jan Kooi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Glial Fibrillary Acidic Protein ◽  
Acidic Protein ◽  
Protein Isoform ◽  
Isoform Expression

P4-216 Proteomic analysis of glial fibrillary acidic protein in Alzheimer's disease brain

2004 ◽  
Vol 25 ◽  
pp. S536-S537
Author(s):  
Minna A. Korolainen ◽  
Seppo Auriola ◽  
Tuula Nyman ◽  
Irina Alafuzoff ◽  
Tuula Pirttilä
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Glial Fibrillary Acidic Protein ◽  
Proteomic Analysis ◽  
Acidic Protein

Proteomic analysis of glial fibrillary acidic protein in Alzheimer's disease and aging brain

2005 ◽  
Vol 20 (3) ◽  
pp. 858-870 ◽  
Author(s):  
Minna A. Korolainen ◽  
Seppo Auriola ◽  
Tuula A. Nyman ◽  
Irina Alafuzoff ◽  
Tuula Pirttilä
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Glial Fibrillary Acidic Protein ◽  
Proteomic Analysis ◽  
Acidic Protein ◽  
Aging Brain

Glial fibrillary acidic protein and Alzheimer's disease

1985 ◽  
Vol 10 (12) ◽  
pp. 1567-1576 ◽  
Author(s):  
S. Scott Panter ◽  
John D. McSwigan ◽  
John R. Sheppard ◽  
Carolyn R. Emory ◽  
William H. Frey
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Glial Fibrillary Acidic Protein ◽  
Acidic Protein

scholarly journals Plasma glial fibrillary acidic protein is an early and specific marker of amyloid‐β pathology in Alzheimer’s disease

2021 ◽  
Vol 17 (S5) ◽  
Author(s):  
Joana B. Pereira ◽  
Shorena Janelidze ◽  
Ruben Smith ◽  
Niklas Mattsson‐Carlgren ◽  
Sebastian Palmqvist ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Glial Fibrillary Acidic Protein ◽  
Amyloid Β ◽  
Acidic Protein ◽  
Specific Marker

scholarly journals Plasma glial fibrillary acidic protein is an early marker of Aβ pathology in Alzheimer’s disease

2021 ◽  
Author(s):  
Joana B. Pereira ◽  
Shorena Janelidze ◽  
Ruben Smith ◽  
Niklas Mattsson-Carlgren ◽  
Sebastian Palmqvist ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Glial Fibrillary Acidic Protein ◽  
Acidic Protein ◽  
Cognitively Impaired ◽  
Cognitively Normal ◽  
Early Marker ◽  
Normal Individuals ◽  
Tau Pet ◽  
Positive Groups

AbstractAlthough recent clinical trials targeting amyloid-β (Aβ) in Alzheimer’s disease (AD) have shown promising results, there is increasing evidence suggesting that understanding alternative disease pathways that interact with Aβ metabolism and amyloid pathology might be important to halt the clinical deterioration. In particular, there is evidence supporting a critical role of astroglial activation and astrocytosis in AD. However, to this date, no studies have assessed whether astrocytosis is independently related to Aβ or tau pathology, respectively, in vivo. To address this question, we determined the levels of the astrocytic marker glial fibrillary acidic protein (GFAP) in plasma and cerebrospinal fluid (CSF) of 217 Aβ-negative cognitively unimpaired individuals, 71 Aβ-positive cognitively unimpaired individuals, 78 Aβ-positive cognitively impaired individuals, 63 Aβ-negative cognitively impaired individuals and 75 patients with a non-AD neurodegenerative disorder from the Swedish BioFINDER-2 study. Subjects underwent longitudinal Aβ (18F-flutemetamol) and tau (18F-RO948) positron emission tomography (PET) as well as cognitive testing. We found that plasma GFAP concentration was significantly increased in all Aβ-positive groups compared with subjects without Aβ pathology (p<0.01). In addition, there were significant associations between plasma GFAP with higher Aβ-PET signal in all Aβ-positive groups, but also in cognitively normal individuals with normal Aβ values (p<0.001), which remained significant after controlling for tau-PET signal. Furthermore, plasma GFAP could predict Aβ-PET positivity with an area under the curve of 0.76, which was greater than the performance achieved by CSF GFAP (0.69) and other glial markers (CSF YKL-40: 0.64, sTREM2: 0.71). Although correlations were also observed between tau-PET and plasma GFAP, these were no longer significant after controlling for Aβ-PET. In contrast to plasma GFAP, CSF GFAP concentration was significantly increased in non-AD patients compared to other groups (p<0.05) and correlated with Aβ-PET only in Aβ-positive cognitively impaired individuals (p=0.005). Finally, plasma GFAP was associated with both longitudinal Aβ-PET and cognitive decline, and mediated the effect of Aβ-PET on tau-PET burden, suggesting that astrocytosis secondary to Aβ aggregation might promote tau accumulation. Altogether, these findings indicate that plasma GFAP is an early marker associated with brain Aβ pathology but not tau aggregation, even in cognitively normal individuals with a normal Aβ status. This suggests that plasma GFAP should be incorporated in current hypothetical models of AD pathogenesis and be used as a non-invasive and accessible tool to detect early astrocytosis secondary to Aβ pathology.

Curcumin as a Potential Treatment for Alzheimer's Disease: A Study of the Effects of Curcumin on Hippocampal Expression of Glial Fibrillary Acidic Protein

2013 ◽  
Vol 41 (01) ◽  
pp. 59-70 ◽  
Author(s):  
Yunliang Wang ◽  
Honglei Yin ◽  
Lin Wang ◽  
Adam Shuboy ◽  
Jiyu Lou ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Glial Fibrillary Acidic Protein ◽  
Spatial Memory ◽  
Amyloid Β ◽  
Amyloid Plaque ◽  
Acidic Protein ◽  
Key Factors ◽  
Sham Control ◽  
The Relationship

Curcumin, an agent traditionally utilized for its preventative action against tumorigenesis, oxidation, inflammation, apoptosis and hyperlipemia, has also been used in the treatment of Alzheimer's disease (AD). Recent advances in the study of AD have revealed astrocytes (AS) as being key factors in the early pathophysiological changes in AD. Glial fibrillary acidic protein (GFAP), a marker specific to AS, is markedly more manifest during morphological modifications and neural degeneration signature during the onset of AD. Several studies investigating the functionality of curcumin have shown that it not only inhibits amyloid sedimentation but also accelerates the disaggregation of amyloid plaque. Thus, we are interested in the relationship between curcumin and spatial memory in AD. In this study, we intend to investigate the effects of curcumin in amyloid-β (Aβ1-40) induced AD rat models on both the behavioral and molecular levels, that is to say, on their spatial memory and on the expression of GFAP in their hippocampi. Our results were statistically significant, showing that the spatial memory of AD rats improved following curcumin treatment (p < 0.05), and that the expression of GFAP mRNA and the number of GFAP positive cells in the curcumin treated rats was decreased relative to the AD group rats (p < 0.05). Furthermore, the expression level of GFAP mRNA in hippocampal AS in the AD rats significantly increased when compared with that in the sham control (p < 0.05). Taken together, these results suggest that curcumin improves the spatial memory disorders (such disorders being symptomatic of AD) in Aβ1-40-induced rats by down regulating GFAP expression and suppressing AS activity.

Glial Fibrillary Acidic Protein in Serum is Increased in Alzheimer’s Disease and Correlates with Cognitive Impairment

2019 ◽  
Vol 67 (2) ◽  
pp. 481-488 ◽  
Author(s):  
Patrick Oeckl ◽  
Steffen Halbgebauer ◽  
Sarah Anderl-Straub ◽  
Petra Steinacker ◽  
André M. Huss ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Glial Fibrillary Acidic Protein ◽  
Acidic Protein
Sign in / Sign up

Export Citation Format

Share Document