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By 2050, it is estimated that more than 150 million people worldwide will be affected by dementia, among which Alzheimer's disease (AD) causes 70% of all cases
.
Although amyloid-β (Aβ) in the brain begins to appear decades before symptoms appear, AD dementia is still largely a clinical diagnosis
diagnosis
Animal and cell studies have shown that there are astrocytes around Aβ plaques, and reactive astrocytes are involved in the production and toxicity of Aβ
.
A PET tracker study with astrocytes as the target showed that astrocyte proliferation is an early feature in the pathological process of AD.
Glial fibrillary acidic protein (GFAP) is expressed in the cytoskeleton of astrocytes and is found to be significantly increased in CSF in AD and other neurodegenerative diseases compared with healthy controls
.
Recently, GFAP in plasma and serum was measured and found that in different neurological diseases, including AD, GFAP will increase
Although previous studies have shown that blood GFAP levels are elevated in AD and can identify the positive status of amyloid-PET, only one study measured GFAP in subjects with normal cognition and followed it for a long time.
Change to dementia (any type)
.
The higher baseline GFAP measured in the serum was associated with an increase in the risk of dementia, but no significant difference was seen in the changes in GFAP levels over time between the cognitively normal group and the dementia group
In this study, Claudia Cicognola and others of Lund University evaluated plasma GFAP as a potential plasma biomarker for MCI patients, and evaluated its association with AD-related Aβ pathology and conversion to AD dementia
.
Early identification of patients who are more likely to have worse cognitive outcomes can have a positive impact on their clinical management and contribute to the rapid diagnosis process; in addition, these patients can be selected for clinical trials of disease correction drugs currently under development In the test
.
The study included 160 subjects with a baseline clinical diagnosis of MCI, followed for an average of 4.
7 years
.
Collect CSF and plasma samples at baseline and follow-up
They followed 160 MCI patients for 4.
7 years (average)
.
Cerebrospinal fluid (CSF) Aβ42/40 and Aβ42/total tau (T-tau) were used to define AD pathology
Baseline plasma GFAP can detect abnormal CSF Aβ42/40 and CSF Aβ42/T-tau, with AUC of 0.
79 (95% CI 0.
72-0.
86) and 0.
80 (95% CI 0.
72-0.
86), respectively
.
When APOE ε4 status is also included as a predictor, the accuracy of the model to detect CSF Aβ42/40 abnormal status is improved (AUC = 0.
86, p = 0.
02)
.
86, p = 0.
02)
.
Plasma GFAP predicted the subsequent conversion to AD dementia with an AUC of 0.
84 (95% CI 0.
77-0.
91).
When APOE ε4 or age was added as a predictor to the model, the prediction results did not improve significantly
.
The longitudinal GFAP slopes of Aβ-positive and MCI progressing to dementia (AD or other) were significantly steeper than the slopes of Aβ-negative (p = 0.
007) and stable MCI (p <0.
0001), respectively
.
The important significance of this study lies in the discovery: plasma GFAP can detect the AD pathology of MCI patients and predict the conversion to AD dementia
.
.
Original source:
Cicognola C, Janelidze S, Hertze J, et al.
Plasma glial fibrillary acidic protein detects Alzheimer pathology and predicts future conversion to Alzheimer dementia in patients with mild cognitive impairment .
Alz Res Therapy.
Plasma glial fibrillary acidic protein detects Alzheimer pathology and predicts future conversion to Alzheimer dementia in patients with mild cognitive impairmentLeave a message here
