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Brain- Plasma glial fibrillary acidic protein, which can reflect Alzheimer’s amyloid changes

 Last Update: 2021-08-03
 Source: Internet
 Author: User

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platelet poor plasma

reactive protein test

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There is increasing evidence that the pathogenesis of Alzheimer's disease (AD) is not limited to amyloid beta (Aβ) plaques and tau tangles, but also includes strong interactions with immunological mechanisms
.
In response to this, astrocytic reactivity or astrocytosis is a well-known pathological process that is usually found around Aβ plaques in the brains of AD patients

immunity

Compared with the relationship between astrocytosis and Aβ plaques, the relationship between reactive astrocytes and tau tangles has been less studied
.
A few existing evaluation studies have shown that reactive astrocytes also interact with tau entanglement, but only in the late stage of AD through the penetration of extracellular ghost tau entanglement

Compared with the relationship between astrocytosis and Aβ plaques, the relationship between reactive astrocytes and tau tangles has been less studied

They identified 217 persons with Aβ-negative cognitive impairment, 71 persons with Aβ-positive cognitive impairment, 78 persons with Aβ-positive cognitive impairment, 63 persons with Aβ-negative cognitive impairment and 75 persons with non-cognitive impairment from the Swedish BioFINDER-2 study.
The levels of astrocyte markers in plasma and cerebrospinal fluid (CSF) of patients with AD neurodegenerative diseases

They found that compared with subjects without Aβ lesions, plasma GFAP concentrations in all Aβ-positive groups were significantly increased (P <0.
01)

Compared with subjects without Aβ lesions, the plasma GFAP concentrations of all Aβ-positive groups were significantly increased (P <0.

Compared with plasma GFAP, the concentration of CSF GFAP in non-AD patients was significantly higher than that in other groups (p <0.

05) , and it was only associated with Aβ-PET in patients with Aβ-positive cognitive impairment (p = 0.
005)
.

Compared with plasma GFAP, the CSF GFAP concentration of non-AD patients was significantly higher than that of other groups (p <0.
05).

Plasma GFAP is an early marker related to brain Aβ pathology, but not tau aggregation.

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