The presence of Glial fibrillary acidic protein (GFAP) in proteomic analyses of age-related neurodegenerative processes is increasingly significant, especially in the context of building early warning biomarker profiles for the development of Alzheimer’s disease. This marker is applicable to the aging of the brain and its supporting cell populations, not limited to Alzheimer’s disease research.
Increased expression of GFAP in astrocyte cells indicates reactive states, commonly associated with damage, altered signaling, and neurodegenerative disease. The consequences of astrocyte reactivity are not fully understood but are clearly linked to the progression of neurodegenerative conditions. Astrocyte reactivity, including increased GFAP levels, has been identified as an early event in preclinical Alzheimer’s disease, making it a key component in the longitudinal progression of blood biomarkers associated with the disease.
Research revealed that plasma GFAP levels are elevated in individuals who later develop cognitive impairment due to Alzheimer’s disease up to 10 years before symptom onset. This elevation is also observed in participants with neuropathologically confirmed Alzheimer’s disease, suggesting that GFAP levels are associated with the severity of the disease’s pathology. Additionally, findings from a transgenic mouse model of Alzheimer’s disease support the role of reactive astrocytosis in the early initiation of Alzheimer’s disease pathogenesis and its potential as a therapeutic target.
