Summary: Higher levels of the GFAP protein in the blood could be used to diagnose Alzheimer’s disease decades before symptoms appear.
Source: Edith Cowan University
A unique brain protein measured in the blood could be used to diagnose Alzheimer’s disease decades before symptoms develop, according to new Edith Cowan University (ECU) research.
Published in Nature journal Translational Psychiatry, the study is the first to find that people with elevated glial fibrillary acidic protein (GFAP) in the blood also have increased amyloid beta in the brain, a known indicator of Alzheimer’s disease.
GFAP is a protein normally found in the brain, but it is released into the blood when the brain is damaged by early Alzheimer’s disease.
Alzheimer’s disease affects more than 340,000 Australians and more than 35 million people in the world. Current diagnosis involves a brain scan or spinal fluid tests.
The study’s lead researcher, ECU Professor Ralph Martins AO, said the discovery offered a promising new avenue for early diagnosis.
“Blood biomarkers are becoming an exciting alternative to the existing expensive and invasive methods of diagnosing Alzheimer’s disease,” said Professor Martins.
“The GFAP biomarker could be used to develop a simple and quick blood test to detect if a person is at very high risk of developing Alzheimer’s.
“Early diagnosis is critical to allow us to implement medication and lifestyle interventions that can help delay the progression of the disease and give people more time before symptoms develop.”
A step forward
Alzheimer’s disease is a degenerative brain condition that can develop silently over years. It leads to memory decline and loss of thinking skills. There is no known cure.
According to Professor Martins, the development of an early blood test for the disease will be revolutionary.
“The technology for detecting biomarkers has developed rapidly, so I think we will begin to see diagnostic blood tests being used for Alzheimer’s in the next few years.
“The current brain imaging and lumbar puncture tests are expensive and invasive and not widely available to the general population. A blood test could open up possibilities for early diagnosis of millions of people and thereby enable earlier interventions.”
The study involved 100 Australians aged between 65 and 90 years of age with no symptoms of Alzheimer’s disease.
Professor Martins said further research is needed to understand GFAP in Alzheimer’s disease.
“Longitudinal studies will provide more insight into how GFAP relates to the progression of Alzheimer’s, which may allow us to determine when symptoms will emerge.”
Professor Martins is also part of a large study exploring interventions for Alzheimer’s disease, with the ultimate goal of finding medications and lifestyle factors that can halt or delay the development of the disease.
“Diagnosis and intervention techniques go hand in hand – if we can use blood biomarkers to detect Alzheimer’s sooner, we can also intervene sooner,” he said.
The study was a collaboration with Dr Pratishtha Chatterjee from Macquarie University, who is the first author on the paper.
Professor Martins is the director of the Centre of Excellence for Alzheimer’s Disease Research and Care and also leads the Western Australian site of the Dominantly Inherited Alzheimer’s Network (DIAN) – a global longitudinal study of people with genetically inherited Alzheimer’s disease.
About this Alzheimer’s disease research news
Source: Edith Cowan University Contact: Kylie Davies – Edith Cowan University Image: The image is in the public domain
Plasma glial fibrillary acidic protein is elevated in cognitively normal older adults at risk of Alzheimer’s disease
Glial fibrillary acidic protein (GFAP), an astrocytic cytoskeletal protein, can be measured in blood samples, and has been associated with Alzheimer’s disease (AD). However, plasma GFAP has not been investigated in cognitively normal older adults at risk of AD, based on brain amyloid-β (Aβ) load.
Cross-sectional analyses were carried out for plasma GFAP and plasma Aβ1–42/Aβ1–40 ratio, a blood-based marker associated with brain Aβ load, in participants (65–90 years) categorised into low (Aβ−, n = 63) and high (Aβ+, n = 33) brain Aβ load groups via Aβ positron emission tomography. Plasma GFAP, Aβ1–42, and Aβ1–40 were measured using the Single molecule array (Simoa) platform. Plasma GFAP levels were significantly higher (p < 0.00001), and plasma Aβ1–42/Aβ1–40 ratios were significantly lower (p < 0.005), in Aβ+ participants compared to Aβ− participants, adjusted for covariates age, sex, and apolipoprotein E-ε4 carriage.
A receiver operating characteristic curve based on a logistic regression of the same covariates, the base model, distinguished Aβ+ from Aβ− (area under the curve, AUC = 0.78), but was outperformed when plasma GFAP was added to the base model (AUC = 0.91) and further improved with plasma Aβ1–42/Aβ1–40 ratio (AUC = 0.92).
The current findings demonstrate that plasma GFAP levels are elevated in cognitively normal older adults at risk of AD. These observations suggest that astrocytic damage or activation begins from the pre-symptomatic stage of AD and is associated with brain Aβ load.
Observations from the present study highlight the potential of plasma GFAP to contribute to a diagnostic blood biomarker panel (along with plasma Aβ1–42/Aβ1–40 ratios) for cognitively normal older adults at risk of AD.