GFAP: What This Brain Marker Reveals About Neuroinflammation

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Written by Liad Stearns, MS

Glial fibrillary acidic protein (GFAP) is a well-established blood-based biomarker in the brain that is elevated in response to brain injury and various neurological disorders. Elevated GFAP levels signal that astrocytes, a star-shaped non-neuronal glial cell, are responding to the injury or disease [1].

Newer technology has made it possible to detect GFAP through a simple blood test (as opposed to previous, more invasive methods like spinal taps or brain tissue sampling), making it more accessible and less intrusive. Clinicians increasingly use GFAP to identify traumatic brain injuries, monitor Alzheimer’s disease progression, and assess neuroinflammation, allowing them to detect neurological issues earlier and more accurately and shifting brain care toward a more proactive approach.

What Is GFAP?

GFAP is a structural protein found in the cytoskeleton of astrocytes, a subtype of glial cells in the central nervous system [2]. You can think of astrocytes like the “gardeners” of the brain: they nurture neurons, prune excess neurotransmitters, and maintain a balanced environment overall. GFAP acts as the trellis they build to stabilize and support delicate structures, which are barely noticeable when everything is thriving, but quickly reinforced when a storm threatens to damage the field.

In healthy individuals, GFAP levels measured in blood or cerebrospinal fluid (CSF) are typically low and stable, reflecting astrocytes’ routine maintenance work. However, when the brain is injured, inflamed, or degenerating, astrocytes enlarge, multiply, and substantially increase GFAP production [3, 4]. This surge serves as a measurable signal that the brain is mounting a protective and repair response to stress.

GFAP and Glial Cells: The Brain’s Support System

To understand GFAP’s role in the brain, it’s important to first understand where it comes from: astrocytes. As mentioned earlier, astrocytes are a subtype of glial cells, non-neuronal cells that perform many of the brain’s essential housekeeping and regulatory functions. To recap, astrocytes are responsible for:

  • Providing structural support to neurons 

  • Reinforcing and regulating the blood-brain barrier

  • Clearing excess neurotransmitters to prevent excitotoxicity (where neurons are damaged or killed by the excessive stimulation of neurotransmitters such as glutamate)

  • Modulating the brain’s immune and inflammatory responses

  • Responding to injury

 

When the brain experiences injury, inflammation, or early signs of disease, astrocytes shift into a “reactive” state, a process known as astrogliosis. In this state, astrocytes proliferate, change shape, and dramatically increase their production of GFAP, a well-established marker of astrocyte activation [5]. 

This reaction is initially protective: reactive astrocytes help contain damage, clear cellular debris, and restore homeostasis. But when the activation becomes prolonged or excessive, such as from chronic neuroinflammation or ongoing neurodegenerative disease, it can turn pathological. Instead of aiding repair, reactive astrocytes may begin to drive inflammation, form scar tissue, and disrupt neuronal communication, potentially accelerating brain damage [6]. 

What Causes GFAP Levels to Rise?

Several factors can cause GFAP levels to rise, and understanding them can help you take a preventative approach to maintaining cognitive health, even as you age. 

1. Brain injury and trauma

Traumatic brain injury (TBI) causes significant elevations in GFAP levels, reflecting astrocyte activation and brain cell degeneration in response to physical damage. Clinical studies show that plasma GFAP levels rise within hours of injury and strongly correlate with injury severity, intracranial pathology, and long-term outcomes, often outperforming other clinical measures [7]. Repeated mild TBI events or concussions demonstrate a consistent upregulation of GFAP as well, suggesting cumulative astrocytic stress and injury even when clinical symptoms are subtle [17].  Similarly, in stroke patients, serum GFAP levels rise sharply and show a strong, positive correlation with stroke severity across multiple time points, including the acute phase (<72 hours), day 7, and day 30 [8]. Together, these findings support GFAP as a reliable marker of acute astrocyte activation and injury severity across various neurological insults, making it a valuable tool for early detection and prognosis in both TBI and stroke.

2. Neurodegenerative diseases

Elevated GFAP levels are increasingly recognized in neurodegenerative conditions such as Alzheimer’s disease, Parkinson’s, and other forms of dementia, even before clinical symptoms appear. GFAP rises in the blood of individuals with mild cognitive impairment and Alzheimer’s, as well as in those with silent amyloid accumulation, reflecting early glial responses to pathology [9]. While amyloid and tau have traditionally dominated the biomarker landscape, GFAP is emerging as a promising complementary tool for detecting early-stage disease and monitoring progression [10]. Its ability to reflect astrocytic stress and neuroinflammation in accessible blood samples may help accelerate diagnosis and improve disease tracking over time.

3. Neuroinflammation (e.g., infections, autoimmune disorders)

Inflammatory conditions of the central nervous system, such as infections, autoimmune disorders (e.g., multiple sclerosis), and chronic systemic inflammation, among others, consistently elevate GFAP levels [11]. This increase reflects astrocyte activation in response to immune-related tissue damage. For example, in MS, both serum and cerebrospinal fluid GFAP levels are significantly elevated compared to healthy controls, particularly in progressive forms of the disease, and these elevations correlate with greater disability and lesion burden [12]. 

4. Age-related changes in GFAP

GFAP levels tend to increase gradually with age, even in healthy individuals [13]. This increase likely reflects a state of chronic, low-grade neuroinflammation as astrocytes become more reactive over time. While modest elevations are considered part of normal aging, disproportionately high levels may signal early vulnerability to neurodegenerative changes. Research analyzing gene expression in the aging human prefrontal cortex demonstrates a consistent upregulation of GFAP alongside declines in synaptic transmission and neurogenesis, suggesting that astrocytic activation is a hallmark of brain aging [13]. 

How GFAP Is Used in Research and Diagnosis

GFAP is a well-known marker for identifying astrocytes in brain tissue, but its real potential lies in its role as a blood-based biomarker. Instead of relying on invasive spinal taps or expensive brain imaging, clinicians can now measure GFAP levels through a simple blood test, making it easier to detect brain injury and neurological disease early and with less burden on the patient.

Clinically and in research, GFAP is already proving valuable in several areas:

  • Diagnosing mild vs. severe traumatic brain injury (TBI): Elevated GFAP levels help distinguish mild concussions from more severe injuries, aiding decisions about further imaging or monitoring [14, 15]. 

  • Predicting Alzheimer’s disease progression: Higher GFAP levels may indicate early Alzheimer’s changes even before cognitive symptoms arise, making it a potential screening tool for at-risk individuals [9].

 

While GFAP is a sensitive marker of astrocyte activation and neuroinflammation, it offers a distinct yet complementary perspective to other biomarkers. For instance, amyloid-beta and tau proteins reflect the hallmark pathology of Alzheimer’s disease, while neurofilament light chain (NfL) indicates axonal damage across various neurodegenerative diseases [16]. GFAP provides additional insight into the inflammatory and structural changes in the brain, helping to build a more complete picture of neurological health and disease progression. 

Is GFAP a Reliable Biomarker?

In short — yes. However, there are some limitations to how GFAP can be used in a clinical context.

Strengths:

Limitations:

  • Not disease-specific — GFAP rises in various conditions, including TBI, Alzheimer’s, MS, and infections

  • Can overlap with other biomarkers, requiring context for accurate interpretation

  • Increases with age, which may complicate its use as a stand-alone indicator [13]

How Nouro Impacts GFAP Levels

Early research by Tonum found that Nouro significantly reduced GFAP levels in mice fed either high-fat or low-fat diets. Across small but standard cohort sizes (6-9 mice per group, 6- and 12-month studies), Nouro lowered GFAP by ~49% in the high-fat group and ~68% in the low-fat group compared to diet-matched controls, indicating less glial reactivity and neuroinflammation. Complementing this effect, Nouro has also been shown to reduce amyloid-beta and neurofilament light chain (NfL), suggesting a broader neuroprotective profile. Because elevated GFAP, amyloid-beta, and NfL are linked to conditions such as repeated mild brain injury, Alzheimer’s disease, and other neurodegenerative processes, these findings demonstrate Nouro’s potential in supporting long-term cognitive health. While confirmation in larger animal studies and human trials is needed, these findings highlight the potential of targeted supplements to support healthier glial function and reduce biomarker levels associated with brain injury and decline, especially in individuals at risk of neuroinflammatory conditions or cognitive impairment.

Takeaways

  • GFAP is a key signal of brain stress. It rises when astrocytes respond to injury, inflammation, or disease, providing insights into neurological challenges like TBI or Alzheimer’s.

  • It’s not a diagnosis, but a warning sign. Elevated GFAP levels tell us that something is wrong, but not exactly what. That’s why it’s used alongside other tools like tau, amyloid-beta, and clinical evaluations.

  • Monitoring GFAP can help us act sooner. By detecting changes earlier, clinicians and individuals have more time to intervene before damage becomes irreversible.

  • GFAP may be modifiable. Early research suggests lifestyle changes and targeted supplements like Nouro could reduce GFAP levels and support healthier brain function.

  • This is a shift toward proactive brain care. Instead of waiting for symptoms, we’re learning to track brain health in real time, opening new doors for prevention, personalization, and empowerment.

References:

  1. https://pmc.ncbi.nlm.nih.gov/articles/PMC11658191/ 

  2. https://pmc.ncbi.nlm.nih.gov/articles/PMC6172254/

  3. https://journals.physiology.org/doi/full/10.1152/physrev.00041.2013?rfr_dat=cr_pub++0pubmed&url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org 

  4. https://pmc.ncbi.nlm.nih.gov/articles/PMC7440737/

  5. https://pmc.ncbi.nlm.nih.gov/articles/PMC11068326/

  6. https://pmc.ncbi.nlm.nih.gov/articles/PMC3629545/ 

  7. https://pmc.ncbi.nlm.nih.gov/articles/PMC4601141/

  8. https://pmc.ncbi.nlm.nih.gov/articles/PMC6542382/

  9. https://pmc.ncbi.nlm.nih.gov/articles/PMC10177296/

  10. https://pmc.ncbi.nlm.nih.gov/articles/PMC11629700/

  11. https://pmc.ncbi.nlm.nih.gov/articles/PMC11279275/

  12. https://pmc.ncbi.nlm.nih.gov/articles/PMC6172254/

  13. https://pmc.ncbi.nlm.nih.gov/articles/PMC7059712/

  14. https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2823148

  15. https://pmc.ncbi.nlm.nih.gov/articles/PMC9743059/

  16. https://pmc.ncbi.nlm.nih.gov/articles/PMC11204270/

  17. https://pmc.ncbi.nlm.nih.gov/articles/PMC4931336/#s010  

 

Liad Stearns, MS, is a health and science writer with a background in neuroscience and functional medicine. She holds a Master’s degree in neuroscience from Tulane University and has professional experience in product development for CGMs and as a functional medicine health coach. Based in San Francisco, Liad specializes in translating complex brain and metabolic health research into clear, actionable content.