Exercise and Brain Health: How Moving Your Body Lowers a Key Dementia Risk Marker
Dementia is now the leading cause of death in Australia (AIHW, 2024). While this statistic is sobering, research continues to show that lifestyle choices — particularly physical activity — can significantly reduce the risk of developing dementia. A new study from the University of Tasmania’s Wicking Dementia Research and Education Centre has revealed a biological link between exercise and reduced levels of a blood protein associated with brain inflammation. In short: moving your body really does help protect your brain.
What the Tasmanian study found
Researchers tapped into the ISLAND project, which follows Tasmanians aged over 50 to identify dementia risk factors. They looked at serum glial fibrillary acidic protein (GFAP) — a biomarker linked to neuroinflammation and brain health.
The study found that people who engaged in higher levels of physical activity had lower levels of GFAP in their blood (Roccati et al., 2024). Crucially, the relationship was strongest in those performing vigorous exercise — the kind that leaves you puffing, like running, swimming, or intense cycling.
Professor James Vickers, director of the Wicking Centre, explained that GFAP is “a good marker for general brain health” and that reducing it may signal better resilience against future dementia (Vickers, 2024).
Why GFAP matters
GFAP is a protein produced by astrocytes, the support cells of the brain. When the brain is under stress — through injury, inflammation, or early degenerative changes — GFAP levels rise. Elevated GFAP has been found in people at risk of Alzheimer’s disease, even before symptoms appear (Chatterjee et al., 2021).
So, lower GFAP levels in active people may reflect healthier brains and lower long-term risk.
What about genetics?The study also looked at the APOE ε4 gene, the strongest known genetic risk factor for Alzheimer’s. Around 25% of people carry one copy, while 2–3% carry two. For these individuals, the protective link between exercise and lower GFAP was weaker.
But here’s the important takeaway: genetics are not destiny. Even if someone carries APOE ε4, physical activity still provides benefits — just perhaps not as strongly reflected in GFAP (Roccati et al., 2024). As Dr Eddy Roccati noted, “You shouldn’t look at genes as determining your fate.”
Intensity matters
Moderate activity (like brisk walking) has benefits, but this study highlights that vigorous activity may give extra protection for the brain. That doesn’t mean everyone needs to start marathon training. Instead, it suggests including activities that make you sweat and breathe harder, as appropriate for your fitness and health status.
Examples include:
Interval jogging or running
Fast swimming
Hill walking or stair climbing
High-intensity cycling
Always check with your GP before starting vigorous exercise, especially if you have underlying health conditions.
Beyond exercise: 14 modifiable risk factors
Physical activity is just one piece of the puzzle. The Lancet Commission on dementia prevention, intervention and care lists 14 modifiable risk factors that, if addressed, could prevent up to 45% of dementia cases (Livingston et al., 2020). These include:
Reducing blood pressure and cholesterol
Treating hearing loss
Improving sleep
Managing obesity and diabetes
Avoiding smoking
Increasing social interaction
Together, these lifestyle changes help create a brain-healthy environment.
Why this matters for Australia
By 2065, almost 1.1 million Australians are predicted to be living with dementia — a 2.5-fold increase (AIHW, 2024). The findings from the ISLAND project highlight the urgent need for proactive prevention strategies.
Encouraging vigorous exercise in midlife may reduce future dementia cases and provide a measurable biological effect — lower GFAP — that could one day help track individual risk.
Key takeaway
Exercise isn’t just about muscles, weight, or heart health. It changes what’s happening inside your brain at a molecular level. Vigorous movement lowers a protein linked to brain inflammation and dementia risk. Whether it’s swimming, running, or dancing until you’re out of breath, your brain will thank you.
References AIHW (2024) Dementia in Australia. Australian Institute of Health and Welfare. Available at: https://www.aihw.gov.au/reports/dementia/dementia-in-australia (Accessed: 22 September 2025).Chatterjee, P. et al. (2021) ‘Plasma glial fibrillary acidic protein is elevated in cognitively normal older adults at risk of Alzheimer’s disease’, Alzheimer’s Research & Therapy, 13, p. 59.Livingston, G. et al. (2020) ‘Dementia prevention, intervention, and care: 2020 report of the Lancet Commission’, The Lancet, 396(10248), pp. 413–446.Roccati, E., Vickers, J., and Wicking Dementia Research and Education Centre (2024) Physical activity and blood-based biomarkers of neurodegeneration in community dwelling Australians from ISLAND. Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring, 16(4), pp. e12422.Vickers, J. (2024) ABC News interview: Protein linked with brain inflammation reduced by exercise. ABC News, 20 September. Available at: https://www.abc.net.au/news/ (Accessed: 22 September 2025).
Ehlers-Danlos Syndrome (EDS) is often misunderstood as simply being “double-jointed” or unusually flexible. In reality, EDS is a complex connective tissue disorder that affects joint stability, proprioception, pain processing, fatigue, autonomic function, and movement control throughout the entire body.
For therapists, this creates a unique clinical challenge. Many traditional rehabilitation approaches that work well for the general population—including aggressive stretching, heavy manual therapy, or isolated strengthening—can sometimes worsen symptoms in people with EDS. What appears to be weakness may actually be instability. What appears to be tightness may be a protective strategy. And what appears to be a local joint problem may reflect a much larger whole-body compensation pattern. Understanding EDS requires a shift away from simply chasing pain or increasing mobility and towards improving control, body awareness, load management, nervous system regulation, and long-term resilience.
In this article, we explore the current evidence surrounding EDS, including proprioception, pain, strength training, autonomic dysfunction, fascia, breathing mechanics, and the role of whole-body assessment. We also examine where emerging concepts such as biotensegrity and fascial therapy may fit within modern clinical practice and discuss the key principles every therapist should understand when working with hypermobile patients.
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Most people assume breathing exercises and breathing retraining are the same thing.
They’re not.
In fact, this misunderstanding may be one of the biggest reasons people continue to struggle with poor sleep, jaw tension, anxiety, headaches, fatigue, and breathing-related problems despite regularly practising breathing techniques.
Think about it.
The average person takes around 20,000 breaths every day.
A five-minute breathing exercise might influence a few dozen of them.
What about the other 19,900?
This is where breathing retraining becomes different. Rather than focusing on a specific exercise, breathing retraining aims to change your everyday breathing patterns—while you’re working, walking, talking, sleeping, exercising, and dealing with stress.
In this article, we’ll explore why breathing exercises alone often fail to create lasting change, the difference between breathwork and breathing retraining, and how improving your default breathing habits may have a greater impact on your health than any breathing technique.
Most of us never think about breathing until something goes wrong.
A blocked nose. Poor sleep. Anxiety. Headaches. Jaw tension. Fatigue.
The common assumption is that we need more oxygen. But what if the problem isn’t a lack of oxygen at all?
Modern research suggests that many people breathe far more than their bodies actually require. In doing so, they may be disrupting the delicate balance between oxygen and carbon dioxide that helps regulate blood flow, nervous system function, sleep quality and even oxygen delivery to the tissues.
In this article, we’ll explore why bigger breaths aren’t always better, why carbon dioxide may be one of the most misunderstood gases in human physiology, and how your breathing habits could be influencing everything from jaw tension and posture to energy levels and recovery.
When most people develop jaw pain, clicking, clenching, or teeth grinding, attention immediately turns to the jaw joint itself.
Makes sense.
After all, that’s where the symptoms are.
But what if the jaw isn’t actually the starting point?
What if it’s simply the place where a much larger story is being expressed?
Emerging research suggests that many cases of TMJ dysfunction may involve far more than joint mechanics alone. Breathing patterns, sleep quality, nervous system regulation, tongue posture, neck tension, stress, and even the way the brain processes sensory information may all play important roles.
In other words, your jaw might not be malfunctioning because it is broken.
It might be working overtime because other systems are struggling.
In this article, we’ll explore the fascinating relationship between the jaw, neck, airway and nervous system—and why treating the jaw alone may not always provide lasting relief.
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Emerging research suggests the jaw is connected to emotional processing, pain perception, breathing, posture and even activity within the brain’s limbic system. Learn how jaw tension, chronic stress and inflammation may be influencing headaches, neck pain, fatigue and persistent pain—and why treating the whole person matters more than chasing symptoms.
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If you’ve ever searched “acupuncture for pain Canberra”, chances are something in your body has decided it’s had enough. Maybe it’s your heel barking every morning, a shoulder that refuses to behave, or a lower back that stiffens the moment you sit down too long.
Acupuncture can be remarkably effective for reducing pain. But here’s the honest truth most clinics won’t say out loud:
Foot shape plays an important role in how the foot absorbs force and distributes pressure during walking. From flatter pes planus feet to the higher-arched pes cavus foot type, these structural differences influence how load travels through the heel and arch.
Understanding how these loading patterns affect the tissues around the heel—including the plantar fascia and Baxter’s nerve—may help explain why some people develop persistent heel pain while others do not.
Most cases of heel pain are quickly labelled plantar fasciitis, but that diagnosis doesn’t always tell the full story.
Research suggests that Baxter’s nerve entrapment—compression of the inferior calcaneal nerve—may account for up to 20% of chronic heel pain cases. Because the symptoms overlap with plantar fasciitis, this nerve condition is frequently overlooked.
Understanding how gait mechanics and medial heel loading influence the tissues surrounding Baxter’s nerve can help explain why some heel pain persists despite traditional treatments.
Most cases of heel pain are quickly labelled plantar fasciitis, but that diagnosis doesn’t always tell the full story.In fact, research suggests that up to 20% of chronic heel pain cases may involve compression of Baxter’s nerve, a small branch of the lateral plantar nerve that runs along the inside of the heel. Because the symptoms overlap, Baxter’s nerve entrapment is frequently mistaken for plantar fasciitis.While plantar fasciitis involves irritation of the plantar fascia, Baxter’s neuropathy is a nerve compression problem, which means the symptoms, mechanics and treatment considerations can be quite different.
Understanding the difference is important. Treatments designed for plantar fascia inflammation may not help nerve-related heel pain—and in some cases may even aggravate the underlying problem.
In this article we explore the key anatomical and biomechanical differences between these two conditions and explain why a deeper look at foot mechanics and gait can be crucial when heel pain persists.
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Most people think stress is all adrenaline and action.
But there’s another version — the quiet one. The one where motivation fades, energy drops, and your nervous system stops fighting and starts conserving.
This isn’t weakness. It’s biology.
Research from Martin Seligman and earlier work by Curt Richter showed that when stress becomes uncontrollable, the brain shifts into a shutdown pattern known as learned helplessness.
At a chemical level, this state is linked to altered acetylcholine signaling, increased nitric oxide, reduced thyroid hormone activity, and impaired mitochondrial energy production. In simple terms? Your metabolism and your mood are having the same conversation.
The good news: the nervous system is plastic. Environment, light exposure, movement, social connection, and metabolic support all influence whether the brain adapts toward resilience — or surrender.
Helplessness isn’t a character flaw.
It’s a reversible physiological state.
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