Dementia is a condition in which cognitive abilities progressively degrade to the point where patients are no longer able to safely care for themselves. It is a blanket term for several conditions: Alzheimer’s, Lewy body dementia, vascular dementia, and frontotemporal dementia, just to name a few.
Currently, about 10% of the US population over age 65 has dementia. This is expected to dramatically increase over the next 20 years. A prospective cohort study published in Nature Medicine by Michael Fang and colleagues in 2025 carefully tracked over 15000 people who had participated in the Atherosclerosis Risk in Communities study.
They found a 42% lifetime risk of dementia after age 55 – double the previous estimates. The rates were about 45-60% higher in Black adults and women. The risk of having dementia increases with age between 65 and 90 years, doubling every 5 years.
We know the key processes that cause dementia: in the case of Alzheimer’s, it is the accumulation of amyloid-beta plaque, tau hyperphosphorylation with neurofibrillary tangles, synaptic dysfunction, neuronal loss, and brain atrophy. Neuroinflammation is a major factor contributing to disease progression.
In vascular dementia, repeated microinfarcts as a result of small vessel cerebellar disease cause chronic hypoperfusion, blood-brain barrier disruption, and white matter injury in brain areas needed for memory and executive function. These areas, specifically the hippocampus and medial temporal lobes, atrophy in dementia.
The pathology of dementia is associated with the conditions we often see in EMS: uncontrolled HTN, diabetes, sedentary lifestyle, obesity, falls, post-stroke deficits, and medication mismanagement. Effective management of these conditions helps to reduce the risk for dementia, just as it does for cardiac disease.
In addition to diet and medical management of risk factors for dementia, exercise has been found to be an additional risk modifier. Large systematic reviews and meta-analyses have consistently found that higher levels of physical activity are associated with a lower risk of all-cause dementia and Alzheimer’s disease.
For example, a meta-analysis published in the British Journal of Sports Medicine found that physically active individuals had a significantly lower incidence of dementia compared with inactive individuals.
The benefits of exercise can be explained by three mechanisms: stimulated brain growth, improved cerebral perfusion, and reduced inflammation.
Brain growth is stimulated by Brain-Derived Neurotrophic Factor, or BDNF. This protein is like fertilizer for brain growth. Its production in the brain is boosted by exercise. During exercise, myokines are released by muscle cells. These molecules improve glucose uptake, increase insulin sensitivity, and promote anti-inflammatory effects. They also boost BDNF and thereby foster neuronal growth and survival of cells in the hippocampus.
A 2011 randomized controlled trial involved 120 sedentary older adults aged 55-80 years who were living independently and did not have dementia or major neurological disorders, who were randomly assigned to one of two groups:
An aerobic exercise group (walking program)
A control group (stretching and toning exercises)
Over 12 months, participants in the aerobic exercise group completed a supervised walking program that gradually increased in intensity and duration, eventually reaching moderate-intensity walking approximately 40 minutes per session, three times per week.
The control group participated in stretching, yoga, and toning activities that involved minimal aerobic exertion. Researchers used several key measurements:
Magnetic resonance imaging (MRI) to measure hippocampal volume
Memory tests, particularly spatial memory tasks
Cardiorespiratory fitness assessments (VO₂ max) to evaluate improvements in aerobic capacity
Blood samples to assess levels of brain-derived neurotrophic factor (BDNF)
Brain scans were performed at baseline, 6 months, and 12 months to track structural changes in the hippocampus.
After one year, the aerobic exercise group experienced approximately a 2% increase in hippocampal volume, reversing about 1–2 years of age-related brain shrinkage. They also showed improvements in spatial memory performance and increased BDNF levels.
Exercise also improves cardiovascular fitness, helping to maintain cerebral perfusion, which is important because vascular injury contributes to cognitive decline and vascular dementia.
Finally, exercise has an anti-inflammatory effect. The brain contains specialized immune cells known as microglia, which serve as the primary immune defense of the central nervous system. These cells constantly monitor the neural environment and, when activated, can remove cellular debris and support neuronal maintenance and remodeling.
Microglia also influence neurogenesis and synaptic development, particularly in the hippocampus; however, aging can lead to dysregulation of microglial activity, causing a chronic pro-inflammatory state sometimes referred to as “inflammaging.”
Persistently activated microglia release inflammatory cytokines and reactive oxygen species that disrupt neuronal signaling, impair neurogenesis, and contribute to neurodegenerative diseases such as Alzheimer’s disease.
Exercise appears to regulate microglia by reducing chronic inflammatory activation and promoting a protective state that supports neuronal survival, neurogenesis, and the clearance of cellular debris.
The importance of regular exercise cannot be overstated with regard to brain health. Current guidelines are 150-300 minutes per week of moderate intensity exercise. Also, strength training at least twice per week is recommended.
Frailty is an independent indicator of cognitive decline and directly correlates with dementia. The younger you are when you start an active lifestyle, the better your baseline will be when you get older, but even elderly people can benefit. We were born to be active.
Sources & More Information:
CDC Physical Activity Basics, https://www.cdc.gov/physical-activity-basics/guidelines/adults.html#:~:. Accessed March 16, 2026.
Erickson, K.I., Voss, M.W., Prakash, R.S., Basak, C., Szabo, A., Chaddock, L., Kim, J.S., Heo, S., Alves, H., White, S.M., Wojcicki, T.R., Mailey, E., Vieira, V.J., Martin, S.A., Pence, B.D., Woods, J.A., McAuley, E. and Kramer, A.F., 2011. Exercise training increases the size of the hippocampus and improves memory. Proceedings of the National Academy of Sciences, 108(7), pp.3017–3022. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3041121/. Accessed March 16, 2026.
Iso-Markku, P., Waller, K., Kujala, U.M. and Kaprio, J., 2022. Physical activity as a protective factor for dementia and Alzheimer’s disease: systematic review, meta-analysis and quality assessment. British Journal of Sports Medicine, 56(12), pp.701–709. Available at: https://bjsm.bmj.com/content/56/12/701. Accessed March 16, 2026.
Iso-Markku, Paula & Kujala, Urho & Knittle, Keegan & Polet, Juho & Vuoksimaa, Eero & Waller, Katja. (2022). Physical activity as a protective factor for dementia and Alzheimer’s disease: systematic review, meta-analysis and quality assessment of cohort and case–control studies. British Journal of Sports Medicine. 56. bjsports-2021. 10.1136/bjsports-2021-104981. https://www.researchgate.net/publication/359314086_Physical_activity_as_a_protective_factor_for_dementia_an.
Accessed March 16, 2026.
Sleiman SF, Henry J, Al-Haddad R, El Hayek L, Abou Haidar E, Stringer T, Ulja D, Karuppagounder SS, Holson EB, Ratan RR, Ninan I, Chao MV. Exercise promotes the expression of brain derived neurotrophic factor (BDNF) through the action of the ketone body β-hydroxybutyrate. Elife. 2016 Jun 2;5:e15092. Available at https://pmc.ncbi.nlm.nih.gov/articles/PMC4915811/. Accessed March 16, 2026.
