06 May 2026, Oslo, Norway

A substance long associated with muscle fatigue may hold unexpected promise for Alzheimer’s disease, according to new research published in the journal Scientific Reports.

The study, led by co-first authors Imen Belhaj and Dr. Ingrid Åmellem from the Brain and Muscle Energy Group at the University of Oslo, found that repeated doses of lactate, a compound produced naturally during exercise, improved memory and triggered widespread beneficial changes in the brains of mice engineered to develop Alzheimer’s-like symptoms.

This is one of several following-up studies of a 2017 important discovery that exercise induces cerebral VEGF and angiogenesis via the lactate receptor HCAR1 pioneered by our NO-Age co-founder Prof. Prof. Linda Hildegard Bergersen. Some of the other co-authors include  Prof. Farrukh A Chaudhry, Prof. Magnar Bjørås , and NO-Age co-founder Prof. Jon Storm-Mathisen.

From metabolic waste to brain signal

Once dismissed as a byproduct of exertion, lactate is increasingly recognised as a key player in brain biology. The new findings add weight to the idea that it may help explain why physical activity is consistently linked to lower dementia risk.

In the study, mice received lactate injections over an 11-week period. Those treated at later stages of disease showed a marked improvement in working memory compared with untreated animals, effectively avoiding the decline seen in controls.

The results, while preliminary, suggest lactate could mimic some of the neurological benefits of exercise a tantalizing prospect for patients unable to maintain high levels of physical activity.

A complex web of effects

Rather than acting on a single pathway, lactate appeared to reshape the brain’s internal environment in multiple ways. Researchers observed:
1) Reduced levels of inflammatory markers linked to neurodegeneration;
2) Strengthening of synaptic proteins critical for communication between neurons;
3) Increased activity in mitochondrial systems that power brain cells; and
4) Elevated expression of growth factors associated with resilience in healthy brains.

At the same time, the treatment did not significantly alter hallmark Alzheimer’s proteins such as amyloid precursors raising the possibility that lactate works by bolstering the brain’s ability to cope with disease rather than directly reversing it.

Subtle differences between sexes

The study also found that the effects of lactate varied between male and female mice an increasingly recognised feature of Alzheimer’s biology. Female animals showed enhanced glutamate receptors, crucial for learning and memory, while males exhibited changes linked to metabolism and gene regulation. Such findings underscore the growing view that future treatments may need to be tailored more precisely, rather than applied uniformly.

Cautious optimism

Despite the striking results, researchers stress that the work remains at an early stage. The experiments were conducted in mice, and translating such findings to humans has historically proved difficult. Still, the study adds to a growing body of evidence suggesting that lactate is far more than a metabolic bystander.

A new angle on an old disease

With few effective treatments for Alzheimer’s and global cases rising, scientists are increasingly exploring unconventional approaches. Lactate sitting at the intersection of metabolism, exercise and brain signalling  offers a fresh angle.

For now, the findings are of clinical relevance. And they reinforce a broader message that has become difficult to ignore: what happens in the body, particularly during exercise, may profoundly shape the fate of the brain.

And in that conversation, lactate, once maligned,  is emerging as a molecule worth watching. In conclusion, short-term lactate exposure may have brain benefit, with further in-depth pre-clinical and large clinical trials needed to validate and potentially optimise its clinical benefits.

Foto: Martin Toft

References
1. Lactate treatment improves brain biochemistry and cognitive function in transgenic Alzheimer’s and wild-type mice – PubMed
2. Exercise induces cerebral VEGF and angiogenesis via the lactate receptor HCAR1 – PubMed