The number of dementia cases worldwide is set to pass 150 million by 2050.
However, it’s estimated that a third of these cases are caused by avoidable risk factors.
With no cure in sight, scientists continue to focus on how lifestyle changes could reduce the risk of the mind-robbing condition.
Now, new research, published in the journal BMJ Medicine, suggested that people with leaner muscles could be less likely to develop Alzheimer’s disease.
Lead author Dr Iyas Daghlas, of the University of California, San Francisco, said: “Despite the steady increase in the prevalence, no effective treatments for this devastating disease exist.
“Prevention of Alzheimer’s through identification of modifiable risk factors is thus a key public health aim.”
Using a technique known as Mendelian randomisation, the research team looked at over a million volunteers, including 450,243 people from the UK Biobank.
“Based on human genetics data, individuals randomised to lifelong higher lean muscle mass had a 12 percent lower risk of Alzheimer’s disease and scored higher for cognitive performance,” Dr Daghlas said.
What’s more, the study results remained “statistically robust” even after taking factors like age, sex and ancestry into account.
Some people are naturally programmed to have lean muscles but they can also be built by combining a healthy diet with resistance training.
Dr Daghlas said: “These analyses provide new evidence supporting a cause-and-effect relation between lean mass and risk of Alzheimer’s disease.
“They also refute a large effect of fat mass on the risk of Alzheimer’s disease and highlight the importance of distinguishing between lean mass and fat mass when investigating the effect of adiposity measures on health outcomes.”
What’s more, the research team suggested that identifying the biological mechanisms behind the phenomenon could open the door to developing new drugs.
Dr Daghlas said: “Several mendelian randomisation analyses have identified the effects of cardiometabolic risk factors on the risk of Alzheimer’s disease, which could be further investigated as potential mediators of the effect of lean mass.”
The effect could also be mediated by mechanisms including circulating myokines, which are proteins released during strenuous exercise.
Dr Daghlas said: “Potentially relevant secreted myokines include irisin, brain-derived neurotrophic factor 5, and cathepsin B.
“Identification of the key causal pathways might lead to the development of treatments that harness and potentiate the neuroprotective effects of lean mass.
“Our findings need to be replicated with independent lines of complementary evidence before informing public health or clinical practice.
“Also, more work is needed to determine the cut-off values for age and degree of pathology of Alzheimer’s disease after which modifications of lean mass might no longer reduce the risk.”
Despite the promising findings, there are still many questions and it’s currently not clear whether increasing lean mass could also cut the risk of Alzheimer’s disease in patients with preclinical disease or mild cognitive impairment.
However, if future studies back the findings, “public health efforts to shift the population distribution of lean mass, potentially through campaigns to promote exercise and physical activity, might reduce the population burden of Alzheimer’s disease”, the expert added.