As we age, a healthy lifestyle becomes more important to not only keep our body in shape but also to protect our brain from decline. Previous studies have shown that nutrition, physical workouts and cognitive exercise can benefit both our muscles and our mind. For the brain, a proactive daily program can slow the effects of normal aging as well as the early onset of dementia. Now, two new studies clarify the situation by better understanding the variables linked to Alzheimer’s disease and finding that healthy living can still help, even if genetic markers put us at risk.
Neuroscientists already know that three contributing factors, age, the presence of amyloid‑β (Aβ) plaque accumulation in the brain and the apolipoprotein E (APOE) ε4 genotype, combine to accelerate the risk of Alzheimer’s disease. Accumulation of Aβ protein in the brain is associated with cognitive decline while the APOE ε4 allele accelerates the loss. “However, what wasn’t known,” says Yen Ying Lim, PhD, a researcher at The Florey Institute of Neuroscience and Mental Health in Melbourne, “was the nature of the relationship between Aβ, APOE ε4, age and memory change over time in the preclinical stages of AD.”
Reviewing the data from 447 cognitively healthy adults from the Australian Imaging, Biomarkers and Lifestyle (AIBL) study, Lim and a team of researchers found that episodic memory composite scores declined faster for Aβ-positive individuals than Aβ-negative individuals and that the rate of decline increased with age. And for those who were Aβ-positive and had the APOE ε4 allele, the decline started seven years earlier.
“We think that these estimates of the combined effect of age and APOE ε4 on amyloid-related cognitive decline provides a foundation for the development of prognostic models of the clinical manifestation of Alzheimer’s disease in the earliest stages,” concluded Dr. Lim.
The study has been published in JAMA Neurology.
Understanding the progression timeline of Alzheimer’s will help educate millions of aging baby boomers on their need to care for their brain. However, for those that know they carry the APOE ε4 allele, there may be some questions around how much good nutrition and exercise will really make a difference.
In June 2015, the results of the two-year Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER) were released showing that a healthy lifestyle could actually reduce cognitive decline by 30%. The study population of 2500 older adults, who had increased risk of dementia but were cognitively normal, was divided into two groups, a control group and an experimental group who followed a recommended healthy diet, exercise regimen and cognitive training program.
“Both the intervention group and the so-called placebo group, where we gave regular health advice, improved during the two years,” said Dr. Miia Kivipelto, MD, principal investigator and professor at Karolinska Institutet. “But the improvement was much higher in the intervention group, in all of the [cognitive] sub-domains: executive function for [information] processing (how quickly people are able to do different tasks) and complex memory tasks. And the risk of cognitive decline was 30% higher for the control group compared to the intervention group.”
However, many of those study participants also carried the APOE ε4 allele. So, Alina Solomon, MD, PhD, of the University of Eastern Finland, and a team of researchers asked if the healthy lifestyle would be as beneficial even in the presence of this genetic risk factor. From the total FINGER population of 2,500 participants, data from 1,109 individuals, of whom 362 carried the APOE ε4 allele, was reviewed. Results from the neuropsychological test battery showed no difference between the allele carriers and the non-carriers, suggesting that the healthy lifestyle could still slow cognitive decline even with the genetic risk.
“Many people worry that genetic risk factors for dementia may thwart potential benefits from healthy lifestyle changes. We were very happy to see that this was not the case in our intervention, which was started early, before the onset of substantial cognitive impairment,” said Dr. Solomon, the lead author of the study, which appears in JAMA Neurology.
In fact, there were signs that the healthy intervention may actually provide better results for the APOE ε4 allele carriers, but more research is needed.
“An extended 7‑year follow-up of the FINGER trial participants is ongoing, and this will tell us more about the longer-term effects of the intervention,” said Dr. Solomon. “Several new clinical trials will be conducted in the worldwide FINGERS initiative, which will tell us more about genetic–environmental interactions in a diversity of populations and help to develop global dementia prevention strategies.”
Indeed, the FINGER framework is being expanded to examine other potential methods to slow down dementia.
“The FINGER intervention model is now being adapted and tested globally in the World Wide FINGERS initiative,” said Dr. Kivipelto. “New clinical trials in diverse populations with a variety of geographical and cultural backgrounds will help us formulate global dementia prevention strategies.”
