That was one of the key takeaways from Senescence Life Sciences founder Shawn Watson's presentation at the recent Healthy Ageing APAC Summit in Singapore, organised by NutraIngredients-Asia and FoodNavigator-Asia.
Drawing from his expertise as a neuroscientist and the extensive research he had conducted on neurodegeneration, Watson said: "Once you become an adult — in your early 20s — brain function starts to decline. We start to see bigger effects in the 40s, and it speeds up past the 60s.
"What we (neuroscientists) know now is the 60s is when the symptoms of Alzheimer's disease start to appear, but in reality, the disease probably starts years or decades earlier.
"In fact, if you're diagnosed with Alzheimer's in your early 60s, it could have started in your 40s. It's not just your parents or grandparents who suffer from Alzheimer's. By mid-life, we need to start doing things to prevent the disease from happening."
He added that the typical life expectancy following a diagnosis is between four and eight years, and the disease has incurred a global cost of US$818bn.
Stagnation in strategy?
The current approach to combating Alzheimer's is characterised by the Amyloid and Tau theories.
The first revolves around beta-amyloid, a microscopic brain protein fragment that accumulates in the brain and disrupts communication between brain cells, eventually killing them.
The second views the brain as having dynamic relations with its environment, instead of as a complex mechanical device whose parts can be individually analysed, suggesting that the risk of developing Alzheimer's could be influenced by external factors.
Watson said that in the US, over 400 clinical trials have tested some type of experimental treatment for Alzheimer's, and between 2002 and 2012, the failure rate for new drugs targeting the disease was 99.6%.
According to Tufts Center for the Study of Drug Development, nearly US$1.4bn in out-of-pocket costs and over US$1.1bn in 'time costs' have been spent on bringing these drugs to market.
Lifestyle factors not helping
A more effective approach, Watson said, might be to target cellular repair through supplementation. In addition to a healthy diet, regular physical activity, social interaction, intellectual engagement and sufficient sleep, this could decrease the incidence of Alzheimer's.
He emphasised the importance of sufficient sleep, saying the modern lifestyle of many in their 20s and 30s does not help to lower Alzheimer's risk.
He shared the results of a study conducted on 27-year-olds who had gone 24 hours without sleep, after which they were found to have a 32.6% increase in amyloid beta and a 19.3% decrease in the ability to clear waste products.
"Sleep is so important because it's when repair happens. Lipids and fats get repaired and inflammation is lowered. We can tell people to change their lifestyles, but that's not going to work. So we need supplementation."
Cells and supplementation
Watson explained the mechanisms of Alzheimer's and how supplementation can help, saying, "One in nine people over the age of 65 will develop dementia. What it is is cell death. In natural, healthy ageing, your brain cells aren't dying.
"In fact, the brain cells you have when you neurologically become an adult are basically the ones you will die with. There is no neurogenesis in the brain — generally speaking, no new brain cells are made, which means if you lose a brain cell, it's gone for good."
"In Alzheimer's, we see severe neuronal atrophy, and what's interesting is that certain areas that are related to learning and memory, like the hippocampus, are one of the first to die."
Increasingly, however, supplementation is being seen as a viable option even for those already diagnosed with Alzheimer's. A clinical trial involving ginseng supplementation showed that Alzheimer's patients experienced improvements in cognitive function after 12 weeks of treatment, and reached a steady state after 96 weeks.
Another trial, which employed turmeric supplementation, found that it inhibited tumour necrosis factor, interleukin-1 and amyloid beta self-assembly, and increased glutathione peroxidase in Alzheimer's patients.
However, they were limited by small sample sizes and supplementation quality, as well as a lack of industry motivation.
Watson said: "Targeted supplementation is a viable strategy to prevent transitions from natural to pathological ageing, but we need longer, more expansive clinical trials, higher standards in manufacturing and more stringent regulations, and increased industry investment into innovation."