According to the U.S. Centers for Disease Control and Prevention (CDC),1 an estimated 5.4 million Americans are living with Alzheimer’s disease, the incidence of which increases as you age and doubles every five years beyond age 65. The National Institute on Aging2,3 suggests Alzheimer’s is the third leading cause of death for older people, falling behind heart disease and cancer. Currently, there is no cure for this irreversible, progressive brain condition.
Due to the seriousness of Alzheimer’s, you’d be wise to proactively address any areas that may be putting you at risk for developing the disease. I’d like to discuss several lifestyle factors that have been linked to this condition, as well as share some healthy prevention tips, in hopes you will take action now to ensure you or someone you love will not become an Alzheimer’s statistic. First, let’s take a look at some genetic links to the disease and recent news on gene research.
The Genetic Links to Alzheimer’s Disease
In the featured video, Dr. Dale Bredesen, director of neurodegenerative disease research at the University of California, Los Angeles (UCLA) School of Medicine, and author of “The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline,” suggests Alzheimer’s is a trillion-dollar global health problem that strikes about 15 percent of the population, making it incredibly common.
He goes on to assert you have the pathophysiology of the disease for about 20 years before the diagnosis is made. By age 85, says Bredesen, nearly half of all people are affected by Alzheimer’s. Bredesen’s breakthrough program is known as ReCODE and later in this article I’ll share more about how it can effectively help you reverse Alzheimer’s. For now, as you may know, the apolipoprotein (ApoE) gene has long been embraced as one of the most important genetic risk factors for Alzheimer’s disease.
Everyone inherits a form of APOE from their parents — either type E2, E3 or E4. Bredesen affirms the common belief that genetic predisposition plays a role, noting an estimated 75 million Americans have the single allele for the problematic ApoE4 (E4) gene, which gives them a 30 percent lifetime risk of developing the disease. Approximately 7 million have two copies of that gene, putting them at a 50 percent lifetime risk. About ApoE, Medical News Today says:4
“Normally, ApoE’s role is to provide instructions for creating the protein of the same name. In combination with fats, ApoE creates lipoproteins, which help transport and regulate levels of cholesterol throughout your bloodstream. However, the E4 version of the gene seems to be particularly damaging to the brain, with several studies showing that this genetic variant increases the risk of toxic beta-amyloid and tau buildup.”
Scientists Identify How E4 Raises Alzheimer’s Disease Risk
Given the genetic links to this disease, in a 2018 study published in the journal Nature Medicine,5 researchers from the Gladstone Institutes in San Francisco, California, sought to find out why the E4 variant was more harmful than the other variants, such as E3, and if anything could be done to correct the faulty gene.
In particular, the researchers investigated whether E4 was causing E3 to lose function or if the presence of more E4 led to the toxic effects. Dr. Yadong Huang, professor of neurology and pathology at the University of California, San Francisco, said in a news release:6
“It’s fundamentally important to address this question because it changes how you treat the problem. If the damage is caused due to the loss of a protein’s function, you would want to increase protein levels to supplement those functions. But if the accumulation of a protein leads to a toxic function, you want to lower production of the protein to block its detrimental effect.”
Another one of the issues Huang and his colleagues hoped to address in their research was the disconnect between the promising results shown through experiments involving lab mice and the subsequent lack of efficacy when the same methods have been applied to human trials. Huang said:7
“Drug development for Alzheimer’s disease has been largely a disappointment over the past 10 years. Many drugs work beautifully in a mouse model, but so far they’ve all failed in clinical trials. One concern within the field has been how poorly these mouse models really mimic human disease.”