CJD happens when proteins called prions, which form incorrectly, find their way into the brain. Prions have the unfortunate, destructive ability to deform the proteins around them as well. As the prions gradually eat away at neurons, they create sponge-like holes in the brain. This leads to dementia, loss of bodily function, and eventually coma and death.

A new study — published last month in the journal Scientific Reports — looked at national data on people 50 years and older from Japan between the years 2005 and 2014 and found a gradual rise in the country’s CJD cases and deaths. The increase in both was most prominent among those older 70, but the Okayama University scientists behind the research saw a rise of CJD even after the data had been corrected for age.

“Given this trend in aging of population, the disease burden of CJD will continue to increase in severity,” the scientists wrote in their paper. “Our findings thus recommend that policymakers be aware of the importance of CJD and focus on preparing to address the increasing prevalence of dementia.”

The researchers found that while equol production did not appear to impact levels of amyloid-beta deposited within the brain, it was associated with reduced white matter lesion volumes. Sekikawa’s team also discovered that high levels of isoflavones—soy nutrients that are metabolized into equol—had no effect on levels of white matter lesions or amyloid-beta when equol wasn’t produced.

According to Sekikawa, the ability to produce equol from soy isoflavones may be the key to unlocking protective health benefits from a soy-rich diet, and his team has previously shown that equol production is associated with a lower risk of heart disease. As heart disease is strongly associated with cognitive decline and dementia, equol production could help protect the aging brain as well as the heart.

A metabolite produced following consumption of dietary soy may decrease a key risk factor for dementia—with the help of the right bacteria, according to a new discovery led by researchers at the University of Pittsburgh Graduate School of Public Health.

Their study, published today in the journal Alzheimer’s & Dementia: Translational Research & Clinical Interventions, reports that elderly Japanese men and women who produce equol—a metabolite of dietary soy created by certain types of gut bacteria—display lower levels of white matter lesions within the brain.

“White matter lesions are significant risk factors for cognitive decline, dementia and all-cause mortality,” said lead author Akira Sekikawa, M.D., Ph.D., associate professor of epidemiology at Pitt Public Health. “We found 50% more white matter lesions in people who cannot produce equol compared to people who can produce it, which is a surprisingly huge effect.”

Our immune system’s capacity to mount a well-regulated defense against foreign substances, including toxins, weakens with age and makes vaccines less effective in people over age 65. At the same time, research has shown that immunotherapy targeting neurotoxic forms of the peptide amyloid beta (oligomeric Aβ) may halt the progression of Alzheimer’s disease, the most common age-related neurodegenerative disease.

A team led by Chuanhai Cao, Ph.D., of the University of South Florida Health (USF Health), has focused on overcoming, in those with impaired immunity, excess inflammation and other complications that interfere with development of a therapeutic Alzheimer’s vaccine.

Now, a preclinical study by Dr. Cao and colleagues indicates that an antigen-presenting dendritic vaccine with a specific antibody response to oligomeric Aβ may be safer and offer clinical benefit in treating Alzheimer’s disease. The vaccine, called E22W42 DC, uses immune cells known as dendritic cells (DC) loaded with a modified Aβ peptide as the antigen.