This was a two-part study, first on mice, then on humans. The researchers found that mice fed a diet high in AGEs had a build-up of amyloid proteins in the brain and impaired cognitive function. Those eating a low-AGE diet, on the other hand, had no amyloid build up! In the second part, a short-term analysis of humans also suggested high levels of AGEs in the blood was linked to cognitive decline.
The most intriguing result from that first part was the fact that mice fed a low-AGE diet had no build of amyloid protein or cognitive decline. This firmly puts 'glycotoxins' as a modifiable risk for Alzheimer's disease.
The researchers point our that AGEs are present in a wide variety of foods in the typical Western diet, and these have previously been linked to a variety of health conditions including diabetes and neurodegenerative disease.
Previously, the mechanisms linking AGEs to health conditions were not know; however, this study provided some new knowledge in this area. The researchers found that older mice on the high-AGE diet, similar to older regular fed controls, developed metabolic syndrome, increased brain amyloid-beta, deposits of AGEs, gliosis, and cognitive deficits, accompanied by suppressed SIRT1,
nicotinamide phosphoribosyltransferase, AGE receptor 1, and PPAR-gamma. Interestingly, these changes were not due to ageing or caloric intake, since these changes were not present in age-matched, low-AGE diet mice.
In the follow-on clinical on 93 healthy humans over the age of 60, the researcher also found that individuals who had high AGEs in their blood also had low SIRT1 levels in their blood and developed cognitive decline and insulin resistance over a nine month follow-up period.
The good new is that activating SIRT1 or correcting its deficiency in humans is both preventable and reversible by AGE reduction. There's a lot of research coming out in this area, so make sure you subscribe Know Guff to stay on top of this!
Source: Oral glycotoxins are a modifiable cause of dementia and the metabolic syndrome in mice and humans
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