Vitamin B12 deficiency is associated with an increased risk of brain disorders with aging, including Alzheimer's disease. But as shown by meta-analyses and randomized controlled research on people aged 70 years and older, compensation deficiency of vitamin B12 does not improve cognitive functions.
As it turned out, it's not the level of vitamin B12 in blood that matters but its content in the frontal cortex. Even at its normal level in blood, the concentration of vitamin B12, especially its active form methylcobalamin, decreases in the frontal cortex after 60 years old 10 times and stays in deficit — even down to zero.
The thing is, transport (carriers and carrier mediators) activity reduces with age, so B12 cannot reach frontal cortex of the brain through the blood-brain barrier. The reduction of these conveyors begins to occur visibly already at the age of 40 and reaches critically low levels at around 60. Starting at 40 the brain begins to accumulate beta-amyloid and after 65 Alzheimer's disease starts to be diagnosed.
What are these carriers and carrier mediators? These are glutathione and megalin, which is partly involved in the amyloid brain liberation. Thus, increasing glutathione and megalin levels, as well as controlling the levels of vitamin B12 in the blood, it is likely to provide a sufficient level of B12 in the brain of older people and prevent a large percentage of cases of Alzheimer's disease.
Clinical trials we plan to conduct at the expense of funds collected via ICO.