Diabetes and Alzheimer's: new data
Diabetes mellitus provokes Alzheimer's disease by hypersynthesis of peripheral beta-amyloid
The downside of the increase in the average life expectancy of a person is an increase in the frequency of so–called age-dependent diseases. It is known that one of these diseases, type 2 diabetes mellitus, is a risk factor for the development of Alzheimer's disease, the main cause of senile dementia. And recently, scientists have managed to find out what mechanism mediates this connection.
Article by Shigemori et al. Peripheral Aß acts as a negative modulator of insulin secrecy is published in the journal Proceedings of the National Academy of Sciences.
Alzheimer's disease is characterized by the accumulation in the brain of the pathological protein beta-amyloid, which triggers the process of neurodegeneration. It is believed that the level of this protein in the blood reflects the pathology of the brain, so it is used as an appropriate diagnostic marker. But beta-amyloid can also be synthesized in other organs, where its molecular precursor and the enzymes necessary for synthesis are produced. However, nothing was known about the physiological role of peripheral beta-amyloid until recently.
Earlier, a group of Japanese scientists found that the level of beta-amyloid in the blood of mice and humans increases in response to the introduction of glucose and the hormone insulin, which regulates carbohydrate metabolism, in particular, glucose utilization. And now scientists have not only confirmed their results, but also found out the mechanism of this phenomenon.
The researchers hypothesized that blood beta-amyloid is produced in the cells of peripheral organs sensitive to glucose and insulin – pancreas, adipose tissue, skeletal muscles, liver – and participates in the regulation of blood glucose levels.
The scientists tested their assumptions in a number of experiments on mice, as well as on isolated tissues of various organs and cell cultures of these animals. In their work, they used lines of laboratory mice in which the synthesis of beta-amyloid was either "disabled" or, on the contrary, hyperactivated by genetic engineering methods.
As you know, after eating, the blood glucose level rises, which, in turn, stimulates the secretion of insulin by the beta cells of the pancreas. At the same time, as it turned out, they begin to synthesize beta-amyloid. The produced insulin acts on its target organs - adipose tissue, muscles and liver, which utilize glucose entering the blood, and the cells of these organs, in turn, also begin to produce and secrete their own beta-amyloid.
All this beta-amyloid from two sources begins to affect beta cells, acting as an insulin synthesis blocker. This two-stage regulation of the production of this hormone helps to maintain the desired level of glucose in the blood.
Based on the results obtained, the researchers suggested a mechanism that may link type 2 diabetes and Alzheimer's disease. As is known, in diabetes, the level of both glucose and insulin is elevated, which causes hypersecretion of peripheral beta-amyloid. And a consistently elevated level of this protein in the blood can affect the balance between the amount of beta-amyloid in the periphery and in the brain, suppressing its outflow through the cerebral glymphatic system. As a result, "excess" beta-amyloid accumulates in the brain, which provokes the development of Alzheimer's disease.
So in the light of new data, the practice of diagnosing Alzheimer's disease by the level of beta-amyloid in the blood looks rather doubtful, given that this level can fluctuate greatly due to organs involved in carbohydrate metabolism.
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