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The level of carbonylation of plasma proteins and peripheral blood leukocytes in patients with different duration of Alzheimer’s disease
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The course of Alzheimer’s disease is associated with an increase in oxidative stress associated with an increase in the production of reactive oxygen species against the background of neurodegenerative inflammation, and a simultaneous depletion of the antioxidant defense capabilities of brain cells. The result is the oxidative modification of macromolecules: proteins, lipids, nucleic acids. Protein carbonylation products accumulate not only in neurons, and in direct correlation with the degree of increase in amyloidosis and neurodegeneration, but also in extra-neuronal tissues, including leukocytes. In the course of this study, the levels of spontaneous and induced oxidative modification of proteins were determined in the blood plasma and fractionated leukocytes of peripheral blood of patients with different durations of Alzheimer’s disease, and the value of the reserve-adaptive potential was assessed as markers of the severity of oxidative stress. It has been established that the course of Alzheimer’s disease has a greater effect on the accumulation of carbonyl derivatives in blood plasma. In patients with a disease duration of 5–10 years, the total level of aldehyde and ketone derivatives of modified plasma proteins exceeds the same indicator in subgroups with a shorter duration of the disease. This tendency is less typical for mononuclear leukocytes. The level of induced oxidative modification of proteins increases to a greater extent in blood plasma than in fractionated leukocytes. This indicates the depletion of the reserve-adaptive potential of plasma antioxidant capabilities, which is more pronounced in patients with a long course of Alzheimer’s disease. For polymorphonuclear leukocytes, such a pattern was not revealed, which is probably associated with a short cell life. In mononuclear leukocytes, as well as in plasma, there is a tendency to depletion of the reserve-adaptive potential, but to a lesser extent.
Title: The level of carbonylation of plasma proteins and peripheral blood leukocytes in patients with different duration of Alzheimer’s disease
Description:
The course of Alzheimer’s disease is associated with an increase in oxidative stress associated with an increase in the production of reactive oxygen species against the background of neurodegenerative inflammation, and a simultaneous depletion of the antioxidant defense capabilities of brain cells.
The result is the oxidative modification of macromolecules: proteins, lipids, nucleic acids.
Protein carbonylation products accumulate not only in neurons, and in direct correlation with the degree of increase in amyloidosis and neurodegeneration, but also in extra-neuronal tissues, including leukocytes.
In the course of this study, the levels of spontaneous and induced oxidative modification of proteins were determined in the blood plasma and fractionated leukocytes of peripheral blood of patients with different durations of Alzheimer’s disease, and the value of the reserve-adaptive potential was assessed as markers of the severity of oxidative stress.
It has been established that the course of Alzheimer’s disease has a greater effect on the accumulation of carbonyl derivatives in blood plasma.
In patients with a disease duration of 5–10 years, the total level of aldehyde and ketone derivatives of modified plasma proteins exceeds the same indicator in subgroups with a shorter duration of the disease.
This tendency is less typical for mononuclear leukocytes.
The level of induced oxidative modification of proteins increases to a greater extent in blood plasma than in fractionated leukocytes.
This indicates the depletion of the reserve-adaptive potential of plasma antioxidant capabilities, which is more pronounced in patients with a long course of Alzheimer’s disease.
For polymorphonuclear leukocytes, such a pattern was not revealed, which is probably associated with a short cell life.
In mononuclear leukocytes, as well as in plasma, there is a tendency to depletion of the reserve-adaptive potential, but to a lesser extent.
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