In the mid extracellular protein at stake is the protein amyloid. It is a membrane protein (located on the cell membrane). This protein detaches from the membrane and enters the extracellular environment. It is then recovered and then deteriorated.
In patients with Alzheimer's disease, this degradation is not total and a fragment called amyloid-β, remains and can not be degraded. These fragments eventually aggregate and form amyloid plaques. And accumulate in the extracellular environment, these plates compress neurons. This phenomenon which leads to dysfunction, which may be followed by neuronal death.
In addition, these plaques will release a peroxide formula H2O2. The link between the two oxygen atoms are very low, it will soon "break". There will be two OH molecules, called free radicals. Free radicals do not respect the rule of bytes, they are unstable. They will seek to combine their free electron. To do so, they will push through a hydrogen atom at the membrane of the neuron (composed of carbon molecules with many hydrogen atoms). The membrane "holes" will leave penetrate other free radicals that attack the DNA of the neuron, resulting in the destruction of the cell functions of private genetic information.
The cause of accumulation also appears with normal aging, but the accumulation at the base of Alzheimer's is unknown.
The only factor is a genetic factor. This concerns another protein that act with this process of formation of amyloid plaques. She called apolipoprotein E. this depends on a protein allele may be three kinds: E2, E3 and E4.
The E2 and E3 alleles are specific to the human species. They come from a mutation of the E4 gene. The most common allele is the E3 allele (70%), followed by E4 allele (20%) then the E2 allele (10%).
The E4 allele is associated with the formation of amyloid plaques. This allele would inhibit the growth neuritique (formation of axons and dendrites). This growth allows the neuronal plasticity. This is very important for the functioning of the central nervous system. The E4 allele is therefore associated with diseases of neuronal dysfunction. The E3 allele promotes neuronal plasticity, but not as much as the E2 allele. It is for this reason that the E2 allele is associated with longevity.
In patients with Alzheimer's disease, this degradation is not total and a fragment called amyloid-β, remains and can not be degraded. These fragments eventually aggregate and form amyloid plaques. And accumulate in the extracellular environment, these plates compress neurons. This phenomenon which leads to dysfunction, which may be followed by neuronal death.
In addition, these plaques will release a peroxide formula H2O2. The link between the two oxygen atoms are very low, it will soon "break". There will be two OH molecules, called free radicals. Free radicals do not respect the rule of bytes, they are unstable. They will seek to combine their free electron. To do so, they will push through a hydrogen atom at the membrane of the neuron (composed of carbon molecules with many hydrogen atoms). The membrane "holes" will leave penetrate other free radicals that attack the DNA of the neuron, resulting in the destruction of the cell functions of private genetic information.
The cause of accumulation also appears with normal aging, but the accumulation at the base of Alzheimer's is unknown.
The only factor is a genetic factor. This concerns another protein that act with this process of formation of amyloid plaques. She called apolipoprotein E. this depends on a protein allele may be three kinds: E2, E3 and E4.
The E2 and E3 alleles are specific to the human species. They come from a mutation of the E4 gene. The most common allele is the E3 allele (70%), followed by E4 allele (20%) then the E2 allele (10%).
The E4 allele is associated with the formation of amyloid plaques. This allele would inhibit the growth neuritique (formation of axons and dendrites). This growth allows the neuronal plasticity. This is very important for the functioning of the central nervous system. The E4 allele is therefore associated with diseases of neuronal dysfunction. The E3 allele promotes neuronal plasticity, but not as much as the E2 allele. It is for this reason that the E2 allele is associated with longevity.
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