Proteins that can cause age-related neurological diseases are found
Last reviewed: 23.04.2024
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Scientists from the Salk Institute for Biological Research (USA) have discovered proteins that can cause age-related neurological diseases, from mild memory deterioration to severe forms of dementia. They, figuratively speaking, open the way for age-related changes in the nerve cell, but are themselves, ironically, called "super-long-living proteins" (or ELLP).
Age-related organ dysfunctions are often associated with disorders of homeostasis, the equilibrium state of cells, or more precisely, molecular machines that support this equilibrium. The cell loses control over the exchange of matter and energy with the environment: poisonous molecules begin to penetrate into it, for example, and garbage ceases to appear from it; as a result, the cell is performing its functions worse and worse. Obviously, in this case, the responsibility lies partly with the proteins that control the transport of substances into and out of the cage. The overdimensional proteins belong precisely to this: they form a nuclear pore complex of neurons, the exchange of substances between the nucleus and the cytoplasm depends on them.
Scientists have examined rat neurons and found that these ELLPs are irremovable, that is, the same protein sits in its place until the animal dies. This is what makes them, perhaps, a weak link: molecules of super-long-living proteins accumulate damage, while not updating themselves. Conventional proteins, after receiving a dose of damage, are turned into scrap, and new molecular machines stand in their place. ELLP in this sense can be likened to the Soviet party functionaries, who left the office only, as they say, with their feet forward. But in the case of these squirrels, their host also carries their feet forward.
Over time, these longevity begin to work poorly: the damage is affected. And this means that unwanted substances begin to penetrate into the nucleus of neurons. They get access to DNA, which can in their own way be modified. As a result, instead of a healthy version of a neural protein, its pathogenic form forming insoluble protein complexes - the characteristic symptoms of neurodegenerative diseases, Alzheimer's syndrome, Parkinson's syndrome, etc. - can begin to be synthesized. Of course, this is only one of the possible consequences that DNA damage can lead to.
Earlier, in the same laboratory, it was possible to establish a connection between the disturbances in the work of the nuclear pore complex and the age-related changes in neurons. Now, it can be said, scientists managed to establish immediate "culprits" of aging nerve cells. It is not yet clear whether there are the same long-living proteins in the nuclei of other types of cells. Perhaps, if one can learn to somehow restrain the aging of such proteins (or even change them to new ones), this will significantly slow down the aging process, at least for nerve cells.
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