Proteins have been discovered that may be responsible for age-related neurological diseases

Scientists from the Salk Institute for Biological Studies (USA) have discovered proteins that may be the cause of age-related neurological diseases, ranging from mild memory loss to severe forms of dementia. They, figuratively speaking, pave the way for age-related changes in the nerve cell, but ironically enough, they themselves are called “ultra-long-lived proteins” (or ELLPs).

Age-related organ dysfunctions are often associated with disturbances in homeostasis, the equilibrium state of cells, or more precisely, the molecular machines that maintain this equilibrium. The cell loses control over the exchange of matter and energy with the environment: for example, toxic molecules begin to penetrate into it, and garbage stops being removed from it; as a result, the cell performs its functions worse and worse. Obviously, in this case, the responsibility partly lies with the proteins that control the transport of substances into and out of the cell. Super-long-lived proteins are just such: they form the nuclear pore complex of neurons, and the exchange of substances between the nucleus and the cytoplasm depends on them.

Scientists have studied rat neurons and discovered that these ELLPs are irreplaceable, meaning that the same protein sits in its place until the animal dies. This is what makes them, perhaps, a weak link: the molecules of super-long-lived proteins accumulate damage without being renewed themselves. Regular proteins, having received a certain amount of damage, are scrapped, and new molecular machines take their place. In this sense, ELLPs can be likened to Soviet party functionaries who left their office only, as they say, feet first. But in the case of these proteins, their owner is also carried feet first.

Over time, these long-livers begin to function poorly: the damage they have received takes its toll. This means that unwanted substances begin to penetrate the nucleus of neurons. They gain access to DNA, which they can modify in their own way. As a result, instead of a healthy version of a neuronal protein, its pathogenic form can begin to be synthesized, forming insoluble protein complexes - characteristic symptoms of neurodegenerative diseases, Alzheimer's, Parkinson's syndromes, etc. Of course, this is only one of the possible consequences that DNA damage can lead to.

Earlier, the same laboratory managed to establish a connection between disturbances in the functioning of the nuclear pore complex and age-related changes in neurons. Now, one can say that scientists have managed to establish the direct "culprits" of nerve cell aging. It is not yet clear whether there are similar long-lived proteins in the nuclei of other types of cells. Perhaps, if we manage to learn how to somehow restrain the aging of such proteins (or even replace them with new ones), this will significantly slow down the aging process, at least in nerve cells.

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