2023-08-03 03:13:17
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If you get clumsy in old age, it doesn’t have to have anything to do with dementia. © Ute Grabowsky/Imago (symbol image)
According to a US study, the dysregulation of a brain protein is responsible for normal mental decline.
Frankfurt – Dementia and an age-related decline in memory and concentration are often equated – although they are fundamentally different. The term dementia describes a range of diseases that are associated with extensive cognitive losses and behavioral changes. On the other hand, non-morbid degradation processes that can set in as we get older must be distinguished: one becomes scatterbrained, forgets more, it is more difficult to learn new things; some people are more affected, others less or not at all.
While it is now assumed that the central mechanisms underlying the clumping of the proteins amyloid beta and tau in the brain are known for Alzheimer’s disease, for example, these have not yet been clearly identified for the “normal” age-related degradation.
Researchers at the Anschutz Medical Campus of the University of Colorado (USA) seem to have struck gold. In the trade magazine Science Signaling they suspect that a dysregulation of the brain protein CaMKII (calcium-calmodulin-dependent protein kinase II) is responsible for cognitive losses in old age. Among other things, this protein regulates the energy metabolism in nerve cells and the synthesis and release of neurotransmitters.
Age-related degradation in the brain: too little nitric oxide
CaMKII is “responsible for memory and learning,” study author Ulli Bayer, professor of pharmacology at the University of Colorado School of Medicine, said in one communication quoted from the university. At the same time, the researchers see their findings as a basis for a therapy that might be used to stop mental deterioration.
In their study, the scientists worked with mice in which they specifically modified the CaMKII protein. That caused cognitive effects that are comparable to those of normal aging, says Bayer. The modification was sufficient “to lead to impairments in synaptic plasticity and memory that are similar to aging,” explains the pharmacologist. He goes on to say that aging changes the so-called S-nitrosylation in both mice and humans – a process with diverse regulatory functions in cells.
Therapy of age-related brain decline
Responsible for this, according to Bayer, is a reduced amount of nitric oxide, which is natural with age. Nitric oxide produced by the body itself has, among other things, a vasodilating and anti-inflammatory effect. According to the study, this decrease in turn reduces nitrosylation – which impairs memory and learning ability.
According to lead author Bayer, these findings open the way for the development of drugs and other forms of therapy aimed at normalizing CaMKII nitrosylation. “That would be the logical step,” he explains. For the pharmacologist, it would offer the opportunity “to treat or stave off normal cognitive decline for an unknown period of time.” Bayer also expressly points out that such a potential treatment would only help with age-related decline and not with dementia diseases. (Pamela Dörhöfer)
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