2023-08-02 19:09:17
Title: Researchers Discover Brain Protein Dysregulation as the Cause of Normal Mental Decline in Old Age
By: Pamela Dörhöfer
Published: 08/02/2023, 7:09 p.m
According to a recent study conducted in the United States, the dysregulation of a brain protein has been identified as the primary factor responsible for the normal cognitive decline associated with old age. While this decline in mental capacity is often equated with dementia, the researchers emphasize that they are fundamentally different phenomena.
Dementia encompasses a range of diseases characterized by extensive cognitive losses and behavioral changes. However, the gradual degradation processes that occur naturally as people age must be distinguished. Symptoms of this normal aging process include forgetfulness, difficulty in learning new things, and scattered thinking, which may affect individuals to varying degrees.
Although the mechanisms underlying the clumping of proteins amyloid beta and tau in the brain have been identified as responsible for Alzheimer’s disease, the same cannot be said for the age-related cognitive decline seen in individuals without dementia.
Researchers at the Anschutz Medical Campus of the University of Colorado in the USA believe they have made significant progress in understanding this process. In a study published in the trade magazine Science Signaling, they propose that dysregulation of the brain protein CaMKII (calcium-calmodulin-dependent protein kinase II) is the root cause of cognitive losses in old age. CaMKII plays a crucial role in regulating energy metabolism in nerve cells, as well as the synthesis and release of neurotransmitters.
Lead author Ulli Bayer, a professor of pharmacology at the University of Colorado School of Medicine, explains that CaMKII is responsible for memory and learning. The researchers consider their findings a potential foundation for developing therapies that could halt mental deterioration associated with old age.
To explore this hypothesis, the scientists conducted experiments using mice in which they specifically modified the CaMKII protein. The resulting cognitive effects observed in the mice were comparable to those seen in normal aging. The pharmacologist explains that the modifications were sufficient to impair synaptic plasticity and memory, thus mimicking the effects of aging. The aging process affects a regulatory function called S-nitrosylation, which is important for both mice and humans.
The reduced amount of nitric oxide, a natural occurrence with age, is believed to be responsible for the decline in S-nitrosylation. Nitric oxide, produced by the body itself, has vasodilating and anti-inflammatory effects. The study suggests that this decrease in nitrosylation further impairs memory and learning abilities.
Lead author Bayer highlights that these findings offer hope for developing drugs or other forms of therapy that target the normalization of CaMKII nitrosylation. This potential treatment could potentially maintain or slow down normal cognitive decline in individuals for an extended period of time. However, Bayer emphasizes that such interventions would only be effective for age-related decline and not for dementia-related conditions.
This groundbreaking research provides valuable insights into the underlying mechanisms of age-related cognitive decline. Further research and clinical trials will be required to explore the feasibility of developing therapies that target the dysregulation of CaMKII and its impact on cognitive decline in old age.
Disclaimer: The content of this article is for informational purposes only and does not constitute medical advice.]
#forgetfulness #age