Study Reveals Tat-HSP10 Protein’s Potential in Enhancing Brain Function and Slowing Cognitive Decline

Addressing the growing issue of cognitive decline in aging populations, this study investigates Tat-heat shock protein 10 (Tat-HSP10) as a potential solution for enhancing brain function and mitigating dementia symptoms.

Old Woman With Dementia

Old Woman With Dementia

Tat-heat shock protein 10 (Tat-HSP10) a protein produced in response to stress improves brain plasticity and stimulates the mitochondrial function of brain cells. In other words, a small supplement of Tat-HSP10 could strengthen the brain and cognition, which decline with age. These results, published in the journal Aging and not yet validated in humans, illustrate the progress made in the search for new therapies to combat cognitive decline and dementia.

Read Also: Adults Still Have Considerable Brain Plasticity and Flexible Learning Due to Silent Synapses

Overview of Tat-HSP10 and Its Potential in Cognitive Health

The Tat-HSP10 protein appears to slow down mitochondrial dysfunction, an important cellular alteration observed in the hippocampus during aging – according to this team from the universities of Seoul, Chungnam, and Gangneung-Wonju in South Korea.

Research Methodology and Experimental Findings

The research carried out at this stage on adult and elderly mice, focused on the effects of the protein on memory function, neurogenesis in the hippocampus, and certain associated genes or proteins. In order to transfer the HSP10 protein to the hippocampus, the Tat-HSP10 fusion protein was synthesized and the researchers administered Tat-HSP10 daily to 3- and 21-month-old mice for 3 months. This experiment revealed :

  • A significant increase in the senescence factor P16 in aged control mice.
  • A significant decrease in P16 expression in the hippocampus of the aged mice treated with Tat-HSP10.
  • These mice also performed better in cognitive tests for mice that included an object recognition test and a water maze test: treatment with Tat-HSP10 significantly reduced the number of exploratory attempts, the number of contacts with objects, and the time spent swimming, in aged mice.
  • The same results were not observed in younger mice that were also treated.
  • Tat-HSP10 administration induced an increase in the proliferation of differentiated neuroblasts in the dentate gyrus of adult and old mice compared to controls.
  • Tat-HSP10 administration significantly reduced the decrease in the levels of mRNA and proteins involved in aging, reducing aging phenotypes in the hippocampus.

Read Also: Adult Brains Also Have Silent Synapses For New Memories, Researchers Find

Implications and Future Research

Taken together, these results, which have not yet been reproduced in humans, suggest that supplementation with Tat-HSP10 or an analog could strengthen mitochondrial function and delay cognitive aging.

Final Thoughts

The study on Tat-HSP10 marks a significant stride in understanding cognitive aging. However, its application in human health remains to be explored. This research paves the way for future investigations, crucial for advancing dementia therapies.

References

Jung, H. Y., Kwon, H. J., Hahn, K. R., Kim, W., Yoo, D. Y., Yoon, Y. S., Kim, D. W., & Hwang, I. K. (2023). Tat-heat shock protein 10 ameliorates age-related phenotypes by facilitating neuronal plasticity and reducing age-related genes in the hippocampus. Aging, 15(22). https://doi.org/10.18632/aging.205182

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