In the second study, the research team measured blood levels for highly sensitive C-reactive protein (hs-CRP) and hemoglobin A1c, which are standard tests for diabetes and systemic inflammation. Using the same conduction studies but evaluating the amplitude of the response to an electrical stimulus rather than its speed, the researchers found decline even in subjects with mild elevations in hs-CRP and hemoglobin A1c. The subjects' levels were within the normal, non-diabetic range for those measures.

"Even within 'normal ranges' for measures of inflammation and glucose metabolism, we are seeing an accelerated aging process that could contribute to progressive neuropathy," said Green. "These findings suggest that age, mild inflammation and mildly impaired glucose metabolism may be bad for nerve cells. Perhaps in the future, we can investigate whether a therapeutic intervention could delay the effect of age on peripheral nerve function. This may just be the tip of the iceberg. We have a lot to learn from this study population."

Both studies are important elements of a broad UCSF effort to learn how nerves age, developed in a groundbreaking collaboration between the UCSF Memory and Aging Center (Drs. Bruce Miller and Joel Kramer), the UCSF Multiple Sclerosis Center (Drs. Stephen Hauser, Ari Green and Jorge Oksenberg) and the UCSF Nerve Injury Clinic (Drs. John Engstrom and Amy Lee). The work was developed in advance of these groups moving together to the new Neurosciences Laboratory and Clinical Research Building at Mission Bay. Laboratory measures were performed in collaboration with the UC Davis Department of Pathology (Drs. Ralph Green and Josh Miller).

The UCSF team is looking at many factors related to how aging effects the connections between nerves and plans many future research studies with this population.

"An important next step is to test whether modification of risk factors like inflammation has an impact on nerve function," Green said.

Source: University of California - San Francisco