Project: Research project

Project Details


DESCRIPTION: This is a request for five years of support of a study of
diabetic neuropathy, a common complication of a common disease. The work is
a continuation and extension of work originally performed as part of a
clinical research center grant. It is an ongoing large-scale
cross-sectional and longitudinal clinical and epidemiological study of
nerve, eye, kidney, and large artery complications in diabetes mellitus in
Rochester, MN (patients of primarily Northern European extraction) and in
Prairie Island, MN (Mdewakanton Dakota native people). The main objectives
are to delineate the frequency, rate of progression, health, work and life
outcomes, and predictive risk profiles in various diabetic neuropathies.
Major efforts during previous funding periods were directed towards
developing diagnostic criteria and quantitative methods for objectively
scoring the severity of peripheral nerve disease. Those tools are now
available and will be used in the proposed studies.

There are four specific aims. The first is to develop and evaluate clinical
end points and composite scores for assessing diabetic polyneuropathy,
proximal diabetic neuropathy, diabetic truncal radiculopathy, and upper limb
mononeuropathies. Normative scales will be developed and changes in these
scores with time will be assessed in the different groups of diabetics. The
second aim is to evaluate the incidence, prevalence, and clinical outcomes
associated with specific manifestations of diabetic neuropathy in the
cohorts of diabetics maintained by the Mayo Clinic and extend these
observations to include a Native American population. Risk profiles will be
developed. The third aim is to identify risk factors for the various
neuropathies and examine whether there are identifiable groups of diabetics
who are at elevated risk of peripheral nerve complications. The fourth aim
is to use the above information to test the following hypotheses: that the
various forms of diabetic neuropathy have different pathogenic mechanisms;
that in diabetic polyneuropathy hyperglycemia either directly damages
Schwann cells or axons or first damages endoneurial microvessels (probably
by mechanisms involving altered blood flow and hypoxia); that immune
mechanisms are involved in the development of proximal diabetic neuropathy,
truncal radiculopathy, and oculomotor neuropathy.
Effective start/end date5/9/975/31/10


  • Medicine(all)
  • Neuroscience(all)