Reduce complications in diabetes

Effectively reduce diabetic brain complications

  • Prevent cognitive dysfunction
  • Reduce cerebrovascular complications
  • Minimize affected brain tissue following stroke
  • Treats other diabetic complications
  • Reduce brain complications
  • Manage blood sugar
  • Targets damaged cells


Licensing Manager: Catherine Murari-Kanti, Ph.D. or 402-559-3265


Effectively reduce diabetic brain complications

Keshore Bidasee, Ph.D., a researcher at the University of Nebraska Medical Center in Omaha, may have found a new way to treat diabetes that could improve the function of damaged organs like the kidneys, heart and eyes while also lowering blood sugar levels.

Keshore Bidasee, Ph.D.

An exciting new development at the University of Nebraska Medical Center helps mitigate the disastrous effects of diabetes—particularly degenerative and destructive brain complications more often seen in the elderly.
Research on diabetic animals show that an enzyme, Glyoxalase-1, could be used to treat common diabetes complications such as blindness, heart disease, kidney failure, and erectile dysfunction.
Even more promising, the therapy also helps improve brain function and minimizes the amount of brain tissue affected by a stroke, all while significantly helping reduce blood sugar levels.
Glyoxalase-1 targets and degrades the suspected cause of these complications—a naturally occurring chemical, methylglyoxal, which is created by damaged cells when blood sugar levels are high.
Currently there are no FDA-approved treatments that target brain complications in diabetes and also help manage blood sugar levels. But with a committed partnership, Glyoxalase-1 could be the first.
To discuss licensing opportunities please contact Catherine Murari-Kanti, Ph.D., at or 402-559-3265.

Technical details

Glyoxalase-1 therapy for complications in diabetes

A wide array of insulins, insulin delivery pumps, glucose monitoring devices and food management/exercise strategies are currently available to help individuals with diabetes mellitus regulate their blood glucose level. Unfortunately, these individuals continue to develop cardiovascular complications including kidney failure, heart failure, stroke, amputations, and blindness at rates 3-4 times higher than that of the general population, for which no specific pharmacological treatments are available.

More recent studies have also recognized cognitive impairment as another prominent co-morbidity in individuals with diabetes. Rather than add to the armamentarium of glucose-lowering strategies, research in Dr. Bidasee’s laboratory focuses on better understanding the underlying causes these cardiovascular complications, with the hope of identify therapeutic strategies that could supplement the existing glucose-lowering drugs.

Of particular interest in Dr. Bidasee’s group are the mono- and di-carbonyl molecules generated from lipid and glucose metabolism known collectively as reactive carbonyl species (RCS). These small molecule electrophiles regulate key physiologic functions including cell growth, differentiation, proliferation, and apoptosis. Furthermore, MGO and other RCS have longer half-lives (minutes to hours) than reactive oxygen species, allowing them to migrate and exert their effects at distant locations. They are also important regulators of anxiety and sleep.

These data help explain the lack of efficacy of anti-oxidant therapy in clinical studies, as RCS, and not reactive oxygen species, are the primary instigators in the disease pathogenesis. In diabetes, production of these molecules exceeds that needed for regulating these physiological functions, resulting in increases in oxidative stress, inflammation, DNA damage and the well-known cardiovascular diseases that cost Americans more than $60 billion annually in health care cost.

Methylglyoxal (MGO), the most potent of these RCS, increases as early as three days after hyperglycemia and could be responsible for vascular/cardiovascular dysfunction. In preliminary studies, brains of steptozotocin-induced diabetes rats contained more than 20 times the amount of MGO than control animals. Because MGO impairs cerebral vascular reactivity, it has been identified as a causative agent of the cognitive decline seen in diabetes.

Dr. Bidasee’s disclosed technology is a viral construct that strategically reduces MGO by overexpressesing glyoxalase-1 (Glo-1), the enzyme that degrades MGO. He identified a key promoter region that allows him to express Glo-1 only in damaged cells that are producing excess MGO. When injected intravenously in diabetic animals, the viral construct improved the functions of the heart, and brain, two key end-organs whose functions are negatively impacted in diabetes. It also improved cognition and reduced stroke damage (cerebral ischemia-reperfusion injury). His viral construct also modestly lowered blood glucose, which is always a good thing from a diabetes management standpoint.

Glo-1 overexpression is a novel therapeutic approach for blunting cerebral vascular dysfunction and cognitive impairment in diabetes. Since microvascular dysfunction is an established cause for other diabetic complications including blindness, kidney failure, diabetic cardiomyopathy, erectile dysfunction, and stroke, lowering MGO levels will also diminish these complications.