TY - JOUR
T1 - Insulin and IGF-1 receptors, nitrotyrosin and cerebral neuronal deficits in two young patients with diabetic ketoacidosis and fatal brain edema
AU - Hoffman, William H.
AU - Andjelkovic, Anuska V.
AU - Zhang, Weixian
AU - Passmore, Gregory G.
AU - Sima, Anders A.F.
N1 - Funding Information:
This work was supported in part by the Thomas Foundation (AAFS). The authors are grateful to Dr. M.F. Casanova for his careful review of the manuscript, and K.K. Smith and D.B. Cawley of the Georgia Research Pathology Service at the Medical College of Georgia for their technical expertise.
PY - 2010/7/9
Y1 - 2010/7/9
N2 - Gray and white matter structural deficits may accompany type 1 diabetes. Earlier experimental studies have demonstrated neuronal deficits associated with impaired neurotrophic support, inflammation and oxidative stress. In this study we demonstrate in two patients with histories of poorly controlled type 1 diabetes and fatal brain edema of ketoacidosis neuronal deficits associated with a decreased presence of insulin and IGF-1 receptors and accumulation of nitrotyrosin in neurons of affected areas and the choroid plexus. The findings add support to the suggested genesis of T1DM encephalopathy due to compromised neurotrophic protection, oxidative stress, inflammation and neuronal deficits, as demonstrated in T1DM encephalopathy in the BB/Wor-rat.
AB - Gray and white matter structural deficits may accompany type 1 diabetes. Earlier experimental studies have demonstrated neuronal deficits associated with impaired neurotrophic support, inflammation and oxidative stress. In this study we demonstrate in two patients with histories of poorly controlled type 1 diabetes and fatal brain edema of ketoacidosis neuronal deficits associated with a decreased presence of insulin and IGF-1 receptors and accumulation of nitrotyrosin in neurons of affected areas and the choroid plexus. The findings add support to the suggested genesis of T1DM encephalopathy due to compromised neurotrophic protection, oxidative stress, inflammation and neuronal deficits, as demonstrated in T1DM encephalopathy in the BB/Wor-rat.
KW - Choroid plexus
KW - Diabetic encephalopathy
KW - Diabetic ketoacidosis
KW - Insulin and IGF-1 receptors
KW - Neuronal deficit
KW - Oxidative/nitrosative stress
KW - Proton magnetic resonance spectroscopy
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U2 - 10.1016/j.brainres.2010.04.042
DO - 10.1016/j.brainres.2010.04.042
M3 - Article
C2 - 20420811
AN - SCOPUS:77953617603
SN - 0006-8993
VL - 1343
SP - 168
EP - 177
JO - Brain Research
JF - Brain Research
ER -