Cholinergic and GABAergic receptor functional deficit in the hippocampus of insulin-induced hypoglycemic and streptozotocin-induced diabetic rats

Hypoglycemic seizures and epilepsy in type I diabetes mellitus

“…Moreover, hypoglycemia may induce acute symptomatic seizures and also predispose to the development of epileptogenic processes. It is generally accepted that recurrent episodes of hypoglycemia can result in epilepsy due to the possible permanent damage in the hippocampus [11]. Our results do not support this idea, as the subjects in our study suffered several episodes (in one case more than 10) of hypoglycemic seizures without becoming epileptic.…”

The mature/pro nerve growth factor ratio is decreased in the brain of diabetic rats: Analysis by ELISA methods

“…Direct cerebral effects of metabolic aberrations caused by DM result in a diabetes durationrelated cognitive decline, so-called primary DE, which has been reported to predispose patients to Alzheimer's disease (AD) (Sims-Robinson et al, 2010). Indeed, a key point emerging from clinical and basic research on DE is that it shares common pathological characteristics with AD (Kroner, 2009), including an early involvement of the brain cholinergic system (Rocco et al, 2013;Sherin et al, 2012;Sposato et al, 2007;Welsh and Wecker, 1991). Our data on experimental diabetes point to an early reduction in the mNGF/proNGF ratio in the hippocampus and cortex of diabetic rats, which is evident at 4 weeks and lasts until 8 weeks after diabetes induction.…”

“…We then selected appropriate antibodies, used them in ELISA and checked for their specificity. Finally, since several reports describe the presence of brain cholinergic dysfunctions in diabetic encephalopathy (DE) (Kamboj et al, 2008;Rocco et al, 2013;Sherin et al, 2012;Sima, 2004;Wahba and Soliman, 1988;Welsh and Wecker, 1991), which could be associated with deregulation in NGF maturation (Rocco et al, 2013;Sposato et al, 2007), we validated our newly-developed ELISA in a study of the dynamics of mNGF/proNGF contents in rat brain during the development and early progression of experimental diabetes.…”

Antidiabetic drugs restore abnormal transport of amyloid-β across the blood–brain barrier and memory impairment in db / db mice

“…The vascular hypothesis on diabetes-associated cognitive dysfunction proposes that structural or functional changes in the BBB lead to accumulation of multiple vasculotoxic and neurotoxic macromolecules in the brain, reductions in cerebral blood flow, and subsequent impairment of hippocampal synaptic neurotransmission and cognition (Huber, 2008;Sherin et al, 2012). Specifically, abnormalities in the BBB may increase RAGE-mediated influx of peripheral Aβ into the brain or decrease LRP1-mediated Aβ efflux from the brain into bloodstream (Shibata et al, 2000), which cause brain Aβ accumulation and memory impairment.…”