Intracerebral streptozotocin model of type 3 diabetes: Relevance to sporadic Alzheimer's disease

Lester-Coll, N.H.; Rivera, Enrique J.; Soscia, Stephanie J.; Doiron, Kathryn; Wands, Jack R.; Monte, Suzanne M. de la

doi:10.3233/jad-2006-9102

Cited by 407 publications

(396 citation statements)

References 90 publications

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“…Supporting the hypothesis that the pathophysiology in the STZ-icv animal models shares huge similarities with the one in AD patients, cholinergic deficits have also been consistently found in various STZ-icv animal AD models (from newborn and adult rats to adult mice treated with STZ-icv), by demonstrating as a decrease in ChAT and an increase in AChE activity in the hippocampus, respectively (Hellweg et al 1992;Blokland and Jolles 1993;Blokland and Jolles 1994;Prickaerts et al 1999;Terwel et al 1995;Sonkusare et al 2005;Ishrat et al 2006;(Lester-Coll et al 2006; de la Monte et al 2006;Kumar et al 2010;Tota et al 2011). Importantly, AChE inhibitors tested so far, have been consistently successful in improving/preventing memory deficits in STZ-icv sAD models.…”

Section: Acetylcholinesterase Inhibitors and Other Cholinergic-relatementioning

confidence: 82%

“…The PPAR agonist-induced effect has been explored also in the 3-day-old rat pups given STZ-icv injection (40 µg/kg) and on the same day treated with a single ip injection of saline or PPAR α/δ/γ agonists with memory evaluation and brain analysis being done 4 weeks after the drug treatment (de la Monte et al 2006). PPAR agonist treatments showed responses in range from being inefficient to partially or completely rescuing the brains from STZ-mediated neurodegeneration.…”

Section: Insulin-sensitizing and Other Anti-diabetic Drugsmentioning

confidence: 99%

“…Following the parenteral administration of high doses, STZ selectively destroys insulin producing/secreting β cells in the pancreas, causing DM type I in adult animals (Szkudelski 2001), while multiple parenteral treatment with low to moderate STZ doses causes insulin resistance by damaging insulin receptor (IR) signalling (Blondel and Portha 1989;Kadowaki et al 1984;Giorgino et al 1992). Intracerebroventricular administration of low, subdiabetogenic doses of STZ has been shown to induce cognitive (Mayer et al 1991;Lannert and Hoyer 1998) and brain cholinergic deficits (Hellweg et al 1992;Blockland andJolles 1993, 1994), oxidative stress (Sharma and Gupta, 2001a;Sharma and Gupta 2002;Ishrat et al 2006;Pathan et al 2006;Shoham et al, 2006;Kumar et al, 2010;Saxena et al, 2011) as well as decrement in brain glucose/energy metabolism (Nitsch and Hoyer 1991;Plaschke et al 1996;Lannert and Hoyer 1998;Hoyer and Lannert 2007), and insulin resistant brain state (Salkovic-Petrisic et al 2006;Gruenblatt et al 2007;Steen 2006;Lester-Coll et al 2006;Agrawal et al 2010). These STZ-icv induced effects have been extensively reviewed elsewhere Salkovic-Petrisic et al 2012), and will not be elaborated here.…”

Section: Introductionmentioning

confidence: 99%

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What have we learned from the streptozotocin-induced animal model of sporadic Alzheimer’s disease, about the therapeutic strategies in Alzheimer’s research

et al. 2012

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Section: Acetylcholinesterase Inhibitors and Other Cholinergic-relatementioning

confidence: 82%

Section: Insulin-sensitizing and Other Anti-diabetic Drugsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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What have we learned from the streptozotocin-induced animal model of sporadic Alzheimer’s disease, about the therapeutic strategies in Alzheimer’s research

et al. 2012

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“…Disturbances in central insulin signaling have also been shown to affect amyloid-beta (Ab) levels and tau protein hyperphosphorylation (Hoyer, 2004;Salkovic-Petrisic et al, 2009), supporting the notion that sAD may be considered to be the brain type of diabetes (Hoyerm 2002;. The intracerebroventricular (icv) administration of the diabetes-inducing drug streptozotocin (icv-STZ) has been investigated as a non-transgenic model of sAD (Lester-Coll et al, 2006;Salkovic-Petrisic and Hoyer, 2007). Subdiabetogenic doses of icv-STZ (1-3 mg/kg) mimic features of human sAD, such as metabolic dysfunctions (Hoyer and Lannert, 2007), brain insulin resistance associated with tau protein hyperphosphorylation (Gru¨nblatt et al, 2007;Barilar et al, 2015), Ab-like aggregation in meningeal vessels (Salkovic-Petrisic et al, 2011), cholinergic deficits (Blokland and Jolles, 1993), and memory impairments (Lannert and Hoyer, 1998;Agrawal et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Chronic nicotine attenuates behavioral and synaptic plasticity impairments in a streptozotocin model of Alzheimer’s disease

et al. 2017

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Abstract-Brain glucose metabolism is altered in sporadic Alzheimer's disease (sAD), whose pathologies are reproduced in rodents by intracerebroventricular (icv) infusion of streptozotocin (STZ) in subdiabetogenic doses. The icv-STZ model also culminates in central cholinergic dysfunctions, which in turn are known to underlie both the sAD cognitive decline, and synaptic plasticity impairments. Considering the cognitive-enhancing potential of chronic nicotine (Nic), we investigated whether it attenuates icv-STZ-induced impairments in recognition memory and synaptic plasticity in a cognition-relevant substrate: the hippocampal CA1-medial prefrontal cortex (mPFC) pathway. Rats treated with icv-STZ were submitted to a chronic Nic regime, and were evaluated for recognition memory. We then examined long-term potentiation (LTP), paired-pulse facilitation (PPF) under urethane anesthesia, and brains were also evaluated for hippocampus-mPFC cell density. We found that Nic treatment prevents icv-STZ-induced disruptions in recognition memory and LTP. STZ did not precipitate neuronal death, while Nic alone was associated with higher neuronal density in CA1 when compared to vehicle-injected animals. Through combining behavioral, neurophysiological, and neuropathological observations into the Nic-STZ interplay, our study reinforces that cholinergic treatments are of clinical importance against earlystage Alzheimer's disease and mild cognitive impairments.

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“…The majority of AD patients are late onset (sporadic) and the disease usually develops after 65 years of age. Sporadic AD (SAD) is associated with peripheral insulin abnormalities, which might influence cerebral glucose metabolism in the brain (Lester-Coll et al 2006). De Santi et al demonstrated the hypometabolism of hippocampal glucose in patients with AD compared to control individuals (De Santi et al 2001), and hypothesised that reduced glucose utilisation and energy metabolism may be two of the main causes of the impaired cognition observed in AD (Rivera et al 2005).…”

Section: Introductionmentioning

confidence: 99%

Curcumin ameliorates impaired insulin/IGF signalling and memory deficit in a streptozotocin-treated rat model

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Ulusoy

et al. 2008

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Increased serum insulin levels and reduced peripheral insulin activities seen in insulin resistance syndrome are associated with age-dependent cognitive impairment and Sporadic Alzheimer's Disease (SAD), suggesting a disturbance in the insulin signalling system in the brain and possibly being one of the causes of dementia. Therefore, the streptozotocin (STZ)-induced animal may be an appropriate model for the investigation of SAD and related dementia. This study was designed to investigate the beneficial effect of Curcumin (CUR), a neuroprotective agent, on intracerebroventricular (ICV) STZ-induced cognitive impairment in rats. For this purpose, adult male Wistar rats were bilaterally ICV injected with STZ (3 mg/kg). An artificial cerebrospinal fluid (aCSF) was given to the control group (SHAM) instead of STZ on days 1 and 3. Learning and memory performance were assessed using the "passive avoidance task" and the "Morris water maze test". After confirmation of acquisition impairment with these tests, the STZ group was divided into two subgroups: STZ+ vehicle (Vh) and STZ+CUR. The rats in the SHAM and STZ+Vh groups were administered intraperitoneally with 0.5 ml Vh and the rats in the STZ+CUR group were treated intraperitoneally with CUR (300 mg kg −1 day −1 in Vh) for 10 days starting from the 25th day after STZ injection. The Morris water maze test was reapplied on the 35th day after STZ injection and all of the rats were sacrificed on day 36 for quantitation of IGF-1 and for histopathological evaluation. Rats in the STZ+CUR group were found to have a higher performance in cognitive tests than rats in the STZ+Vh group (P<0.01). In parallel with the cognitive tests, IGF-1 levels were decreased in all of the STZ-injected groups (1.78±0.34) compared to the SHAM group (3.46±0.41). In contrast, CUR treatment significantly increased IGF-1 levels (P<0.001). The degree of neuronal loss decreased after CUR treatment compared to the SHAM group (P< 0.02). These results clearly indicate that CUR treatment is effective in reducing the cognitive impairment caused AGE

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Intracerebral streptozotocin model of type 3 diabetes: Relevance to sporadic Alzheimer's disease

Cited by 407 publications

References 90 publications

What have we learned from the streptozotocin-induced animal model of sporadic Alzheimer’s disease, about the therapeutic strategies in Alzheimer’s research

What have we learned from the streptozotocin-induced animal model of sporadic Alzheimer’s disease, about the therapeutic strategies in Alzheimer’s research

Chronic nicotine attenuates behavioral and synaptic plasticity impairments in a streptozotocin model of Alzheimer’s disease

Curcumin ameliorates impaired insulin/IGF signalling and memory deficit in a streptozotocin-treated rat model

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