(Val8) glucagon-like peptide-1 prevents tau hyperphosphorylation, impairment of spatial learning and ultra-structural cellular damage induced by streptozotocin in rat brains

Lin, Li; Zhang, Zhifeng; Hölscher, Christian; Gao, Chong; Jiang, Yuan‐Hong; Liu, Yueze

doi:10.1016/j.ejphar.2011.11.005

Cited by 77 publications

(57 citation statements)

References 22 publications

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“…Furthermore, in an AD rat model induced by the intrahippocampal injection of Aβ, liraglutide (Han et al, 2013) and Val(8)GLP-1 (Wang et al, 2010 activate cAMP signaling in the brain and protect rats against the Aβ-induced impairments of spatial memory and deficit of LTP in a dose-dependent manner. In the rodent model of sporadic AD by intracerebroventricular injection with streptozotocin (STZ), liraglutide (Xiong et al, 2013), (Chen et al, 2012), Val(8)GLP-1 (Li et al, 2012a), and geniposide (Gao et al, 2014) decrease the hyperphosphorylation of τ and neurofilament proteins. In the P301L mouse model of tauopathy, liraglutide furthermore reduced the levels of tangles and hyperphosphorylated τ (Hansen et al, 2015).…”

Section: Effects Of Glp-1 On Neurodegenerative Diseasementioning

confidence: 99%

Incretin-based therapy for type 2 diabetes mellitus is promising for treating neurodegenerative diseases

Hölscher

2016

Reviews in the Neurosciences

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AbstractIncretin hormones include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Due to their promising action on insulinotropic secretion and improving insulin resistance (IR), incretin-based therapies have become a new class of antidiabetic agents for the treatment of type 2 diabetes mellitus (T2DM). Recently, the links between neurodegenerative diseases and T2DM have been identified in a number of studies, which suggested that shared mechanisms, such as insulin dysregulation or IR, may underlie these conditions. Therefore, the effects of incretins in neurodegenerative diseases have been extensively investigated. Protease-resistant long-lasting GLP-1 mimetics such as lixisenatide, liraglutide, and exenatide not only have demonstrated promising effects for treating neurodegenerative diseases in preclinical studies but also have shown first positive results in Alzheimer’s disease (AD) and Parkinson’s disease (PD) patients in clinical trials. Furthermore, the effects of other related incretin-based therapies such as GIP agonists, dipeptidyl peptidase-IV (DPP-IV) inhibitors, oxyntomodulin (OXM), dual GLP-1/GIP, and triple GLP-1/GIP/glucagon receptor agonists on neurodegenerative diseases have been tested in preclinical studies. Incretin-based therapies are a promising approach for treating neurodegenerative diseases.

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Section: Effects Of Glp-1 On Neurodegenerative Diseasementioning

confidence: 99%

Incretin-based therapy for type 2 diabetes mellitus is promising for treating neurodegenerative diseases

Hölscher

2016

Reviews in the Neurosciences

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“…In recent studies, GLP-1 or analogs were shown to ameliorate neurodegeneration and cognitive performance in icv-STZ rats with impaired insulin signaling in the brain. Treatment with exedin-4 (Ex-4), a long-acting GLP-1 receptor agonist, or (Val 8 )GLP-1 improved learning and memory in the Morris water maze and reversed icv-STZ-induced tau phosphorylation (Li et al, 2012b) via down-regulation of GSK3β activity (Chen et al, 2012). Ex-4 was also shown to improve cognitive behavior and neurogenesis in the hippocampus of adult rodents (Isacson et al, 2011) and in a mouse model of obesity and insulin-resistance (Gault et al, 2010).…”

Section: Insulinmentioning

confidence: 99%

Food for thought: The role of appetitive peptides in age-related cognitive decline

Fadel

Jolivalt

Reagan

2013

Ageing Research Reviews

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Through their well described actions in the hypothalamus, appetitive peptides such as insulin, orexin and leptin are recognized as important regulators of food intake, body weight and body composition. Beyond these metabolic activities, these peptides also are critically involved in a wide variety of activities ranging from modulation of immune and neuroendocrine function to addictive behaviors and reproduction. The neurological activities of insulin, orexin and leptin also include facilitation of hippocampal synaptic plasticity and enhancement of cognitive performance. While patients with metabolic disorders such as obesity and diabetes have greater risk of developing cognitive deficits, dementia and Alzheimer’s disease (AD), the underlying mechanisms that are responsible for, or contribute to, age-related cognitive decline are poorly understood. In view of the importance of these peptides in metabolic disorders, it is not surprising that there is a greater focus on their potential role in cognitive deficits associated with aging. The goal of this review is to describe the evidence from clinical and pre-clinical studies implicating insulin, orexin and leptin in the etiology and progression of age-related cognitive decline. Collectively, these studies support the hypothesis that leptin and insulin resistance, concepts normally associated with the hypothalamus, are also applicable to the hippocampus.

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“…On the 18th day of the study, spatial learning and memory of the animals were tested in Morris water maze (Joseph et al 2006;Li et al 2012). MWM was employed to assess learning and memory of the animals, wherein the animal learned to escape on to a hidden platform.…”

Section: Evaluation Of Spatial Memory By Morris Water Maze Test (Mwm)mentioning

confidence: 99%

Pterostilbene ameliorates intracerebroventricular streptozotocin induced memory decline in rats

2016

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There is strong evidence that mitochondrial dysfunction mediated oxidative stress results in aging and energy metabolism deficits thus playing a prime role in pathogenesis of Alzheimer's disease, neuronal death and cognitive dysfunction. Evidences accrued in empirical studies suggest the antioxidant, anticancer and anti-inflammatory activities of the phytochemical pterostilbene (PTS). PTS also exhibits favourable pharmacokinetic attributes compared to other stilbenes. Hence, in the present study, we explored the neuroprotective role of PTS in ameliorating the intracerebroventricular administered streptozotocin (STZ) induced memory decline in rats. PTS at doses of 10, 30 and 50 mg/kg, was administered orally to STZ administered Sprague-Dawley (SD) rats. The learning and memory tests, Morris water maze test and novel object recognition test were performed which revealed improved cognition on PTS treatment. Further, there was an overall improvement in brain antioxidant parameters like elevated catalase and superoxide dismutase activities, GSH levels, lowered levels of nitrites, lipid peroxides and carbonylated proteins. There was improved cholinergic transmission as evident by decreased acetylcholinesterase activities. The action of ATPases (Na ? K ? , Ca 2? and Mg 2? ) indicating the maintenance of cell membrane potential was also augmented. mRNA expression of battery of genes involved in cellular mitochondrial biogenesis and inflammation showed variations which extrapolate to hike in mitochondrial biogenesis and abated inflammation. The histological findings corroborated the effective role of PTS in countering STZ induced structural aberrations in brain.

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(Val8) glucagon-like peptide-1 prevents tau hyperphosphorylation, impairment of spatial learning and ultra-structural cellular damage induced by streptozotocin in rat brains

Cited by 77 publications

References 22 publications

Incretin-based therapy for type 2 diabetes mellitus is promising for treating neurodegenerative diseases

Incretin-based therapy for type 2 diabetes mellitus is promising for treating neurodegenerative diseases

Food for thought: The role of appetitive peptides in age-related cognitive decline

Pterostilbene ameliorates intracerebroventricular streptozotocin induced memory decline in rats

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