Potential effects of current drug therapies on cognitive impairment in patients with type 2 diabetes

Palleria, Caterina; Leporini, Christian; Maida, Francesca; Succurro, Elena; Sarro, Giovambattista De; Arturi, Franco; Russo, Emilio

doi:10.1016/j.yfrne.2016.07.002

Cited by 50 publications

(56 citation statements)

References 240 publications

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“…2) [13, 63–68]. Dr. Yoshinori Ohsumi discovered autophagy-related genes (ATGs) using a genetic screening approach in Saccharomyces cerevisiae and awarded the 2016 Nobel Prize in Physiology or Medicine for his remarkable contribution to autophagy research [1, 4, 69–71]. …”

Section: Programmed Cell Death (Pcd)mentioning

confidence: 99%

Autophagy and its link to type II diabetes mellitus

Yang¹,

Lu²,

Kuo³

et al. 2017

BioMedicine

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Autophagy, a double-edged sword for cell survival, is the research object on 2016 Nobel Prize in Physiology or Medicine. Autophagy is a molecular mechanism for maintaining cellular physiology and promoting survival. Defects in autophagy lead to the etiology of many diseases, including diabetes mellitus (DM), cancer, neurodegeneration, infection disease and aging. DM is a metabolic and chronic disorder and has a higher prevalence in the world as well as in Taiwan. The character of diabetes mellitus is hyperglycemia resulting from defects in insulin secretion, insulin action, or both. Type 2 diabetes mellitus (T2DM) is characterized by insulin resistance and failure of producing insulin on pancreatic beta cells. In T2DM, autophagy is not only providing nutrients to maintain cellular energy during fasting, but also removes damaged organelles, lipids and miss-folded proteins. In addition, autophagy plays an important role in pancreatic beta cell dysfunction and insulin resistance. In this review, we summarize the roles of autophagy in T2DM.

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Section: Programmed Cell Death (Pcd)mentioning

confidence: 99%

Autophagy and its link to type II diabetes mellitus

Yang¹,

Lu²,

Kuo³

et al. 2017

BioMedicine

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“…There are previous review articles that discuss the association between T2DM and PD [4,[11][12][13][14][15] or the common therapeutic approaches to T2DM and PD [4,13,16,17]. Our review provides an updated discussion on the epidemiological association between T2DM and PD, the shared pathways involved in T2DM and PD pathophysiology, and the common therapeutic approaches to T2DM and PD.…”

Section: Introductionmentioning

confidence: 99%

The Association Between Type 2 Diabetes Mellitus and Parkinson’s Disease

Cheong

Pablo-Fernández

Foltynie

et al. 2020

JPD

134

120

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In recent years, an emerging body of evidence has forged links between Parkinson's disease (PD) and type 2 diabetes mellitus (T2DM). In observational studies, those with T2DM appear to be at increased risk of developing PD, as well as experiencing faster progression and a more severe phenotype of PD, with the effects being potentially mediated by several common cellular pathways. The insulin signalling pathway, for example, may be responsible for neurodegeneration via insulin dysregulation, aggregation of amyloids, neuroinflammation, mitochondrial dysfunction and altered synaptic plasticity. In light of these potential shared disease mechanisms, clinical trials are now investigating the use of established diabetes drugs targeting insulin resistance in the management of PD. This review will discuss the epidemiological links between T2DM and PD, the potential shared cellular mechanisms, and assess the relevant treatment options for disease modification of PD.

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“…Considering the pathogenesis of T2DM and brain dysfunction, antidiabetic drugs may also exert beneficial effects on neuronal metabolism, which could be clinically significant for the treatment of CNS complications in DM and other neurological diseases (12). Glucagon-like peptide-1 (GLP-1) receptor agonists are a novel type of hypoglycemic drug used in clinical practice, which have been reported to possess numerous Liraglutide improves cognitive impairment via the AMPK and PI3K/Akt signaling pathways in type 2 diabetic rats potential benefits in improving capacity in various animal models of neurodegeneration (13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

Liraglutide improves cognitive impairment via the AMPK and PI3K/Akt signaling pathways in type 2 diabetic rats

Yang

Fang

et al. 2018

Mol Med Report

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Liraglutide is a type of glucagon‑like‑peptide 1 receptor agonist, which has been reported as a novel type of antidiabetic agent with numerous benefits, including cardiovascular and neuroprotective effects. To the best of our knowledge, few studies to date have reported the potential mechanism underlying the neuroprotective effects of liraglutide on rats with type 2 diabetes mellitus (T2DM). The present study aimed to investigate the neuroprotective actions of liraglutide in diabetic rats and to determine the mechanisms underlying these effects. A total of 30 male T2DM Goto‑Kakizaki (GK) rats (age, 32 weeks; weight, 300‑350 g) and 10 male Wistar rats (age, 32 weeks; weight, 300‑350 g) were used in the present study. Wistar rats received vehicle treatment, and GK rats randomly received treatment with vehicle, low dose of liraglutide (75 µg/kg) or high dose of liraglutide (200 µg/kg) for 28 days. Cognitive deficits were evaluated using the Morris water maze test. The expression levels of phosphoinositide 3‑kinase (PI3K), protein kinase B (Akt), phosphorylated (p)‑Akt, AMP‑activated protein kinase (AMPK), mammalian target of rapamycin (mTOR), Beclin‑1, microtubule‑associated protein light chain 3 (LC)‑3 II, caspase‑3, B‑cell lymphoma 2 (Bcl‑2)‑associated X protein and Bcl‑2 were assessed by western blot analysis. The results demonstrated that diabetic GK rats exhibited cognitive dysfunction, whereas treatment with liraglutide alleviated the learning and memory deficits, particularly in the high‑dose liraglutide group. The expression levels of Beclin‑1 and LC‑3 II were decreased in GK rats; however, this decrease was alleviated in the presence of liraglutide. Liraglutide also reversed T2DM model‑induced increases in mTOR, and decreases in p‑AMPK, PI3K and p‑Akt expression, and modulated the expression of apoptosis‑associated proteins. Furthermore, the administration of liraglutide inhibited apoptosis and exerted a protective effect against cognitive deficits via the activation of autophagy. In conclusion, the protective effects of liraglutide may be associated with increased mTOR expression via activation of the AMPK and PI3K/Akt signaling pathways.

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Potential effects of current drug therapies on cognitive impairment in patients with type 2 diabetes

Cited by 50 publications

References 240 publications

Autophagy and its link to type II diabetes mellitus

Autophagy and its link to type II diabetes mellitus

The Association Between Type 2 Diabetes Mellitus and Parkinson’s Disease

Liraglutide improves cognitive impairment via the AMPK and PI3K/Akt signaling pathways in type 2 diabetic rats

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