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Cells
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The Link between Diabetes and Neurodegenerative Diseases
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The Link between Diabetes and Neurodegenerative Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Autophagy".

Deadline for manuscript submissions: closed (5 November 2022) | Viewed by 7851

Special Issue Editor

Dr. Carlos Guillén Viejo

E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Biology, Faculty of Pharmacy, Complutense University of Madrid, Ciudad Universitaria s/n, 28040 Madrid, Spain
Interests: mtorc1; autophagy; pancreatic beta cells; diabetes; mitophagy; tsc2; er-stress; mvb; exosomes; aging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Nowadays, our society has a long life expectancy. Diabetes and neurodegeneration are two progressive and age-related groups of diseases, being interconnected. Although both pathologies have a genetic component, many other factors are involved in the appearance of both disorders. During recent years, different mechanisms have been proposed in the linkage between these two groups of affections. However, the precise molecular and cellular actors in the connection are unknown to this date.

In this Special Issue, the main pathways, molecules and structures implicated in the appearance, progression and susceptibility to suffer a neurodegenerative disease whilst having diabetes and vice versa will be analyzed.

Dr. Carlos Guillén Viejo
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • type 2 diabetes
  • Alzheimer’s
  • Parkinson’s
  • neurodegeneration
  • exosomes
  • amylin
  • protein aggregates
  • mitochondrial dysfunction
  • ER stress
  • autophagy
  • mitophagy
  • alpha-synuclein
  • insulin resistance
  • brain insulin resistance
  • obesity
  • aging

Published Papers (2 papers)

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Research

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18 pages, 3287 KiB  
Article
Empagliflozin Induced Ketosis, Upregulated IGF-1/Insulin Receptors and the Canonical Insulin Signaling Pathway in Neurons, and Decreased the Excitatory Neurotransmitter Glutamate in the Brain of Non-Diabetics
by Konstantinos I. Avgerinos, Roger J. Mullins, Michael Vreones, Maja Mustapic, Qinghua Chen, Denise Melvin, Dimitrios Kapogiannis and Josephine M. Egan
Cells 2022, 11(21), 3372; https://doi.org/10.3390/cells11213372 - 25 Oct 2022
Cited by 10 | Viewed by 2943
Abstract
Sodium-glucose cotransporter-2 inhibitors (SGLT2is), such as empagliflozin, lower blood glucose in type 2 diabetes mellitus and improve cardiorenal outcomes regardless of diabetes presence. Whether SGLT2is exert any effects on the brain’s metabolism has not been studied. We conducted a single-arm clinical trial to [...] Read more.
Sodium-glucose cotransporter-2 inhibitors (SGLT2is), such as empagliflozin, lower blood glucose in type 2 diabetes mellitus and improve cardiorenal outcomes regardless of diabetes presence. Whether SGLT2is exert any effects on the brain’s metabolism has not been studied. We conducted a single-arm clinical trial to investigate the effects of once daily administration of oral empagliflozin (25 mg) for 14 days on systemic and brain metabolism in 21 non-diabetics aged 55 years old or older. Empagliflozin lowered circulating insulin and elevated β-hydroxybutyrate over 34-h periods, both following its first administration and after 14 days of daily administration, with minor alterations in glucose homeostasis. Levels of phosphorylated insulin-like growth factor-1 receptor (pIGF-1R), phosphorylated insulin receptor (pIR), phosphorylated-in-tyrosine insulin receptor substrate-1 (pY-IRS-1), and phosphorylated protein kinase B or AKT (pAKT) were increased in extracellular vesicles enriched for neuronal origin (NEVs) following the first empagliflozin administration, but not after 14 days. Our finding of IGF-1R upregulation in NEVs is promising because several post-mortem and epidemiological studies support the idea that upregulation of IGF signaling may protect against Alzheimer’s disease (AD). Moreover, our finding showing activation of insulin signaling and, in particular, the canonical pathway (pIR, pY-IRS-1, pAKT) in NEVs is important because such changes have been repeatedly associated with neuronal survival. Using brain magnetic resonance spectroscopy (MRS), we detected decreased concentrations of the excitatory neurotransmitter glutamate and its precursor glutamine after empagliflozin administration. This finding is also encouraging since glutamatergic excitotoxicity has long been implicated in AD pathology. Overall, our findings may motivate the repurposing of SGLT2is for use in AD and other, related diseases that are characterized by downregulation of IGF-1/insulin signaling in neurons and excitotoxicity. Full article
(This article belongs to the Special Issue The Link between Diabetes and Neurodegenerative Diseases)
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Review

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21 pages, 6103 KiB  
Review
Development of Dementia in Type 2 Diabetes Patients: Mechanisms of Insulin Resistance and Antidiabetic Drug Development
by Desh Deepak Singh, Ali A. Shati, Mohammad Y. Alfaifi, Serag Eldin I. Elbehairi, Ihn Han, Eun-Ha Choi and Dharmendra K. Yadav
Cells 2022, 11(23), 3767; https://doi.org/10.3390/cells11233767 - 25 Nov 2022
Cited by 7 | Viewed by 3860
Abstract
Dementia is reported to be common in those with type 2 diabetes mellitus. Type 2 diabetes contributes to common molecular mechanisms and an underlying pathology with dementia. Brain cells becoming resistant to insulin leads to elevated blood glucose levels, impaired synaptic plasticity, microglial [...] Read more.
Dementia is reported to be common in those with type 2 diabetes mellitus. Type 2 diabetes contributes to common molecular mechanisms and an underlying pathology with dementia. Brain cells becoming resistant to insulin leads to elevated blood glucose levels, impaired synaptic plasticity, microglial overactivation, mitochondrial dysfunction, neuronal apoptosis, nutrient deprivation, TAU (Tubulin-Associated Unit) phosphorylation, and cholinergic dysfunction. If insulin has neuroprotective properties, insulin resistance may interfere with those properties. Risk factors have a significant impact on the development of diseases, such as diabetes, obesity, stroke, and other conditions. Analysis of risk factors of importance for the association between diabetes and dementia is important because they may impede clinical management and early diagnosis. We discuss the pathological and physiological mechanisms behind the association between Type 2 diabetes mellitus and dementia, such as insulin resistance, insulin signaling, and sporadic forms of dementia; the relationship between insulin receptor activation and TAU phosphorylation; dementia and mRNA expression and downregulation of related receptors; neural modulation due to insulin secretion and glucose homeostasis; and neuronal apoptosis due to insulin resistance and Type 2 diabetes mellitus. Addressing these factors will offer clinical outcome-based insights into the mechanisms and connection between patients with type 2 diabetes and cognitive impairment. Furthermore, we will explore the role of brain insulin resistance and evidence for anti-diabetic drugs in the prevention of dementia risk in type 2 diabetes. Full article
(This article belongs to the Special Issue The Link between Diabetes and Neurodegenerative Diseases)
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