Xourgia E, Papazafiropoulou A, Melidonis A. Antidiabetic treatment on memory and spatial learning: From the pancreas to the neuron. World J Diabetes 2019; 10(3): 169-180 [PMID: 30891152 DOI: 10.4239/wjd.v10.i3.169]
Corresponding Author of This Article
Athanasia Papazafiropoulou, MD, MSc, PhD, Attending Doctor, Research Scientist, 1st Department of Internal Medicine and Diabetes Center, Tzaneio General Hospital of Piraeus, 1 Zanni and Afentouli Street, Athens 18536, Greece. pathan@ath.forthnet.gr
Research Domain of This Article
Endocrinology & Metabolism
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Diabetes. Mar 15, 2019; 10(3): 169-180 Published online Mar 15, 2019. doi: 10.4239/wjd.v10.i3.169
Antidiabetic treatment on memory and spatial learning: From the pancreas to the neuron
Eleni Xourgia, Athanasia Papazafiropoulou, Andreas Melidonis
Eleni Xourgia, Athanasia Papazafiropoulou, Andreas Melidonis 1st Department of Internal Medicine and Diabetes Center, Tzaneio General Hospital of Piraeus, Athens 18536, Greece
Author contributions: All authors equally contributed to this paper with conception and design of the study, literature review and analysis, drafting and critical revision and editing, and final approval of the final version.
Conflict-of-interest statement: No potential conflicts of interest. No financial support.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Athanasia Papazafiropoulou, MD, MSc, PhD, Attending Doctor, Research Scientist, 1st Department of Internal Medicine and Diabetes Center, Tzaneio General Hospital of Piraeus, 1 Zanni and Afentouli Street, Athens 18536, Greece. pathan@ath.forthnet.gr
Telephone: +30-697-996483
Received: February 20, 2019 Peer-review started: February 20, 2019 First decision: February 26, 2019 Revised: March 1, 2019 Accepted: March 8, 2019 Article in press: March 8, 2019 Published online: March 15, 2019 Processing time: 24 Days and 14.8 Hours
Abstract
The detrimental effects of constant hyperglycemia on neural function have been quantitatively and qualitatively evaluated in the setting of diabetes mellitus. Some of the hallmark features of diabetic encephalopathy (DE) are impaired synaptic adaptation and diminished spatial learning capacity. Chronic and progressive cognitive dysfunction, perpetuated by several positive feedback mechanisms in diabetic subjects, facilitates the development of early-onset dementia and Alzheimer’s disease. Despite the numerous clinical manifestations of DE having been described in detail and their pathophysiological substrate having been elucidated in both type 1 and type 2 diabetes mellitus, an effective therapeutic approach is yet to be proposed. Therefore, the aim of this review is to summarize the growing body of evidence concerning the effect of current antidiabetic treatment options on diabetic and non-DE.
Core tip: In this review, we aim to create a concise overview of the effects exerted by hyperglycemia on neural tissue, while describing the potential of each antidiabetic drug to improve functional and cognitive capacity in subjects with diabetic encephalopathy.
