Alterations in glucose metabolism on cognition: A possible link between diabetes and dementia
The use of the carbohydrate glucose as an energetic source is essential for an adequate function of the human body. The complex regulation of this molecule involves the coordinated action of various organs such as pancreas, liver and brain. Any disruption of this physiological balance may result in...
- Autores:
- Tipo de recurso:
- Fecha de publicación:
- 2016
- Institución:
- Universidad del Rosario
- Repositorio:
- Repositorio EdocUR - U. Rosario
- Idioma:
- eng
- OAI Identifier:
- oai:repository.urosario.edu.co:10336/26673
- Acceso en línea:
- https://doi.org/10.2174/1381612822666151209152013
https://repository.urosario.edu.co/handle/10336/26673
- Palabra clave:
- Diabetes
Alzheimer Disease
Dementia
Insulin resistance
Antidiabetic drugs
- Rights
- License
- Restringido (Acceso a grupos específicos)
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799427726007caa7b58-f3f2-44b1-8bd1-894c2ae24046-1c4e0e11b-1bf6-4831-a478-a2269f284892-1756df063-3b80-4568-a1b7-e90dcd52fcca-12020-08-19T14:40:01Z2020-08-19T14:40:01Z2016-02-01The use of the carbohydrate glucose as an energetic source is essential for an adequate function of the human body. The complex regulation of this molecule involves the coordinated action of various organs such as pancreas, liver and brain. Any disruption of this physiological balance may result in a dangerous compromise of general metabolic activities increasing the possibility of developing T1DM, T2DM and possibly AD. Astrocytes convert glucose into lactate and transfer it to neurons. This lactate is essential for neuronal metabolism and for various processes including the formation of synapses, dendrites and the expression of genes involved in memory. The brain is highly susceptible to variations in glucose blood levels, and both hypoglycemia and hyperglycemia can be dangerous. Pathological hyperglycemia induces changes in plasmatic osmotic pressure, mitochondrial production of free radicals, oxidative stress and activation of neuronal apoptosis, among others. Both AD and diabetes are chronic diseases having age as an important risk factor. As the brain ages, it seems to become much more susceptible to cellular damage induced by excess of circulating glucose and this could explain the appearance of cognitive changes observed in some patients with diabetes. Excessive circulation of pro-inflammatory agents has been observed in insulin resistance and is likely that some of these mediators may cross the bloodbrain barrier and induce abnormal neuroinflammation. GSK-3 is overexpressed in diabetes and also has been reported to regulate tau phosphorylation and production of A? peptides in the brain. Currently, diabetes (hyperglycemia) is considered as a risk factor for the development of AD. A novel therapeutic approach, using intranasal insulin and anti-diabetic medications in patients suffering from AD is being explored and is discussed in this review.application/pdfhttps://doi.org/10.2174/1381612822666151209152013ISSN: 1381-6128EISSN: 1873-4286https://repository.urosario.edu.co/handle/10336/26673engBentham Science818No. 7812Current Pharmaceutical DesignVol. 22Current Pharmaceutical Design, ISSN:1381-6128;EISSN:1873-4286, Vol.22, No.7 (2016); pp. 812 - 818https://benthamscience.com/journals/current-pharmaceutical-design/volume/22/issue/7/page/812/Restringido (Acceso a grupos específicos)http://purl.org/coar/access_right/c_16ecCurrent Pharmaceutical Designinstname:Universidad del Rosarioreponame:Repositorio Institucional EdocURDiabetesAlzheimer DiseaseDementiaInsulin resistanceAntidiabetic drugsAlterations in glucose metabolism on cognition: A possible link between diabetes and dementiaAlteraciones en el metabolismo de la glucosa en la cognición: un posible vínculo entre la diabetes y la demenciaarticleArtículohttp://purl.org/coar/version/c_970fb48d4fbd8a85http://purl.org/coar/resource_type/c_6501González Reyes, Rodrigo EstebanAliev, GjumrakchAvila-Rodrigues, MarcoBarreto, George E.10336/26673oai:repository.urosario.edu.co:10336/266732021-06-03 00:49:57.255https://repository.urosario.edu.coRepositorio institucional EdocURedocur@urosario.edu.co |
dc.title.spa.fl_str_mv |
Alterations in glucose metabolism on cognition: A possible link between diabetes and dementia |
dc.title.TranslatedTitle.spa.fl_str_mv |
Alteraciones en el metabolismo de la glucosa en la cognición: un posible vínculo entre la diabetes y la demencia |
title |
Alterations in glucose metabolism on cognition: A possible link between diabetes and dementia |
spellingShingle |
Alterations in glucose metabolism on cognition: A possible link between diabetes and dementia Diabetes Alzheimer Disease Dementia Insulin resistance Antidiabetic drugs |
title_short |
Alterations in glucose metabolism on cognition: A possible link between diabetes and dementia |
title_full |
Alterations in glucose metabolism on cognition: A possible link between diabetes and dementia |
title_fullStr |
Alterations in glucose metabolism on cognition: A possible link between diabetes and dementia |
title_full_unstemmed |
Alterations in glucose metabolism on cognition: A possible link between diabetes and dementia |
title_sort |
Alterations in glucose metabolism on cognition: A possible link between diabetes and dementia |
dc.subject.keyword.spa.fl_str_mv |
Diabetes Alzheimer Disease Dementia Insulin resistance Antidiabetic drugs |
topic |
Diabetes Alzheimer Disease Dementia Insulin resistance Antidiabetic drugs |
description |
The use of the carbohydrate glucose as an energetic source is essential for an adequate function of the human body. The complex regulation of this molecule involves the coordinated action of various organs such as pancreas, liver and brain. Any disruption of this physiological balance may result in a dangerous compromise of general metabolic activities increasing the possibility of developing T1DM, T2DM and possibly AD. Astrocytes convert glucose into lactate and transfer it to neurons. This lactate is essential for neuronal metabolism and for various processes including the formation of synapses, dendrites and the expression of genes involved in memory. The brain is highly susceptible to variations in glucose blood levels, and both hypoglycemia and hyperglycemia can be dangerous. Pathological hyperglycemia induces changes in plasmatic osmotic pressure, mitochondrial production of free radicals, oxidative stress and activation of neuronal apoptosis, among others. Both AD and diabetes are chronic diseases having age as an important risk factor. As the brain ages, it seems to become much more susceptible to cellular damage induced by excess of circulating glucose and this could explain the appearance of cognitive changes observed in some patients with diabetes. Excessive circulation of pro-inflammatory agents has been observed in insulin resistance and is likely that some of these mediators may cross the bloodbrain barrier and induce abnormal neuroinflammation. GSK-3 is overexpressed in diabetes and also has been reported to regulate tau phosphorylation and production of A? peptides in the brain. Currently, diabetes (hyperglycemia) is considered as a risk factor for the development of AD. A novel therapeutic approach, using intranasal insulin and anti-diabetic medications in patients suffering from AD is being explored and is discussed in this review. |
publishDate |
2016 |
dc.date.created.spa.fl_str_mv |
2016-02-01 |
dc.date.accessioned.none.fl_str_mv |
2020-08-19T14:40:01Z |
dc.date.available.none.fl_str_mv |
2020-08-19T14:40:01Z |
dc.type.eng.fl_str_mv |
article |
dc.type.coarversion.fl_str_mv |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
dc.type.coar.fl_str_mv |
http://purl.org/coar/resource_type/c_6501 |
dc.type.spa.spa.fl_str_mv |
Artículo |
dc.identifier.doi.none.fl_str_mv |
https://doi.org/10.2174/1381612822666151209152013 |
dc.identifier.issn.none.fl_str_mv |
ISSN: 1381-6128 EISSN: 1873-4286 |
dc.identifier.uri.none.fl_str_mv |
https://repository.urosario.edu.co/handle/10336/26673 |
url |
https://doi.org/10.2174/1381612822666151209152013 https://repository.urosario.edu.co/handle/10336/26673 |
identifier_str_mv |
ISSN: 1381-6128 EISSN: 1873-4286 |
dc.language.iso.spa.fl_str_mv |
eng |
language |
eng |
dc.relation.citationEndPage.none.fl_str_mv |
818 |
dc.relation.citationIssue.none.fl_str_mv |
No. 7 |
dc.relation.citationStartPage.none.fl_str_mv |
812 |
dc.relation.citationTitle.none.fl_str_mv |
Current Pharmaceutical Design |
dc.relation.citationVolume.none.fl_str_mv |
Vol. 22 |
dc.relation.ispartof.spa.fl_str_mv |
Current Pharmaceutical Design, ISSN:1381-6128;EISSN:1873-4286, Vol.22, No.7 (2016); pp. 812 - 818 |
dc.relation.uri.spa.fl_str_mv |
https://benthamscience.com/journals/current-pharmaceutical-design/volume/22/issue/7/page/812/ |
dc.rights.coar.fl_str_mv |
http://purl.org/coar/access_right/c_16ec |
dc.rights.acceso.spa.fl_str_mv |
Restringido (Acceso a grupos específicos) |
rights_invalid_str_mv |
Restringido (Acceso a grupos específicos) http://purl.org/coar/access_right/c_16ec |
dc.format.mimetype.none.fl_str_mv |
application/pdf |
dc.publisher.spa.fl_str_mv |
Bentham Science |
dc.source.spa.fl_str_mv |
Current Pharmaceutical Design |
institution |
Universidad del Rosario |
dc.source.instname.none.fl_str_mv |
instname:Universidad del Rosario |
dc.source.reponame.none.fl_str_mv |
reponame:Repositorio Institucional EdocUR |
repository.name.fl_str_mv |
Repositorio institucional EdocUR |
repository.mail.fl_str_mv |
edocur@urosario.edu.co |
_version_ |
1814167713436663808 |