uu.seUppsala universitets publikasjoner
Endre søk
RefereraExporteraLink to record
Permanent link

Direct link
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Annet format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annet språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf
Insulin Resistance as a Therapeutic Target in the Treatment of Alzheimer's Disease: A State-of-the-Art Review
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Funktionell farmakologi.ORCID-id: 000-0002-8911-4068
Univ South Carolina, Sch Med, Dept Pharmacol Physiol & Neurosci, Columbia, SC 29208 USA..
2018 (engelsk)Inngår i: Frontiers in Neuroscience, ISSN 1662-4548, E-ISSN 1662-453X, Vol. 12, artikkel-id 215Artikkel, forskningsoversikt (Fagfellevurdert) Published
Abstract [en]

Research in animals and humans has shown that type 2 diabetes and its prodromal state, insulin resistance, promote major pathological hallmarks of Alzheimer's disease (AD), such as the formation of amyloid plaques and neurofibrillary tangles (NFT). Worrisomely, dysregulated amyloid beta (A beta) metabolism has also been shown to promote central nervous system insulin resistance; although the role of tau metabolism remains controversial. Collectively, as proposed in this review, these findings suggest the existence of a mechanistic interplay between AD pathogenesis and disrupted insulin signaling. They also provide strong support for the hypothesis that pharmacologically restoring brain insulin signaling could represent a promising strategy to curb the development and progression of AD. In this context, great hopes have been attached to the use of intranasal insulin. This drug delivery method increases cerebrospinal fluid concentrations of insulin in the absence of peripheral side effects, such as hypoglycemia. With this in mind, the present review will also summarize current knowledge on the efficacy of intranasal insulin to mitigate major pathological symptoms of AD, i.e., cognitive impairment and deregulation of A beta and tau metabolism.

sted, utgiver, år, opplag, sider
FRONTIERS MEDIA SA , 2018. Vol. 12, artikkel-id 215
Emneord [en]
intranasal insulin, diabetes, mild cognitive impairment, amyloid beta, neurofibrillary tangles
HSV kategori
Identifikatorer
URN: urn:nbn:se:uu:diva-357169DOI: 10.3389/fnins.2018.00215ISI: 000429596300001OAI: oai:DiVA.org:uu-357169DiVA, id: diva2:1238797
Forskningsfinansiär
Swedish Research Council, 2015-03100Tilgjengelig fra: 2018-08-14 Laget: 2018-08-14 Sist oppdatert: 2018-08-14bibliografisk kontrollert

Open Access i DiVA

fulltext(1253 kB)68 nedlastinger
Filinformasjon
Fil FULLTEXT01.pdfFilstørrelse 1253 kBChecksum SHA-512
82707638bb9ca44872150fee660955720c64aa60e952552e3cc20af4080319832eeeb2b88bc61a642b940184eb9b034bd96bb590ec17b38fdd778fba6a25bd0c
Type fulltextMimetype application/pdf

Andre lenker

Forlagets fulltekst

Personposter BETA

Benedict, Christian

Søk i DiVA

Av forfatter/redaktør
Benedict, Christian
Av organisasjonen
I samme tidsskrift
Frontiers in Neuroscience

Søk utenfor DiVA

GoogleGoogle Scholar
Totalt: 68 nedlastinger
Antall nedlastinger er summen av alle nedlastinger av alle fulltekster. Det kan for eksempel være tidligere versjoner som er ikke lenger tilgjengelige

doi
urn-nbn

Altmetric

doi
urn-nbn
Totalt: 184 treff
RefereraExporteraLink to record
Permanent link

Direct link
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Annet format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annet språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf