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Insulin Resistance as a Therapeutic Target in the Treatment of Alzheimer's Disease: A State-of-the-Art Review
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Functional Pharmacology.ORCID iD: 000-0002-8911-4068
Univ South Carolina, Sch Med, Dept Pharmacol Physiol & Neurosci, Columbia, SC 29208 USA..
2018 (English)In: Frontiers in Neuroscience, ISSN 1662-4548, E-ISSN 1662-453X, Vol. 12, article id 215Article, review/survey (Refereed) 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.

Place, publisher, year, edition, pages
FRONTIERS MEDIA SA , 2018. Vol. 12, article id 215
Keywords [en]
intranasal insulin, diabetes, mild cognitive impairment, amyloid beta, neurofibrillary tangles
National Category
Neurosciences
Identifiers
URN: urn:nbn:se:uu:diva-357169DOI: 10.3389/fnins.2018.00215ISI: 000429596300001OAI: oai:DiVA.org:uu-357169DiVA, id: diva2:1238797
Funder
Swedish Research Council, 2015-03100Available from: 2018-08-14 Created: 2018-08-14 Last updated: 2018-08-14Bibliographically approved

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