Abstract
Individuals with type 2 diabetes have an increased risk for developing Alzheimer's disease (AD), although the causal relationship remains poorly understood. Alterations in insulin signaling (IS) are reported in the AD brain. Moreover, oligomers/fibrils of amyloid-ß (Aß) can lead to neuronal insulin resistance and intranasal insulin is being explored as a potential therapy for AD. Conversely, elevated insulin levels (ins) are found in AD patients and high insulin has been reported to increase Aß levelsand tau phosphorylation, which could exacerbate AD pathology. Herein, we explore whether changes in ins and IS are a cause or consequence of AD.
| Original language | English |
|---|---|
| Pages (from-to) | 1375-1385 |
| Number of pages | 11 |
| Journal | Journal of Experimental Medicine |
| Volume | 213 |
| Issue number | 8 |
| DOIs | |
| State | Published - Jul 25 2016 |
Bibliographical note
Funding Information:This work was supported by a National Science Foundation Graduate Research Fellowship (DGE-1143954; M. Stanley), National Institute on Ageing grant K01 AG050719 (S.L. Macauley), National Institute of Neurological Disorders and Stroke grants F32 NS080320 (S.L. Macauley) and P01 NS080675 (D.M. Holtzman), New Vision Award through Donors Cure Foundation (S.L. Macauley), and the JPB Foundation (D.M. Holtzman). D.M. Holtzman co-founded and is on the scientific advisory board of C2N Diagnostics. D.M. Holtzman consults for Genentech, AbbVie, Eli Lilly, Neurophage, and Denali. SML consults for Denali. The authors declare no additional competing financial interests.
Publisher Copyright:
© 2016 Stanley et al.
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
