TY - JOUR
T1 - Changes in insulin and insulin signaling in Alzheimer's disease
T2 - Cause or consequence?
AU - Stanley, Molly
AU - Macauley, Shannon L.
AU - Holtzman, David M.
N1 - Publisher Copyright:
© 2016 Stanley et al.
PY - 2016/7/25
Y1 - 2016/7/25
N2 - 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.
AB - 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.
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U2 - 10.1084/jem.20160493
DO - 10.1084/jem.20160493
M3 - Article
C2 - 27432942
AN - SCOPUS:84983002115
SN - 0022-1007
VL - 213
SP - 1375
EP - 1385
JO - Journal of Experimental Medicine
JF - Journal of Experimental Medicine
IS - 8
ER -
