Table 1.
Insulin-related changes in AD
ParameterAD ↑ ↓ StudyDetails
Blood insulin  Bucht et al., 1983; Fujisawa et al., 1991; Stolk et al., 1997; Craft et al., 1998; Ma et al., 2016  -Fasting or after glucose tolerance test -In women only (1 study) -Only in non-APOE4 and moderate/severe AD (1 study) -Meta-analysis of 11 studies: 5 report overall ↑, 1 ↑ in women, 1 ↑ with advanced stage (Ma et al., 2016) 
CSF insulin  Fujisawa et al., 1991  -Also found small increase with vascular dementia 
 Craft et al., 1998; Gil-Bea et al., 2010  -Only in non-APOE4 and moderate/severe AD -No relationship to APOE or AD severity  
No change Molina et al., 2002  -No relationship with AD severity or cognition 
Brain insulin No change Frölich et al., 1998  -Comparing controls >65 y/o and AD patients 
 Frölich et al., 1998; Rivera et al., 2005; Steen et al., 2005  -Comparing controls <65 y/o and AD patients -mRNA: in hippocampus and hypothalamus -mRNA: progressive reduction with Braak stage 
Brain IR (total)  Frölich et al., 1998; Rivera et al., 2005; Steen et al., 2005  -Comparing controls <65 y/o and AD patients -mRNA and protein -mRNA: progressive reduction with Braak stage 
 Frölich et al., 1998   -Comparing controls >65 y/o and AD patients 
No change Moloney et al., 2010; Liu et al., 2011; Ho et al., 2012; Talbot et al., 2012  -Potential changes in cellular distribution -Also no change in p-IR -Only reduced in patients with T2D and AD 
Brain p-IR and activity  Frölich et al., 1998; Rivera et al., 2005; Steen et al., 2005  -In hippocampus -Reduced insulin binding -TK activity reduced compared to all controls 
Brain IRS1 (total)  Steen et al., 2005; Moloney et al., 2010  -mRNA in 3 regions -Also reductions in IRS2 
No change Liu et al., 2011; Talbot et al., 2012  -Also no change in IRS2 -Only reduced in patients with T2D and AD 
Brain p(Ser)-IRS1  Moloney et al., 2010 ,Talbot et al., 2012 ,Bomfim et al., 2012 ,Yarchoan et al., 2014  -Regardless of APOE status and reduced ex vivo insulin stimulation -Highest in AD, but also elevated in some tauopathies 
Brain AKT (total)  Griffin et al., 2005; Liu et al., 2011  -Reduced in AD and in patients with T2D and AD 
No change Steen et al., 2005; Talbot et al., 2012   
Brain p-AKT  Pei et al., 2003; Griffin et al., 2005; Talbot et al., 2012; Yarchoan et al., 2014  -Associated with tangles 
 Steen et al., 2005  -In hippocampus 
No change Liu et al., 2011  -Only reduced in patients with T2D and AD 
Brain GSK3 (total)  Ho et al., 2012  -With advanced AD 
No change Steen et al., 2005; Liu et al., 2011; Talbot et al., 2012  -Only reduced in patients with T2D or T2D and AD 
Brain p(Ser)-GSK3  Steen et al., 2005 ,Griffin et al., 2005  -In hippocampus 
No change Liu et al., 2011  -Only reduced in patients with T2D or T2D and AD 
Brain p-GSK3   Pei et al., 2003  -Associated with tangles 
Brain p-JNK  Bomfim et al., 2012; Talbot et al., 2012   
Other IR signaling molecules  Griffin et al., 2005; Liu et al., 2011; Talbot et al., 2012  -PDK1, p-PDK1 and p-PI3K -PIP3, PKC, p-mTOR, p-ERK2 -PTEN 
ParameterAD ↑ ↓ StudyDetails
Blood insulin  Bucht et al., 1983; Fujisawa et al., 1991; Stolk et al., 1997; Craft et al., 1998; Ma et al., 2016  -Fasting or after glucose tolerance test -In women only (1 study) -Only in non-APOE4 and moderate/severe AD (1 study) -Meta-analysis of 11 studies: 5 report overall ↑, 1 ↑ in women, 1 ↑ with advanced stage (Ma et al., 2016) 
CSF insulin  Fujisawa et al., 1991  -Also found small increase with vascular dementia 
 Craft et al., 1998; Gil-Bea et al., 2010  -Only in non-APOE4 and moderate/severe AD -No relationship to APOE or AD severity  
No change Molina et al., 2002  -No relationship with AD severity or cognition 
Brain insulin No change Frölich et al., 1998  -Comparing controls >65 y/o and AD patients 
 Frölich et al., 1998; Rivera et al., 2005; Steen et al., 2005  -Comparing controls <65 y/o and AD patients -mRNA: in hippocampus and hypothalamus -mRNA: progressive reduction with Braak stage 
Brain IR (total)  Frölich et al., 1998; Rivera et al., 2005; Steen et al., 2005  -Comparing controls <65 y/o and AD patients -mRNA and protein -mRNA: progressive reduction with Braak stage 
 Frölich et al., 1998   -Comparing controls >65 y/o and AD patients 
No change Moloney et al., 2010; Liu et al., 2011; Ho et al., 2012; Talbot et al., 2012  -Potential changes in cellular distribution -Also no change in p-IR -Only reduced in patients with T2D and AD 
Brain p-IR and activity  Frölich et al., 1998; Rivera et al., 2005; Steen et al., 2005  -In hippocampus -Reduced insulin binding -TK activity reduced compared to all controls 
Brain IRS1 (total)  Steen et al., 2005; Moloney et al., 2010  -mRNA in 3 regions -Also reductions in IRS2 
No change Liu et al., 2011; Talbot et al., 2012  -Also no change in IRS2 -Only reduced in patients with T2D and AD 
Brain p(Ser)-IRS1  Moloney et al., 2010 ,Talbot et al., 2012 ,Bomfim et al., 2012 ,Yarchoan et al., 2014  -Regardless of APOE status and reduced ex vivo insulin stimulation -Highest in AD, but also elevated in some tauopathies 
Brain AKT (total)  Griffin et al., 2005; Liu et al., 2011  -Reduced in AD and in patients with T2D and AD 
No change Steen et al., 2005; Talbot et al., 2012   
Brain p-AKT  Pei et al., 2003; Griffin et al., 2005; Talbot et al., 2012; Yarchoan et al., 2014  -Associated with tangles 
 Steen et al., 2005  -In hippocampus 
No change Liu et al., 2011  -Only reduced in patients with T2D and AD 
Brain GSK3 (total)  Ho et al., 2012  -With advanced AD 
No change Steen et al., 2005; Liu et al., 2011; Talbot et al., 2012  -Only reduced in patients with T2D or T2D and AD 
Brain p(Ser)-GSK3  Steen et al., 2005 ,Griffin et al., 2005  -In hippocampus 
No change Liu et al., 2011  -Only reduced in patients with T2D or T2D and AD 
Brain p-GSK3   Pei et al., 2003  -Associated with tangles 
Brain p-JNK  Bomfim et al., 2012; Talbot et al., 2012   
Other IR signaling molecules  Griffin et al., 2005; Liu et al., 2011; Talbot et al., 2012  -PDK1, p-PDK1 and p-PI3K -PIP3, PKC, p-mTOR, p-ERK2 -PTEN 

Reported alterations in ins and brain IS in AD are categorized by the specific component measured, whether there have been reports of an increase, decrease (up and down arrows), or no change in individuals with AD, the studies that report this specific alteration, and important details. For blood and CSF insulin, AD diagnosis was based on clinical criteria. For postmortem analysis of brain insulin and IS components, AD was confirmed by clinical diagnosis and histological analyses. All reported changes were at the protein level unless mRNA is specified in the details. Overall, data from this table supports a higher level of blood insulin in individuals with AD and some degree of brain insulin resistance.

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