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Table 1 Comprehensive overview of end point immunohistochemistry and longitudinal FDG-PET findings in treated and untreated hTau mice

From: Late-stage Anle138b treatment ameliorates tau pathology and metabolic decline in a mouse model of human Alzheimer’s disease tau

 

hTau Anle138b

hTau Vehicle

hTau pooled Baseline

Non-carrier controls (pooled)

Immunohistochemistry

Frontal cortex (%-area)

6.1 ± 1.9**

12.9 ± 1.8

 

0

Immunohistochemistry

Frontal cortex (CP13+ neurons, N/mm2)

1366 ± 116**

2039 ± 153

 

0

Immunohistochemistry

Hippocampus (%-area)

1.9 ± 1.4**

4.8 ± 0.4

 

0

Immunohistochemistry

Hippocampus (CP13+ neurons, N/mm2)

534 ± 18**

619 ± 13

 

0

FDG-PET baseline

Frontal cortex (SUVR)

0.97 ± 0.02

1.02 ± 0.09

1.00 ± 0.07#

1.10 ± 0.10

FDG-PET follow-up

Frontal cortex (SUVR)

1.03 ± 0.05*

0.95 ± 0.03#

 

1.09 ± 0.06

FDG-PET change

Frontal cortex (ΔSUVR)

+ 0.06 ± 0.06*

− 0.07 ± 0.09

 

+ 0.01 ± 0.05

FDG-PET baseline

Hippocampus (SUVR)

0.93 ± 0.03

0.98 ± 0.10

0.96 ± 0.08#

1.06 ± 0.10

FDG-PET follow-up

Hippocampus (SUVR)

1.00 ± 0.07

0.93 ± 0.05##

 

1.05 ± 0.07

FDG-PET change

Hippocampus (ΔSUVR)

+ 0.06 ± 0.05

− 0.05 ± 0.10

 

+ 0.00 ± 0.05

  1. Results summary: “*” indicates p < 0.05 and “**” indicates p < 0.005 in the direct comparison of hTau treatment and vehicle groups. “#” indicates p < 0.05 and “##” indicates p < 0.005 in the comparison of hTau groups (pooled baseline or treatment/vehicle during follow-up) versus non-carrier controls