Table 1 Human postmortem samples from BA9 prefrontal cortex, that were used in this study

M

0

n/a

Normal adult brain

M

0

n/a

Normal adult brain

M

0

2/3

Ageing changes (mild)

F

0

2/3

Argyrophilic grains low to moderate density

F

I

3/3

Control brain with some tau deposition

F

I

n/a

Minimal tau pathology consistent with HP-tau stage-I

F

I

3/3

Mild ageing changes Braak I

M

I

n/a

control—old cerebral infarct (Braak I)

M

II

3/3

Mild alzheimer-type changes—Braak II

F

II

n/a

Alzheimer changes Braak II consistent with normal ageing

F

II

n/a

Very mild Alzheimer’s disease type changes BNE stage 2, control

M

III

n/a

Mild alzheimer-type changes—Braak III

F

III

n/a

Possible AD (CERAD) Braak III (limbic) BNE stage III

M

III

n/a

Alzheimer type changes (ageing), BNE stage 2, control

F

III

n/a

Alzheimer’s disease BNE IV, CERAD probable; TDP-43 pathology (hippocampus and amygdala)

F

III

3/3

Alzheimer’s disease pathology (BNE stage IV) with amyloid angiopathy & limbic TDP-43 pathology but cognitively not impaired

M

IV

n/a

AD (modified Braak IV) with limbic TDP-43 pathology

M

IV

n/a

AD (modified Braak IV) with extensive severe amyloid angiopathy

F

IV

n/a

AD (limbic stage-modified Braak IV) with moderate–severe amyloid angiopathy

F

IV

n/a

AD HP tau stage 4, severely affecting limbic system and moderately extending to neocortex

M

IV

n/a

Alzheimer’s disease (BNE stage 4)

F

V

3/4

AD Braak V with mild amyloid angiopathy

M

V

4/4

AD Braak V with moderate amyloid angiopathy

F

V

4/4

Alzheimer’s disease Braak 5

F

V

3/3

Alzheimer’s disease Braak V

M

VI

3/3

AD Braak VI with marked amyloid angiopathy

F

VI

3/4

Alzheimer’s disease, Braak VI