Ageing and amyloidosis underlie the molecular and pathological alterations of tau in a mouse model of familial Alzheimer’s disease

Neurofibrillary pathology in aged APPswe/PS1ΔE9 mice

Fresh-frozen brain sections from APPswe/PS1ΔE9 transgenic (TG) mice and their wild-type (WT) counterparts were processed along with human brain sections for the detection of neurofibrillary alterations with the Gallyas silver stain. Co-staining for amyloid and Gallyas was used to probe the relationship between amyloidosis and tau-associated pathology.

Aβ deposition was the predominant lesion in the 6-month-old APPswe/PS1ΔE9 brain (Fig. 1a,b), with age-dependent increases in argyrophilic density observed exclusively in TG mice (Fig. 1c-f). Only mild and diffuse silver staining was observed in the neocortex of 6-month-old animals (Fig. 1g). Densely-labelled, plaque-like structures, surrounded by a halo of argyrophilic staining, constituted the majority of Gallyas-positive signal in the neuropil of the neocortex and hippocampus…

Read more…