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Fig. 1 | Acta Neuropathologica Communications

Fig. 1

From: Different tau species lead to heterogeneous tau pathology propagation and misfolding

Fig. 1

Tau misfolding and hyperphosphorylation in human brains with AD and genetic FTLD-Tau. (a, b and c) human brain sections from a genetic FTLD-Tau case (a), a Braak IV AD case (b) and a Braak VI AD case (c) stained with AT8 (green), Alz50 (red) and Dapi (blue) showing neurons Alz50 and AT8 positive (arrows), neurons only AT8 positive (arrowhead) and neurons only Alz50 positive (star). Scale bars represent 20 μm (d) Quantification of the percentage of neurons single or double positive for Alz50 and AT8 in MAPT mutants (n = 4, top panels) or AD cases (n = 6, low panels) in hippocampus (left), temporal cortex (middle) and visual cortex (right). The percentages for each category: double positive (brown), AT8 only (green) and Alz50 only (red) are indicated along with standard deviations. Statistical test used: Pearson’s Chi-squared test with Yates’ continuity correction was used to assess the distribution of Alz50-only neurons and AT8-only neurons in mutant versus AD cases. The presence of Alz50-only positive neurons was significantly linked to the presence of a MAPT mutation both taking into account all regions (p < .001; chi2 = 391) and in the hippocampus (p < .001; chi2 = 656). The presence of AT8-only positive neurons could only be linked with the presence of a mutation taking into account all regions (p < .001; chi2 = 171)

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