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Reduction of aggregated Tau in neuronal processes but not in the cell bodies after Abeta42 immunisation in Alzheimer’s disease


Boche, Delphine, Donald, Jane, Love, Seth, Harris, Scott, Neal, James W., Holmes, Clive, Nicoll, James A. R.


Acta Neuropathologica, Volume: 120, No.: 1, Pages.: 13-20

Year of Publication



Alzheimer’s disease (AD) pathology is characterised by aggregation in the brain of amyloid-beta (Abeta) peptide and hyperphosphorylated tau (phospho-tau), although how these proteins interact in disease pathogenesis is unclear. Abeta immunisation results in removal of Abeta from the brain but cognitive decline continues to progress, possibly due to persistent phospho-tau. We quantified phospho-tau and Abeta42 in the brains of 10 AD patients (iAD) who were actively immunised with Abeta42 (AN1792, Elan Pharmaceuticals) compared with 28 unimmunised AD cases (cAD). The phospho-tau load was lower in the iAD than the cAD group in the cerebral cortex (cAD 1.08% vs. iAD 0.72%, P = 0.048), CA1 hippocampus (cAD 2.26% vs. iAD 1.05%; P = 0.001), subiculum (cAD 1.60% vs. iAD 0.31%; P = 0.001) and entorhinal cortex (cAD 1.10% vs. iAD 0.18%; P < 0.001). Assessment of the localisation within neurons of phospho-tau indicated that the Abeta immunotherapy-associated reduction was confined to neuronal processes, i.e. neuropil threads and dystrophic neurites. However, the phospho-tau accumulation in the neuronal cell bodies, contributing to neurofibrillary tangles, appeared not to be affected. In showing that Abeta immunisation can influence phospho-tau pathology, we confirm the position of Abeta as a target for modifying tau accumulation in AD and demonstrate a link between these proteins. However, the continuing progression of cognitive decline in AD patients after Abeta immunisation may be explained by its lack of apparent effect on tangles.;

Bibtex Citation

@article{Boche_2010, doi = {10.1007/s00401-010-0705-y}, url = {}, year = 2010, month = {jun}, publisher = {Springer Science $mathplus$ Business Media}, volume = {120}, number = {1}, pages = {13--20}, author = {Delphine Boche and Jane Donald and Seth Love and Scott Harris and James W. Neal and Clive Holmes and James A. R. Nicoll}, title = {Reduction of aggregated Tau in neuronal processes but not in the cell bodies after A$upbeta$42 immunisation in Alzheimer's disease}, journal = {Acta Neuropathologica} }


abeta, aged, aged, 80 and over, alzheimer disease, ca1 region hippocampal, entorhinal cortex, female, humans, immunisation, immunization, immunohistochemistry, immunology, male, metabolism, middle aged, neocortex, neurites, neurofibrillary tangles, neurons, pathology, peptide fragments, phosphorylation, phosphotau, tau proteins, therapy, treatment outcome

Countries of Study


Types of Dementia

Alzheimer’s Disease

Types of Study

Case Control Study

Type of Outcomes


Type of Interventions

Pharmaceutical Interventions

Pharmaceutical Interventions