Soluble amyloid β-protein is increased in frontotemporal dementia with tau gene mutations

Antonella Vitali, Alessandra Piccini, Roberta Borghi, Pantaleo Fornaro, Sandra L. Siedlak, Mark A. Smith, Pierluigi Gambetti, Bernardino Ghetti, Massimo Tabaton

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

The relationship between senile plaques and neurofibrillary tangles, the main pathologic lesions of Alzheimer's disease, is not completely understood. We addressed this issue examining the type and amount of amyloid β-protein (Aβ) associated with the soluble and insoluble tissue fractions in the frontal cortex of 8 cases with frontotemporal dementia with parkinsonism caused by mutations of the Tau gene (FTDP-17), in which the intracellular accumulation of polymerised tau is definitely the primary cause of neurodegeneration. As control, we examined 7 cases with frontotemporal dementia lacking distinctive histopathology (DLDH) as well as 8 pathologically normal subjects. In all cases the presence of Aβ deposits was ruled out using immunocytochemistry on sections adjacent to those used for biochemical analysis. ELISA analysis showed a 2.7 and 2.1 fold (p < 0.01) increase of soluble Aβ42 and Aβ40 in FTDP-17, compared to normal and DLDH brains, both of which had comparable levels of Aβ species. Furthermore, the immunoreactivity of the intracellular Aβ42 was significantly increased in cortical neurons of subjects affected with FTDP-17. The results demonstrate that the aggregation of tau protein produces an accumulation of Aβ, which, however, does not reach the critical concentration needed for AO plaques formation.

Original languageEnglish
Pages (from-to)45-51
Number of pages7
JournalJournal of Alzheimer's Disease
Volume6
Issue number1
StatePublished - Feb 2004

Fingerprint

Amyloidogenic Proteins
Frontotemporal Dementia
Mutation
Genes
Serum Amyloid A Protein
tau Proteins
Neurofibrillary Tangles
Amyloid Plaques
Frontal Lobe
Dementia
Alzheimer Disease
Enzyme-Linked Immunosorbent Assay
Immunohistochemistry
Neurons
Brain

Keywords

  • Alzheimer's disease
  • Amyloid β-protein
  • FTDP-17
  • Tau pathology
  • Tau protein

ASJC Scopus subject areas

  • Neuropsychology and Physiological Psychology

Cite this

Vitali, A., Piccini, A., Borghi, R., Fornaro, P., Siedlak, S. L., Smith, M. A., ... Tabaton, M. (2004). Soluble amyloid β-protein is increased in frontotemporal dementia with tau gene mutations. Journal of Alzheimer's Disease, 6(1), 45-51.

Soluble amyloid β-protein is increased in frontotemporal dementia with tau gene mutations. / Vitali, Antonella; Piccini, Alessandra; Borghi, Roberta; Fornaro, Pantaleo; Siedlak, Sandra L.; Smith, Mark A.; Gambetti, Pierluigi; Ghetti, Bernardino; Tabaton, Massimo.

In: Journal of Alzheimer's Disease, Vol. 6, No. 1, 02.2004, p. 45-51.

Research output: Contribution to journalArticle

Vitali, A, Piccini, A, Borghi, R, Fornaro, P, Siedlak, SL, Smith, MA, Gambetti, P, Ghetti, B & Tabaton, M 2004, 'Soluble amyloid β-protein is increased in frontotemporal dementia with tau gene mutations', Journal of Alzheimer's Disease, vol. 6, no. 1, pp. 45-51.
Vitali A, Piccini A, Borghi R, Fornaro P, Siedlak SL, Smith MA et al. Soluble amyloid β-protein is increased in frontotemporal dementia with tau gene mutations. Journal of Alzheimer's Disease. 2004 Feb;6(1):45-51.
Vitali, Antonella ; Piccini, Alessandra ; Borghi, Roberta ; Fornaro, Pantaleo ; Siedlak, Sandra L. ; Smith, Mark A. ; Gambetti, Pierluigi ; Ghetti, Bernardino ; Tabaton, Massimo. / Soluble amyloid β-protein is increased in frontotemporal dementia with tau gene mutations. In: Journal of Alzheimer's Disease. 2004 ; Vol. 6, No. 1. pp. 45-51.
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