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Tau is essential to β-amyloid-induced neurotoxicity
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| Zeitschriftentitel: | Proceedings of the National Academy of Sciences |
|---|---|
| Personen und Körperschaften: | , , , , |
| In: | Proceedings of the National Academy of Sciences, 99, 2002, 9, S. 6364-6369 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Proceedings of the National Academy of Sciences
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| Schlagwörter: |
| author_facet |
Rapoport, Mark Dawson, Hana N. Binder, Lester I. Vitek, Michael P. Ferreira, Adriana Rapoport, Mark Dawson, Hana N. Binder, Lester I. Vitek, Michael P. Ferreira, Adriana |
|---|---|
| author |
Rapoport, Mark Dawson, Hana N. Binder, Lester I. Vitek, Michael P. Ferreira, Adriana |
| spellingShingle |
Rapoport, Mark Dawson, Hana N. Binder, Lester I. Vitek, Michael P. Ferreira, Adriana Proceedings of the National Academy of Sciences Tau is essential to β-amyloid-induced neurotoxicity Multidisciplinary |
| author_sort |
rapoport, mark |
| spelling |
Rapoport, Mark Dawson, Hana N. Binder, Lester I. Vitek, Michael P. Ferreira, Adriana 0027-8424 1091-6490 Proceedings of the National Academy of Sciences Multidisciplinary http://dx.doi.org/10.1073/pnas.092136199 <jats:p>Senile plaques and neurofibrillary tangles, the two hallmark lesions of Alzheimer's disease, are the results of the pathological deposition of proteins normally present throughout the brain. Senile plaques are extracellular deposits of fibrillar β-amyloid peptide (Aβ); neurofibrillary tangles represent intracellular bundles of self-assembled hyperphosphorylated tau proteins. Although these two lesions are often present in the same brain areas, a mechanistic link between them has yet to be established. In the present study, we analyzed whether tau plays a key role in fibrillar Aβ-induced neurite degeneration in central neurons. Cultured hippocampal neurons obtained from wild-type, tau knockout, and human tau transgenic mice were treated with fibrillar Aβ. Morphological analysis indicated that neurons expressing either mouse or human tau proteins degenerated in the presence of Aβ. On the other hand, tau-depleted neurons showed no signs of degeneration in the presence of Aβ. These results provide direct evidence supporting a key role for tau in the mechanisms leading to Aβ-induced neurodegeneration in the central nervous system. In addition, the analysis of the composition of the cytoskeleton of tau-depleted neurons suggested that the formation of more dynamic microtubules might confer resistance to Aβ-mediated neurodegeneration.</jats:p> Tau is essential to β-amyloid-induced neurotoxicity Proceedings of the National Academy of Sciences |
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Proceedings of the National Academy of Sciences, 2002 |
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| title |
Tau is essential to β-amyloid-induced neurotoxicity |
| title_unstemmed |
Tau is essential to β-amyloid-induced neurotoxicity |
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Tau is essential to β-amyloid-induced neurotoxicity |
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Tau is essential to β-amyloid-induced neurotoxicity |
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Tau is essential to β-amyloid-induced neurotoxicity |
| title_short |
Tau is essential to β-amyloid-induced neurotoxicity |
| title_sort |
tau is essential to β-amyloid-induced neurotoxicity |
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Multidisciplinary |
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http://dx.doi.org/10.1073/pnas.092136199 |
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2002 |
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<jats:p>Senile plaques and neurofibrillary tangles, the two hallmark lesions of Alzheimer's disease, are the results of the pathological deposition of proteins normally present throughout the brain. Senile plaques are extracellular deposits of fibrillar β-amyloid peptide (Aβ); neurofibrillary tangles represent intracellular bundles of self-assembled hyperphosphorylated tau proteins. Although these two lesions are often present in the same brain areas, a mechanistic link between them has yet to be established. In the present study, we analyzed whether tau plays a key role in fibrillar Aβ-induced neurite degeneration in central neurons. Cultured hippocampal neurons obtained from wild-type, tau knockout, and human tau transgenic mice were treated with fibrillar Aβ. Morphological analysis indicated that neurons expressing either mouse or human tau proteins degenerated in the presence of Aβ. On the other hand, tau-depleted neurons showed no signs of degeneration in the presence of Aβ. These results provide direct evidence supporting a key role for tau in the mechanisms leading to Aβ-induced neurodegeneration in the central nervous system. In addition, the analysis of the composition of the cytoskeleton of tau-depleted neurons suggested that the formation of more dynamic microtubules might confer resistance to Aβ-mediated neurodegeneration.</jats:p> |
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| author | Rapoport, Mark, Dawson, Hana N., Binder, Lester I., Vitek, Michael P., Ferreira, Adriana |
| author_facet | Rapoport, Mark, Dawson, Hana N., Binder, Lester I., Vitek, Michael P., Ferreira, Adriana, Rapoport, Mark, Dawson, Hana N., Binder, Lester I., Vitek, Michael P., Ferreira, Adriana |
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| description | <jats:p>Senile plaques and neurofibrillary tangles, the two hallmark lesions of Alzheimer's disease, are the results of the pathological deposition of proteins normally present throughout the brain. Senile plaques are extracellular deposits of fibrillar β-amyloid peptide (Aβ); neurofibrillary tangles represent intracellular bundles of self-assembled hyperphosphorylated tau proteins. Although these two lesions are often present in the same brain areas, a mechanistic link between them has yet to be established. In the present study, we analyzed whether tau plays a key role in fibrillar Aβ-induced neurite degeneration in central neurons. Cultured hippocampal neurons obtained from wild-type, tau knockout, and human tau transgenic mice were treated with fibrillar Aβ. Morphological analysis indicated that neurons expressing either mouse or human tau proteins degenerated in the presence of Aβ. On the other hand, tau-depleted neurons showed no signs of degeneration in the presence of Aβ. These results provide direct evidence supporting a key role for tau in the mechanisms leading to Aβ-induced neurodegeneration in the central nervous system. In addition, the analysis of the composition of the cytoskeleton of tau-depleted neurons suggested that the formation of more dynamic microtubules might confer resistance to Aβ-mediated neurodegeneration.</jats:p> |
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| institution | DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3 |
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| spelling | Rapoport, Mark Dawson, Hana N. Binder, Lester I. Vitek, Michael P. Ferreira, Adriana 0027-8424 1091-6490 Proceedings of the National Academy of Sciences Multidisciplinary http://dx.doi.org/10.1073/pnas.092136199 <jats:p>Senile plaques and neurofibrillary tangles, the two hallmark lesions of Alzheimer's disease, are the results of the pathological deposition of proteins normally present throughout the brain. Senile plaques are extracellular deposits of fibrillar β-amyloid peptide (Aβ); neurofibrillary tangles represent intracellular bundles of self-assembled hyperphosphorylated tau proteins. Although these two lesions are often present in the same brain areas, a mechanistic link between them has yet to be established. In the present study, we analyzed whether tau plays a key role in fibrillar Aβ-induced neurite degeneration in central neurons. Cultured hippocampal neurons obtained from wild-type, tau knockout, and human tau transgenic mice were treated with fibrillar Aβ. Morphological analysis indicated that neurons expressing either mouse or human tau proteins degenerated in the presence of Aβ. On the other hand, tau-depleted neurons showed no signs of degeneration in the presence of Aβ. These results provide direct evidence supporting a key role for tau in the mechanisms leading to Aβ-induced neurodegeneration in the central nervous system. In addition, the analysis of the composition of the cytoskeleton of tau-depleted neurons suggested that the formation of more dynamic microtubules might confer resistance to Aβ-mediated neurodegeneration.</jats:p> Tau is essential to β-amyloid-induced neurotoxicity Proceedings of the National Academy of Sciences |
| spellingShingle | Rapoport, Mark, Dawson, Hana N., Binder, Lester I., Vitek, Michael P., Ferreira, Adriana, Proceedings of the National Academy of Sciences, Tau is essential to β-amyloid-induced neurotoxicity, Multidisciplinary |
| title | Tau is essential to β-amyloid-induced neurotoxicity |
| title_full | Tau is essential to β-amyloid-induced neurotoxicity |
| title_fullStr | Tau is essential to β-amyloid-induced neurotoxicity |
| title_full_unstemmed | Tau is essential to β-amyloid-induced neurotoxicity |
| title_short | Tau is essential to β-amyloid-induced neurotoxicity |
| title_sort | tau is essential to β-amyloid-induced neurotoxicity |
| title_unstemmed | Tau is essential to β-amyloid-induced neurotoxicity |
| topic | Multidisciplinary |
| url | http://dx.doi.org/10.1073/pnas.092136199 |