The Exceptional Vulnerability of Humans to Alzheimer’s Disease
Like many humans, non-human primates deposit copious misfolded Aβ protein in the brain as they age. Nevertheless, the complete behavioral and pathologic phenotype of Alzheimer’s disease, including Aβ plaques, neurofibrillary (tau) tangles, and dementia, has not yet been identified in a non-human spe...
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| Veröffentlicht in: | Trends in molecular medicine 2017-06, Vol.23 (6), p.534-545 |
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| creator | Walker, Lary C Jucker, Mathias |
| description | Like many humans, non-human primates deposit copious misfolded Aβ protein in the brain as they age. Nevertheless, the complete behavioral and pathologic phenotype of Alzheimer’s disease, including Aβ plaques, neurofibrillary (tau) tangles, and dementia, has not yet been identified in a non-human species. Recent research suggests that the crucial link between Aβ aggregation and tauopathy is somehow disengaged in aged monkeys. Understanding why Alzheimer’s disease fails to develop in species that are biologically proximal to humans could disclose new therapeutic targets in the chain of events leading to neurodegeneration and dementia. |
| doi_str_mv | 10.1016/j.molmed.2017.04.001 |
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| ispartof | Trends in molecular medicine, 2017-06, Vol.23 (6), p.534-545 |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | aging Alzheimer Disease - drug therapy Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer Disease - physiopathology amyloid Amyloid beta-Peptides - metabolism Animals dementia Humans neurodegeneration non-human primate Pathology prion proteopathy seeding Species Specificity tau |
| title | The Exceptional Vulnerability of Humans to Alzheimer’s Disease |
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